Journal of Integrative Neuroscience

Published by World Scientific Publishing
Print ISSN: 0219-6352
Publications
Sensing and perceiving involve enormous numbers of widely distributed dendritic and action potentials in cortex, before, during and after stimulus arrival but with differing spatiotemporal patterns. Stimulus-activated receptors drive cortical neurons directly (olfactory) or indirectly through thalamocortical relays. The driven activity induces hemisphere-wide, self-organized patterns of neural activity called wave packets. Three levels of brain function are hypothesized to mediate transition from sensation and perception. Microscopic activity expressed by action potentials is sensory. Macroscopic activity of the whole forebrain expressed by behavior is perceptual. Mesoscopic activity bridges the gap by the formation of wave packets. They form when sensory input destabilizes the primary receiving areas by local state transitions. The sensory-driven action potentials condense into mesoscopic wave packets like molecules forming raindrops from vapor. The condensation disks sustain 2D spatial patterns of phase and amplitude of carrier waves in the beta and gamma EEG. The AM patterns correlate not with features but with the context and value of sensory stimuli for the subjects, in a word, their meaning. The wave packets from all sensory areas are broadly transmitted through the forebrain. They induce the formation of macroscopic patterns that coalesce like scintillating pools over much and perhaps all of each hemisphere. The prediction is made for clinical testing that wave packets are precursor to states of awareness. They are not by themselves accessible to experience, as may be the macroscopic states initiated by global state transitions.
 
The opioidergic hypothesis suggests an association between genetic variations at the opioid receptor mu 1 (OPRM1) gene locus and opiate addiction. The OPRM1 gene, which encodes for mu opioid receptor, contains several single nucleotide polymorphisms (SNPs) in exon I. Two of these, C17T and A118G, have been reported to be associated with substance abuse. The present study aims to delineate the frequency of these variants in the subjects of Indian origin and study their association with the phenotype of opioid dependence. A118G (rs 1799971) and C17T (rs 1799972) were genotyped using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. For 118G allele, the control subjects (n = 156) showed a frequency of 0.12 while the opioid dependents (n = 126) had an approximately 2.5-fold higher frequency of 0.31 (Odds Ratio 3.501; CI(95%) 2.212-5.555; p < 0.0001). For C17T polymorphism, the controls (n = 57) showed a frequency of 0.89 for C allele versus 0.83 seen in dependents (n = 123; odds ratio of 0.555; CI(95%) 0.264-1.147; p = 0.121). A significant association was observed between the 118G allele and no association was seen with C17T polymorphism and opioid dependence.
 
Upper graph shows target ERP components recorded at Fz during the auditory oddball paradigm. Arrow indicates reduced N2 amplitude in the ELS-exposed (red) group. Lower graph shows posterior (Pz) EEG power spectra recorded during the eyes closed paradigm. Arrow indicates that the ELS-exposed group show significantly reduced low frequency EEG power compared to subjects with no ELS exposure. 
Early Life Stress (ELS) has been associated with a range of adverse outcomes in adults, including abnormalities in electrical brain activity [1], personality dimensions [40], increased vulnerability to substance abuse and depression [14]. The present study seeks to quantify these proposed effects in a large sample of non-clinical subjects. Data for the study was obtained from The Brain Resource International Database (six laboratories: two in USA, two in Europe, two in Australia). This study analyzed scalp electrophysiological data (EEG eyes open, closed and target auditory oddball data) and personality (NEO-FFI), history of addictive substance use and ELS) data that was acquired from 740 healthy volunteers. The ELS measures were collected via a self-report measure and covered a broad range of events from childhood sexual and physical abuse, to first-hand experience of traumatizing accidents and sustained domestic conflict [41]. Analysis of covariance, controlling for age and gender, compared EEG data from subjects exposed to ELS with those who were unexposed. ELS was associated with significantly decreased power across the EEG spectrum. The between group differences were strongest in the eyes closed paradigm, where subjects who experienced ELS showed significantly reduced beta (F1,405=12.37, p=.000), theta (F1,405=20.48, p=.000), alpha (F1,405=9.65, p=.002) and delta power (F1,450=36.22, p=.000). ELS exposed subjects also showed a significantly higher alpha peak frequency (F1,405=6.39, p=.012) in the eyes closed paradigm. Analysis of covariance on ERP components revealed that subjects who experienced ELS had significantly decreased N2 amplitude (F1,405=7.73, p=.006). Analyses of variance conducted on measures of personality revealed that subjects who experienced ELS had significantly higher levels of neuroticism (F1,264=13.39, p=.000) and openness (F1,264=17.11, p=.000), but lower levels of conscientiousness, than controls (F1,264=4.08, p=.044). The number of ELS events experienced was shown to be a significant predictor of scores on the DASS questionnaire [27], which rates subjects on symptoms of depression (F3,688=16.44, p=.000, R2=.07), anxiety (F3,688=14.32, p=.000, R2=.06) and stress (F3,688=20.02, p=.000, R2=.08). Each additional early life stressor was associated with an increase in these scores independent of age, gender and the type of stressor. Furthermore, the number of ELS experiences among smokers was also found to be a positive predictor of the nicotine dependency score (Faegstrom Test For Nicotine Dependence, [19]) (F3,104=10.99, p=.000, R2=.24), independent of age, gender and type of stressor. In conclusion, we highlight the impact of a history of ELS showed significant effects on brain function (EEG and ERP activity), personality dimensions and nicotine dependence.
 
Drug addiction is an important social problem in many countries. Genetic and environmental factors contribute to the predisposition of drug addiction. Genetic variations at the μ opioid receptor (OPRM1) gene locus have been associated with opiate addiction. The present study aims to delineate the frequency of A118G allele of OPRM1 among Malaysian subjects. The frequency of A allele and G allele were 51% and 49%, respectively for addicts and about 73% and 27% respectively for healthy volunteers. The frequency of G allele was 1.77-fold higher in addicts by odds ratio calculation at 95% Cl, which indicate the G allele to be strongly associated with addiction X(2) = 15.31,P < 0.0001; odds ratio 2.51; 95% Cl (1.575-3.994), compared to healthy volunteers. A significant association was observed between A118G polymorphism in μ opioid receptor gene and drug addiction.
 
Electrotonic potentials allow the accommodative processes to polarizing stimuli to be assessed. Electrotonic potential transients in response to applied polarizing stimuli are caused by the kinetics of underlying axonal conductances. Here, we study these transients using our multi-layered model of the human motor nerve, in three simulated cases of the motor neuron disease amyotrophic lateral sclerosis (ALS): ALS1, ALS2 and ALS3 are three consecutively greater degrees of uniform axonal dysfunctions along the human motor nerve fibre. The results show that the responses in the ALS1 case are quite similar to the normal case. In contrast, in the ALS2 and ALS3 cases, long-lasting (100 ms) subthreshold depolarizing stimuli activate the classical "transient" Na(+) channels in the nodal and in the internodal axolemma beneath the myelin sheath; this leads to action potential generation during the early parts of the electrotonic responses in all compartments along the fibre length. The results also show that the electrotonic potentials in response to long-lasting (100 ms) subthreshold hyperpolarizing stimuli in the ALS1 and ALS2 cases are quiet similar to those of the normal case. However, the current kinetics in the ALS3 case differs from the normal case after the termination of the long-lasting hyperpolarizing stimuli. In the most abnormal ALS3 case, the activation of the Na(+) channels in the nodal and in the internodal axolemma leads to repetitive action potential generation in the late parts (100-200 ms) of the hyperpolarizing electrotonic responses. The results show that the repetitive firing, due to the progressively increased nodal and internodal ion channel dysfunction, are consistent with the loss of functional potassium channels involving both the fast and the slow potassium channel types. The results confirm that the electrotonic potentials in the three simulated ALS cases are specific indicators for the motor neuron disease ALS. The mechanisms underlying the simulated ALS are also discussed.
 
This study provides numerical simulations of some of the abnormalities in the potentials and axonal excitability indices of human motor nerve fibers in simulated cases of internodal, paranodal and simultaneously of paranodal internodal demyelinations, each of them systematic or focal. A 70% reduction of the myelin lamellae (defining internodal demyelination), or of the paranodal seal resistance (defining paranodal demyelination), or simultaneously both of them (defining paranodal internodal demyelination) was uniform along the fiber length for the systematically demyelinated subtypes. These permutations were termed internodal systematic demyelination (ISD), paranodal systematic demyelination (PSD) and paranodal internodal systematic demyelination (PISD). In other tests, the same reductions of the myelin sheath parameters were used but restricted to only three (8th, 9th and 10th) consecutive internodes. Such fiber demyelinations were termed internodal focal demyelination (IFD), paranodal focal demyelination (PFD) and paranodal internodal focal demyelination (PIFD). The computations used our previous double cable model of the fibers. The axon model was comprised of 30 nodes and 29 internodes. The 70% reduction value was not sufficient to develop conduction block in all investigated demyelinations, which were regarded as mild. The membrane property abnormalities obtained in the ISD, PSD and PISD cases were quite different and abnormally greater than those in the IFD, PFD and PIFD cases. The changes in the excitability indices such as strength-duration time constants, rheobasic currents and recovery cycles in the focally demyelinated subtypes were so slight as to be essentially indistinguishable from normal values. Consequently, the excitability based approaches that have shown strong potential as diagnostic tools in systematically demyelinated conditions may not be useful in detecting mild focal demyelinations. The membrane property changes simulated in the systematically demyelinated subtypes are in good accordance with the data from patients with Charcot-Marie-Tooth disease type 1A (CMT1A) and chronic inflammatory demyelinating polyneuropathy (CIDP). The excitability abnormalities obtained in each focally demyelinated subtype match those observed in vivo in patients with demyelinating forms of Guillain-Barré syndrome (GBS). The results indicate that the model that was used is a rather promising tool in studying the membrane property abnormalities of hereditary, chronic and acquired demyelinating neuropathies, which up till now, have not been sufficiently well understood.
 
The present study investigates action potential abnormalities obtained in simulated cases of three progressively greater degrees of uniform axonal dysfunctions. The kinetics of the currents, defining the action potential propagation through the human motor nerve in the normal and abnormal cases, are also given and discussed. These computations use our previous multi-layered model of the myelinated motor axon, without taking into account the aqueous layers within the myelin sheath. The results show that the classical "transient" Na(+) current contributes mainly to the action potential generation in the nodal segments, as the contribution of the nodal fast and slow potassium currents to the total nodal ionic current is negligible. However, the ionic channels beneath the myelin sheath are insensitive to the short-lasting current stimuli and do not contribute to action potential generation in the internodal compartments along the fibre length. The slight changes obtained in the currents underlying the generated action potentials in the three amylotropic lateral sclerosis cases are consistent with the effect of uniform axonal dysfunction along the fibre length. Nevertheless that the uniform axonal dysfunction progressively increases in the nodal and internodal segments of each next simulated amylotropic lateral sclerosis case, the action potentials cannot be regarded as definitive indicators for the progressive degrees of this disease.
 
Epilepsy is a serious neurodegenerative disorder with a high incidence and a variety of presentations and causes. Studies on brain from various animal models including chronic models: Genetic Absence Epilepsy Rats from Strasbourg (GAERS) are very useful for understanding the fundamental mechanisms associated with human epilepsy. Individual regions of the brain have different protein composition in different conditions. Therefore, proteomic analyses of the brain compartments are preferred for the development of new therapeutic targets in different pathophysiological conditions like neurodegenerative disorders. In this study, we describe a proteomic profiling of membrane fraction of cortex tissue from epileptic GAERS and non-epileptic Wistar rat brain by two-dimensional gel electrophoresis coupled with matrix-assisted laser desorption/ionization mass spectroscopy. Comparing the optical density of spots between groups, we found that one protein expression was significantly down-regulated (guanine nucleotide-binding protein G(I)/G(S)/G(T) subunit beta-1) and one protein expression was significantly up-regulated (14-3-3 protein epsilon isoform) in GAERS group. Our results indicate that these proteins might have played a significant role in epilepsy and may be considered as valuable therapeutic targets in the absence of epilepsy.
 
The review deals with the morphology, physiology, topography, and central projections of direction-selective cells of the accessory optic system in vertebrates.
 
Mean constant error (± SD) in the rigid support conditions. First, control session (RS1) — open circles and the second, final session (RS2) — solid diamond. The area within the dotted lines indicates the range of sufficiently accurate performance (± 2.5 @BULLET ). Subjects' data were ordered and displayed according to increases in the mean error in RS1 condition.  
Mean constant error (± SD) of elbow matching (the large reference elbow angles-circle, small angles-square) in three experimental conditions. The area within the dotted lines indicates the range of sufficiently accurate performance (± 2.5 • ).
The percentage of trials where the absolute errors are identified as a higher score. Note that the absolute error was higher in the HS condition (gray part of HS column) even if the elbow backward motion was similar (less then 7 cm) in HS and LS.  
The aim of the present work was to determine if the elbow joint instability and translatory movements during elbow flexion lead to significant errors in elbow angle perception. The matching elbow was fixed on a rocking platform of two different heights so that the elbow flexion was associated with tilting movement of the support and the angle/torque relationship changed depending on the height of the platform. The matching on any of the rocking supports did not cause an over-flexion constant error but it did increase the error variance, especially in the high rocking support condition. An adaptation to the rocking support condition was revealed by an after-effect resulting in an overestimation of the reference angle in the final testing on a rigid support. It is concluded that the elbow angle perception is modified as a result of adaptation to the rocking support, which is associated with recalibration of position sense during the experimental session. The results are consistent with the hypothesis that the estimation of the elbow joint angle depends on the internal representation of the arm's dynamics.
 
In this study, we evaluated the acute effects of central NAC administration on baroreflex in juvenile SHR and Wistar Kyoto (WKY) rats. Male SHR and WKY rats (8-10 weeks old) were implanted with a stainless steel guide cannula into the fourth cerebral ventricle (4th V). The femoral artery and vein were cannulated for mean arterial pressure (MAP) and heart rate (HR) measurement and drug infusion, respectively. After basal MAP and HR recordings, the baroreflex was tested with a pressor dose of phenylephrine (PHE, 8 μg/kg, bolus) and a depressor dose of sodium nitroprusside (SNP, 50 μg/kg, bolus). Baroreflex was evaluated before, 5, 15, 30 and 60 minutes after NAC injection into the 4th V. Vehicle treatment did not change baroreflex responses in WKY and SHR. Central NAC slightly but significantly increased basal HR at 15 minutes and significantly reduced PHE-induced increase in MAP 30 and 60 minutes after NAC injection (p < 0.05) in WKY rats. In relation to SHR, NAC decreased HR range 15 and 30 minutes after its administration. In conclusion, acute NAC into the 4th V does not improve baroreflex in juvenile SHR.
 
A schematic illustration of a dendrite of diameter d( μ m) studded with clusters or hot- spots of Na + ionic channels. Each hot-spot reflects the notion of I Na representing a point source of 
The attenuation of passive bAPs measured at three distinct locations mediated by an input functional representation of an action potential at the point x = 0 (denoting a point close to the soma) with varying leakage conductance values: (i) Rm = 500 Ωcm 2 , (ii) Rm = 1000 Ωcm 2 , (iii) Rm = 5000 Ωcm 2 , and (iv) Rm = 10000 Ωcm 2. The following other parameters were used: R i = 70 Ωcm, Cm = 1 µF/cm 2 and d = 4 µm. Note the change in time scales as a result of the non-constant Rm. The abscissa is time in msec, and the ordinate is voltage in mV.
The attenuation of active bAPs measured at 91, 182 and 267 µm from the location of the activated action potential mediated by Na + hot-spots distributed: (a) near the x = 0 region (up to 27 µm from the location of the input site), and (b) uniformly for 267 µm from the location of the input site. The number of hot-spots is assumed to be N = 10 in each case, together the following parameters were used: R i = 70 Ωcm, Cm = 1 µF/cm 2 and Rm = 500 Ωcm 2 , d = 4µm, λ = 0.0267 cm, g Na = 0.143 µS/cm, and the value of g Na was based on the number of sodium channels per hot-spot of N * = 10/πd. The abscissa is time in msec, and the ordinate is voltage in mV.
The attenuation of active bAPs measured at 91, 182 and 267 µm from the location of the input site mediated by Na + hot-spots distributed uniformly for three different numbers of hot-spots: (a) N = 5, (c) N = 20 (d) N = 40. The abscissa is time in msec, and the ordinate is voltage in mV. The same parameters as those in Fig. 4 are used. In (b) the nonlinear functional f[Vo(λ, t)]G(x, λ; t) is shown representing the integrand in the convolution integral of the first-order perturbation. Note that in (b) the ordinate has dimension of µV.
The attenuation of active bAPs measured at 91, 182 and 267 µm from the location of the input site mediated by Na + hot-spots distributed uniformly with varying densities. The number of Na + channels per hot-spot is assumed to be equal with (a) Na * = 6/πd (i.e. g Na = 0.0858 µS/cm), (b) Na * = 12/πd (i.e., g Na = 0.1716 µS/cm), (c) Na * = 24/πd (i.e. g Na = 0.2288 µS/cm), and (d) Na * = 36/πd (i.e., g Na = 0.2860 µS/cm). The abscissa is time in msec, and the ordinate is voltage is mV. The same parameters are used as in Fig. 4, but the number of hot-spots is N = 5.
Hodgkin and Huxley's ionic theory of the nerve impulse embodies principles, applicable also to the impulses in vertebrate nerve fibers, as demonstrated by Bernhard Frankenhaeuser and Andrew Huxley 40 years ago. Frankenhaeuser and Huxley reformulated the classical Hodgkin-Huxley equations, in terms of electrodiffusion theory, and computed action potentials specifically for saltatory conduction in myelinated axons. In this paper, we obtain analytical solutions to the most difficult nonlinear partial differential equations in classical neurophysiology. We solve analytically the Frankenhaeuser-Huxley equations pertaining to a model of sparsely excitable, nonlinear dendrites with clusters of transiently activating, TTX-sensitive Na(+) channels, discretely distributed as point sources of inward current along a continuous (non-segmented) leaky cable structure. Each cluster or hot-spot, corresponding to a mesoscopic level description of Na(+) ion channels, includes known cumulative inactivation kinetics observed at the microscopic level. In such a third-order system, the 'recovery' variable is an electrogenic sodium-pump imbedded in the passive membrane, and the system is stabilized by the presence of a large leak conductance mediated by a composite number of ligand-gated channels permeable to monovalent cations Na(+) and K(+). In order to reproduce antidromic propagation and attenuation of action potentials, a nonlinear integral equation must be solved (in the presence of suprathreshold input, and a constant-field equation of electrodiffusion at each hot-spot with membrane gates controlling the flow of current). A perturbative expansion of the non-dimensional membrane potential (Phi) is used to obtain time-dependent analytical solutions, involving a voltage-dependent Na(+) activation (micro) and a state-dependent inactivation (eta) gating variables. It is shown that action potentials attenuate in amplitude in accordance with experimental findings, and that the spatial density distribution of transient Na(+) channels along a long dendrite contributes significantly to their discharge patterns. A major significance of the analytical modeling, in contrast to the computational modeling of backpropagating action potentials, is the provision of a continuous description of the voltage as a function of position, allowing for greater feasibility in developing large-scale biophysical neural networks, without the need for ad hoc computational modeling.
 
The basal ganglia system has been proposed as a possible neural substrate for action selection in the vertebrate brain. We describe a robotic implementation of a model of the basal ganglia and demonstrate the capacity of this system to generate adaptive switching between several acts when embedded in a robot that has to "survive" in a laboratory environment. A comparison between this brain-inspired selection mechanism and classical "winner-takes-all" selection highlights some adaptive properties specific to the model, such as avoidance of dithering and energy-saving. These properties derive, in part, from the capacity of simulated basal ganglia-thalamo-cortical loops to generate appropriate "behavioral persistence".
 
Among Esther Thelen's most important contributions to developmental theory is that there is no single factor that has priority in driving development. In this paper, we discuss how this notion influenced our research on perceptual-motor development. We show that multiple factors constrain perceptual-motor development, but that a relatively minor change in one of them may lead to significant changes in the observed perceptual-motor behavior.
 
Neurophysiological mechanisms of recognition of verbal and nonverbal stimuli have been studied. It was determined that subjects solved nonverbal tasks faster and more effectively with their left hands, while they used two strategies of recognition to solve verbal tasks (fast reactions with right and left hand). Analysis of spectral characteristics of EEG revealed that mechanisms of both anterior and posterior attention systems were simultaneously involved in the process of effective recognition of nonverbal stimuli and ineffective recognition of verbal stimuli. Analysis of the event-related potentials (ERPs) showed that ineffective recognition of verbal and nonverbal stimuli resulted in an increase in the amplitude of sensory components of ERPs (N1m, P1m), while effective recognition increased the amplitude of cognitive components of ERPs (P2m, P3m).
 
The non-classical, but frequently reported behavior of GABA(A) receptor-mediated excitation in mature CNS has long been regarded as a puzzle. We theorize that the function of cortical GABAergic interneurons, which might constitute a subsystem of brain's GABA interneurons, is their ability of switching from inhibitory action to excitatory action depending on the level of spatio-temporal activity in progress. From the perspective of a dynamical systems approach, such "excitatory" GABAergic responses may serve to temporarily invoke attractor-like memories when extensively activated by, for example, top-down signals as category information or attention, while an ongoing background state of GABA changes its action to inhibition, returning the dynamical nature of the memory structure back to attractor ruins.
 
The aim of this study was to extend our understanding of the "asynchrony" phenomenon by examining the existence of several additional differences in brain activity. The differences which were investigated were the difference between the left and right hemisphere processing, the anterior and posterior areas processing and the differences between the different stages of information processing. These differences could account as an additional explanation for word decoding failure among individuals with dyslexia. The research utilized behavioral and electrophysiological (ERP - Event Related Potentials) measures in skilled and dyslexic university students. The subjects performed a lexical decision task presented in the visual and auditory modalities. The dyslexics exhibited a larger processing time interval between the activation of the P2 and P3 components, between the left and right hemisphere and between posterior and anterior regions of the cortex. Disharmony of the dyslexic brain is suggested as a possible explanation for the dyslexia phenomenon.
 
SK channels are responsible for long-lasting hyperpolarization following action potential and contribute to the neuronal integration signal. This study evaluates the involvement of SK channels on learning and memory in rats, by comparing the effects of two SK channel blockers, i.e., apamin which recognizes SK2 and SK3 channels, and lei-Dab7 which binds SK2 channels only. lei-Dab7 totally competes and contests apamin binding on whole brain sections (IC(50): 11.4 nM). Using an olfactory associative task, intracerebroventricular blocker injections were tested on reference memory. Once the task was mastered with one odor pair, it was then tested with a new odor pair. Apamin (0.3 ng), injected before or after the acquisition session, improved new odor pair learning in a retention session 24 hours later, whereas lei-Dab7 (3 ng) did not significantly affect the mnesic processes. These results indicated that the blockage of SK channels by apamin facilitates consolidation on new odor associations; lei-Dab7, containing only SK2 subunits, remains without effect suggesting an involvement of SK3 channels in the modulation of the mnesic processes.
 
Significant increased coherences for the dyslexic vs. the control group for the different frequency bands. Red connections are from homologous pairs (equal right and left) and purple connections are unique right or left hemispheric increased coherences. All p values’s < 0 . 001. 
Significant correlations between dyslexia subscales and significant EEG coherences in the different EEG bands. Red = Delta Coherence; Orange = Theta Coherence; Light Blue = Alpha Coherence; Dark Blue = Beta Coherence. Thick lines represent significances of p < 0 . 001 and thin- ner lines of p < 0 . 05. Note the specific independent patterns for some of the patterns especially Articulation with a centro-temporal pattern but also the continuous involvement of the right temporal region for all measures. Also note the clear differences between the slow (Delta and Theta; Red and Orange) vs. higher (Alpha and Beta; Light and Dark Blue) EEG frequencies and the similarities between Delta/Theta and Alpha/Beta. 
QEEG and neuropsychological tests were used to investigate the underlying neural processes in dyslexia. A group of dyslexic children were compared with a matched control group from the Brain Resource International Database on measures of cognition and brain function (EEG and coherence). The dyslexic group showed increased slow activity (Delta and Theta) in the frontal and right temporal regions of the brain. Beta-1 was specifically increased at F7. EEG coherence was increased in the frontal, central and temporal regions for all frequency bands. There was a symmetric increase in coherence for the lower frequency bands (Delta and Theta) and a specific right-temporocentral increase in coherence for the higher frequency bands (Alpha and Beta). Significant correlations were observed between subtests such as Rapid Naming Letters, Articulation, Spelling and Phoneme Deletion and EEG coherence profiles. The results support the double-deficit theory of dyslexia and demonstrate that the differences between the dyslexia and control group might reflect compensatory mechanisms. INTEGRATIVE SIGNIFICANCE: These findings point to a potential compensatory mechanism of brain function in dyslexia and helps to separate real dysfunction in dyslexia from acquired compensatory mechanisms.
 
This article presents a novel method for activation detection in task-related functional magnetic resonance imaging (fMRI) based on the Empirical Mode Decomposition (EMD) algorithm. The basic concept stems mainly from the idea that the EMD performs well in isolating the imbedded stimulus from the activated Blood Oxygen Level Dependent (BOLD) signal. The power of the proposed method was compared with the General Linear Model (GLM), spatial Independent Component Analysis (ICA) and Region Growing (RG) methods on simulated and real datasets. Experimental results suggest an almost identical performance for the proposed method compared with the standard approach of fMRI signal detection (the GLM), which indicates that it is to become a viable alternative to fMRI analysis.
 
The paper presents a review of electrophysiological data which indicate the integrative mechanisms of information coded in the human and animal peripheral skin receptors. The activity of the skin sensory receptors was examined by applying various natural stimuli. It was revealed that numerous identical receptors respond to various stimuli (mechanical, temperature, and pain ones), but the spike patterns of these receptors were found to be specific for each stimulus. The description of characteristic structures of spike patterns in the cutaneous nerve fibers in response to five major modalities, namely: "touch", "pain", "vibration/breath", "cold", and "heat", is being presented. The recordings of the cutaneous physical state revealed a correlation between the patterns of spatiotemporal skin deformation and the receptors activity. A rheological state of the skin can be changed either in response to external temperature variation or by the sympathetic pilomotor activation. These results indicate that the skin sensory receptors activity may be considered as an integrative process. It depends not only on the receptors themselves, but also on the changes in the surrounding tissue and on the adaptive influence of the central nervous system. A new framework for the sensory channel system related to the skin is proposed on the basis of experimental results.
 
Vascular dementia is one of the most important causes that account for 20-40% of all dementia cases. The aim of this study was to investigate whether electroacupuncture can reduce behavior deficit and long-term potentiation (LTP) in vascular dementia. Here we used a middle cerebral artery occlusion (MCAo) technique to induce a vascular dementia model with additional electroacupuncture (EA) manipulation. Behaviors were impaired in animals with MCAo, and similar results were observed with long-term potentiation induction. MCAo decreased the expression of LTP from 180.4±14.9% to 112.5±18.3%, suggesting that cerebral ischemia could impair the hippocampal LTP. In addition, immunostaining results showed that the expressions of N-methyl-D-aspartate receptor subtype 1 (NR1) and transient receptor potential vanilloid subtype 1 (TRPV1) receptors were significantly increased in the hippocampal CA1 areas. Noticeably, these phenomena can be reversed by 2 Hz EA at Baihui acupoint (GV20) for six consecutive days. Our results support a rescue role of 2 Hz EA for MCAo-induced behavior and LTP impairment. These results also suggest that NMDAR1 and TRPV1 may be involved in this pathway.
 
Stress is any condition that seriously affects the balance of the organism physiologically and psychologically. Stress activates the hypothalamic-pituitary-adrenal (HPA) releasing glucocorticoid hormones that produce generalized effects on different body systems including the nervous system. This study aimed to investigate the effect of acute restraint stress (ARS) on cognitive performance by measuring spatial working memory in Y-maze, behavior (anxiety and exploratory behavior) in open field test, expression of synaptophysin and glial fibrillary acidic protein (GFAP) in the hippocampus by immunohistochemistry, dopaminergic receptors (D2) in the basal ganglia by gene expression and comparing the effect of ghrelin and quetiapine on the previous parameters. 36 adult male albino rats constituted the animal model of this work and have been divided into six groups: control group, control group exposed to ARS, quetiapine group, quetiapine group exposed to ARS, ghrelin group and ghrelin group exposed to ARS. We demonstrated more neuroprotective effect for quetiapine compared to ghrelin on stress response, anxiety behavior and working spatial memory impairment due to ARS.
 
The number of males and [females] and mean age (standard deviation) of participants according to age-grouping and diagnostic group. 
Mean P3a (a) amplitude and (b) latency topographies from the child and adolescent AD/HD-com, AD/HD-in and control groups along with significant univariate results; and (c) ERPs from over the CPz site displayed for the child and adolescent groups, with the arrow pointing to the P3a component.
The current study aimed to investigate whether children and adolescents diagnosed with Attention Deficit/Hyperactivity Disorder Predominantly Inattentive (AD/HD-in; Child n = 24, Adolescent n = 33) and Combined (AD/HD-com; Child n = 30, Adolescent n = 42) subtypes were more distractible than controls (Child n = 54; Adolescents n = 75), by assessing event-related potential (ERP), performance and peripheral arousal measures. All AD/HD groups displayed smaller amplitudes and/or shorter latencies of the P3a ERP component - thought to reflect involuntary attention switching - following task-deviant novel stimuli (checkerboard patterns) embedded in a Working Memory (WM) task. The P3a results suggested that both AD/HD-in and AD/HD-com subtypes ineffectively evaluate deviant stimuli and are hence more "distractible". These abnormalities were most pronounced over the central areas. AD/HD groups did not display any abnormalities in averaged heart rate over the WM task, a measure of peripheral arousal. They did display abnormalities in performance measures from the task, but these were unrelated to P3a abnormalities. AD/HD groups also displayed a number of deficits on Switching of Attention and Verbal Memory tasks, however, the pattern of abnormality mostly reflected general cognitive deficits rather than resulting from distraction.
 
It was explored if the speed with which an individual learns to deal with new environments and challenges can be predicted on the basis of his/her brain's response to irrelevant (repeating) and novel auditory stimuli. In this study, 26 subjects threw 30 light-weight balls at a target with and without vision-distorting goggles. The horizontal displacement from a bull's-eye target was measured and the rate and degree of adaptation were computed. The adaptation parameters were correlated with evoked and event-related potential (EP/ERP) measures of the subject's ability to suppress irrelevant information and respond to novel stimuli. Only a weak (or a trend to) correlation was found between the behavioral adaptation and some of the EP/ERP measures. The correlations were limited to EP parameters in the 100 to 200 ms post-stimulus range reflecting the ability to suppress irrelevant information. Thus we conclude that the speed with which an individual adapts to a new environment is at best weakly correlated with brain activity associated with stimulus memory and classification.
 
In this article, we establish a model to delineate the emergence of "self" in the brain making recourse to the theory of chaos. Self is considered as the subjective experience of a subject. As essential ingredients of subjective experiences, our model includes wakefulness, re-entry, attention, memory, and proto-experiences. The stability as stated by chaos theory can potentially describe the non-linear function of "self" as sensitive to initial conditions and can characterize it as underlying order from apparently random signals. Self-similarity is discussed as a latent menace of a pathological confusion between "self" and "others". Our test hypothesis is that (1) consciousness might have emerged and evolved from a primordial potential or proto-experience in matter, such as the physical attractions and repulsions experienced by electrons, and (2) "self" arises from chaotic dynamics, self-organization and selective mechanisms during ontogenesis, while emerging post-ontogenically as an adaptive pressure driven by both volume and synaptic-neural transmission and influencing the functional connectivity of neural nets (structure).
 
Mechanisms involved in the multiple biochemical interactions between adenosine A 1 , dopamine D 1 and NMDA receptors in the GABAergic dynorphinergic neuron. A cyclase, adeny- 
Long-lasting, activity-dependent changes in synaptic efficacy at excitatory synapses are critical for experience-dependent synaptic plasticity. Synaptic plasticity at excitatory synapses is determined both presynaptically by changes in the probability of neurotransmitter release, and postsynaptically by changes in the availability of functional postsynaptic glutamate receptors. Two kinds of synaptic plasticity have been described. In homosynaptic or Hebbian plasticity, the events responsible for synaptic strengthening occur at the same synapse as is being strengthened. Homosynaptic plasticity is activity-dependent and associative, because it associates the firing of a postsynaptic neuron with that of the presynaptic neuron. Heterosynaptic plasticity, on the other hand, is activity-independent and the synaptic strength is modified as a result of the firing of a third, modulatory neuron. It has been suggested that long-term changes in synaptic strength, which are associated with gene transcription, can only be induced with the involvement of heterosynaptic plasticity. The neuromodulator adenosine plays an elaborated pre- and postsynaptic control of glutamatergic neurotransmission. This paper reviews the evidence suggesting that in some striatal excitatory synapses, adenosine can provide the heterosynaptic-like modulation essential for stabilizing homosynaptic plasticity without the need of a "third, modulatory neuron".
 
This study demonstrates that the EEG phenotypes as described by Johnstone, Gunkelman & Lunt are identifiable EEG patterns with good inter-rater reliability. Furthermore, it was also demonstrated that these EEG phenotypes occurred in both ADHD subjects as well as healthy control subjects. The Frontal Slow and Slowed Alpha Peak Frequency and the Low Voltage EEG phenotype discriminated ADHD subjects best from controls (however the difference was not significant). The Frontal Slow group responded to a stimulant with a clinically relevant decreased number of false negative errors on the CPT. The Frontal Slow and Slowed Alpha Peak Frequency phenotypes have different etiologies as evidenced by the treatment response to stimulants. In previous research Slowed Alpha Peak Frequency has most likely erroneously shown up as a frontal theta sub-group. This implies that future research employing EEG measures in ADHD should avoid using traditional frequency bands, but dissociate Slowed Alpha Peak Frequency from frontal theta by taking the individual alpha peak frequency into account. Furthermore, the divergence from normal of the frequency bands pertaining to the various phenotypes is greater in the clinical group than in the controls. Investigating EEG phenotypes provides a promising new way to approach EEG data, explaining much of the variance in EEGs and thereby potentially leading to more specific prospective treatment outcomes.
 
There have been significant advances in understanding the neurobiology of Attention-Deficit/Hyperactivity Disorder (ADHD) and it is timely to examine the ability of biological and psychological markers to predict medication response in this disorder. We evaluated prediction of medication response in adolescent ADHD using neuropsychological testing and psychophysiological measures of central and autonomic function. Fifty ADHD adolescents participated in pre- and post-stimulant medication testing. Separately ranked performance in auditory oddball and visual Working Memory (WM) tasks determined 20 "responders" and 20 "non-responders" with 10 "neutrals" excluded from the discriminant function analyses (DFA). For both oddball and WM performance rankings, the two groups did not differ in age, sex, or handedness. However, responders did have higher levels of symptomatology than non-responders at baseline. Pre-stimulant medication psychophysiology variables were used as predictors in each DFA. Oddball performance correctly classified 85.0% of responders and 95.0% of non-responders. Better response was associated with increased resting beta power (left posteriorly), delayed oddball target N1 (frontally), decreased oddball target P2 (left posteriorly) and decreased WM distractor P3 (right frontally). Working memory performance classified 80.0% of responders and 90.0% of non-responders, with a broadly similar profile of psychophysiological predictors. These finding indicate the value of integrating neuropsychological and psychophysiological data in predicting medication response in ADHD.
 
A recently developed quantitative model of cortical activity is used that permits data comparison with experiment using a quantitative and standardized means. The model incorporates properties of neurophysiology including axonal transmission delays, synaptodendritic rates, range-dependent connectivities, excitatory and inhibitory neural populations, and intrathalamic, intracortical, corticocortical and corticothalamic pathways. This study tests the ability of the model to determine unique physiological properties in a number of different data sets varying in mean age and pathology. The model is used to fit individual electroencephalographic (EEG) spectra from post-traumatic stress disorder (PTSD), schizophrenia, first episode schizophrenia (FESz), attention deficit hyperactivity disorder (ADHD), and their age/sex matched controls. The results demonstrate that the model is able to distinguish each group in terms of a unique cluster of abnormal parameter deviations. The abnormal physiology inferred from these parameters is also consistent with known theoretical and experimental findings from each disorder. The model is also found to be sensitive to the effects of medication in the schizophrenia and FESz group, further supporting the validity of the model.
 
Electrophysiological and ultrastructural studies have demonstrated that gap junctions connect diverse types of neurons in the central nervous system, permitting direct electrical and metabolic coupling. A member of gap junction channel subunit connexin36 (Cx36), is probed for the location of cell-to-cell communication in the mammalian retina, where gap junction networks of major classes of neurons are present. We present an analysis of the expression and localization of Cx36 protein in adult Wistar rat retina, using a newly generated polyclonal antibody against a sequence in the predicted cytoplasmic loop of the Cx36 amino acid alignment, deduced from the cDNA sequence. The affinity-purified antibody, recognizing a single 36-kDa protein, consistently labeled discrete puncta of subcellular structures likely to be associated with gap junctions in the inner plexiform layer, and also cytoplasm within somata and dendrites of retinal amacrine and ganglion cells, following examination with various fixation protocols and double labeling immuno-fluorescence. These results provide that prominent cell-to-cell communication appears in mature excitatory neurons such as retinal ganglion cells, in addition to inhibitory amacrine cells, mediated by gap junctions in the adult retina.
 
Several effects of neonatal handling on brain and behavior have been reported. We investigated the effects of neonatal handling on behaviors that have been shown to be sexually dimorphic in rats using an open-field test. "Gender differences" were observed in locomotor activity, exploratory behavior and grooming in the handled group. However, clear gender differences in these behaviors were not observed in the non-handled group. Our findings show that brief daily handling sessions (~ 1 min) in the first 2 weeks of postnatal life increased locomotor activity and exploratory behavior, and that these effects were more pronounced in females. Moreover, many rats in the non-handling group exhibited an increase in defecation relative to the handling group during the 10-min observation period. This suggests that the non-handling group experienced more stress in response to the novel open-field arena, and that this resulted in the absence of gender differences. Notably, this anxiety-related response was attenuated by neonatal handling. Our study underscores the impact of brief neonatal handling on sexually dimorphic behaviors, and indicates that caution should be exercised in controlling for the effects of handling between experimental groups, particularly in neurotoxicological studies that evaluate gender differences.
 
Number of successful retrievals on testing sessions before and after TBI surgery. All the animals showed severe de¯cits in reaching and grasping single pellet at 2 weeks after the surgery. Rats in Groups A (mild CCI) and B (moderate CCI) showed gradual improvement over the course of the study, and the pellet retrievals approximately reached the pre-lesion baseline. While the rats in Groups C (severe CCI) and D (cortical resection) showed severe functional impairment of the right forelimbs in skilled reaching task at the end of the study, although spontaneous recovery was also recorded through the test sessions. Data are represented as mean AE SD (*p < 0:05 compared to the other groups).  
The aim of this study was to evaluate the validity of the model that could produce reproducible and persistent motor weakness and define the accurate tasks and testing parameters for longitudinal assessment of neurological deficits after traumatic brain injury (TBI). We compared the effects of two rat models that suffered different controlled cortical impact (CCI) injury, as well as extensive motor cortex resection model, on behavior recovery and brain morphology. Behavioral tests including the skilled reaching task, limb-use asymmetry test and the grasping test were employed to evaluate neurofunctional recovery from pre- to 12 weeks after the injury. The results demonstrated that all the rats in four groups showed spontaneous functional improvement with the past of time after surgery, especially in rats with mild and moderate CCI injury. At the end of the experiment, the animals' performance reached preoperative base lines on reaching task and limb-use asymmetry test in mild and moderate groups, while severe motor weakness could be observed in rats with severe CCI injury, as well as rats with extended motor cortex resection. Overall, the results of this study indicated that both models with severe CCI injury and extended resection of the motor cortex developed reproducible and long-lasting motor weakness, comparable in severity and duration and identified skilled reaching task, as well as limb-use asymmetry test, as sensitive assessments for slight neurological deficits after brain injury. This will help to provide the basis for further research of the processes after the TBI and development of novel therapies.
 
Mean performance of di®erent syntactic structures (oral and written comprehension combined). 
Oral sentence comprehension results. 
The current study explores sentence comprehension impairments among adults following moderate closed head injury. It was hypothesized that if the factor of syntactic complexity significantly affects sentence comprehension in these patients, it would testify to the existence of syntactic processing deficit along with working-memory problems. Thirty-six adults (18 closed head injury patients and 18 healthy controls matched in age, gender, and IQ) participated in the study. A picture-sentence matching task together with various tests for memory, language, and reading abilities were used to explore whether sentence comprehension impairments exist as a result of a deficit in syntactic processing or of working-memory dysfunction. Results indicate significant impairment in sentence comprehension among adults with closed head injury compared with their non-head-injured peers. Results also reveal that closed head injury patients demonstrate considerable decline in working memory, short-term memory, and semantic knowledge. Analysis of the results shows that memory impairment and syntactic complexity contribute significantly to sentence comprehension difficulties in closed head injury patients. At the same time, the presentation mode (spoken or written language) was found to have no effect on comprehension among adults with closed head injury, and their reading abilities appear to be relatively intact.
 
Configural processing is considered to be the hallmark of face expertise, which has been widely investigated by face global inversion (inversion effect) and local inversion (Thatcher effect). Using a passive detection task in which face stimuli are task-irrelevant, both the face inversion effect and the Thatcher effect on race perception of faces were investigated. We found that although the N170 inversion effect (enhanced and delayed N170 for inverted than upright condition) was similar across races of faces, Chinese participants showed a larger N170 Thatcher effect (enhanced N170 to Thatcherized faces than normal faces) for Mongoloid faces. The present data indicates the perceptual advantage of configural changes for in-group than out-group faces.
 
Exogenous catalase influences neural control of cardiovascular system; however, we do not know yet if its inhibition into the fourth cerebral ventricle (4(th) V) influences baroreflex regulation. We evaluated the effects of central catalase inhibition on baroreflex in conscious Wistar rats. We used males Wistar rats (320-370 g), which were implanted with a stainless steel guide cannula into 4(th) V. The femoral artery and vein were cannulated for mean arterial pressure (MAP) and heart rate (HR) measurement and drug infusion, respectively. After basal MAP and HR recordings, the baroreflex was tested with a pressor dose of phenylephrine (PHE, 8 μg/kg, bolus) and a depressor dose of sodium nitroprusside (SNP, 50 μg/kg, bolus). Baroreflex was evaluated before 5, 15, 30 and 60 minutes after 3-amino-1, 2, 4-triazole (ATZ, 0.001 g/100 μL) injection into the 4(th) V. Vehicle treatment did not change baroreflex responses. ATZ attenuated bradycardic peak and reduced HR range at 30 minutes. ATZ into the 4(th) V reduced bradycardic and tachycardic reflex responses to increase and decrease MAP, respectively (p<0.05) 30 minutes after its microinjection without significantly changing the basal MAP and HR. In conclusion, central catalase inhibition influenced the highest parasympathetic response to MAP increase in conscious Wistar rats without change baroreflex gain.
 
We employ computer simulations to explore the effect of different temporal patterns of afferent impulses on the evoked discharge of a model cerebellar Purkinje cell. We show that the frequency and temporal correlation of impulses across afferent fibers determines which of four regimes of discharge activity is evoked. In the uncorrelated, here Poissonian, case, (i) cell discharge is determined by the total stimulation rate and temporal patterns of discharge are the same for different combinations of afferent fiber number and mean impulse rate per fiber giving the same total stimulation. Alternatively, if temporal correlations are present in the stimulus, (ii) for stimulation frequencies of 4 to at least 64 Hz there is a narrow range of afferent fiber number for which every stimulus pulse (composed of a single impulse on each afferent fiber) evokes a single action potential. In this case cell discharge is frequency locked to the stimulus with a concomitant reduction in discharge variability. (iii) For lower fiber numbers and thus discharge frequencies lower than the locking frequency, the variability of cell discharge is typically independent of afferent impulse timing, whereas, (iv) at higher fiber numbers and thus higher discharge frequencies, the reverse is true. We conclude that in case (iii) the cell acts as an integrator and discharge is determined by the stimulation rate, whereas in case (iv) the cell acts as a coincidence detector and the timing of discharge is determined by the temporal pattern of afferent stimulation. We discuss our results in terms of their significance for neuronal activity at the network level and suggest that the reported effects of varying stimulus timing and afferent convergence can be expected to obtain also with other principal cell types within the central nervous system.
 
Studies exploring the endogenous mechanism that modulates locomotion in Cryptomys sp, a bathyergid of the subterranean hystricomorph African mole-rat species might contribute to the understanding of the interrelations between external variables and internal mechanisms that controls the diverse patterns of locomotion in mole-rats. It has been shown that environmental variables contribute to the inter-individual variations in the daily patterns of locomotion, however, it is not well known if endogenous mechanism such as M1 receptor that regulates locomotion in surface dwelling rodents could as well regulate locomotion in the subterranean dwelling rodent. The present study explores this issue in Cryptomys sp a subterranean African mole-rat species. Using both specific and non-specific antagonists and agonists of M1 receptor, we manipulated the centrally expressed M1 receptor activity and characterized the effects of such manipulations on locomotor activity of Cryptomys sp. Our results indicate that infusion of M1 receptor specific and non-specific antagonists into the left or right ventricle impaired translatory movements, resulting in the display of abnormal complex rotatory locomotion. Based on the findings of this study, we suggest that M1 receptor activity might be part of the endogenous mechanisms that regulate the locomotor activity of Cryptomys sp.
 
State transition diagram depicts the interactions in the pet zoo game. When the block representing an animal is “hungry” it has to be placed in a vicinity of a food block. The timer in the food block will be reset and the block will revive its full color. 
Observed repetitive and exploratory behavior by the tested autistic children expressed in percentage of time of the test duration. The data shows pronounced exploratory behavior by most of the children.
Number of social interactions per group for both games. The lighter bars show the number of social interactions by pet zoo game.
The ability of autistic children to learn by applying logical rules has been used widely in behavioral therapies for social training. We propose to teach social skills to autistic children through games that simultaneously stimulate social behavior and include recognition of elements of social interaction. For this purpose we created a multi-agent platform of interactive blocks, and we created appropriate games that require shared activities leading to a common goal. The games included perceiving and understanding elements of social behavior that non-autistic children can recognize. We argue that the importance of elements of social interaction such as perceiving interaction behaviors and assigning metaphoric meanings has been overlooked, and that they are very important in the social training of autistic children. Two games were compared by testing them with users. The first game focused only on the interaction between the agents and the other combined interaction between the agents and metaphoric meanings that are assigned to them. The results show that most of the children recognized the patterns of interaction as well as the metaphors when they were demonstrated through embodied agents and were included within games having features that engage the interest of this user group. The results also show the potential of the platform and the games to influence the social behavior of the children positively.
 
The cerebral blood flow values used in experimental and clinical investigations as the informative criteria for brain blood supply are often misleading. The correlation between the cerebral blood supply and brain function is not proven in all cases. An increase of brain activity is known to be accompanied by a rise of blood flow in activated regions, while a decreased activity results in a decreased blood flow. This demonstrates the close correlation between the brain blood supply and its activity. Such a correlation had not been noted in the age-dependent decrease of cerebral blood flow, suggesting the existence of special age-related mechanisms that develop with age to maintain brain metabolism. The biomechanical properties are of special significance as predicted in the early 20th century. Only recently were they validated by the simultaneous recording of Transcranial Dopplerogram and Rheoencephalogram with in-depth analysis focused on single cardiac cycles. Functioning of the intracranial blood and cerebrospinal fluid dynamics was integrated with a special physiological test "Prognosis-2" to measure brain cognitive function. Correlation was demonstrated with the circulatory-metabolic state of brain activity, especially in people with changing cognitive function. The data supports a conceptual model of adequate circulatory-metabolic supply of brain activity, showing the functional unity, which follows from integration of the mentioned systems.
 
Increasing age is the strongest risk factor for Alzheimer's disease (AD). Yet, departure from normal age-related decline for established markers of AD including memory, cognitive decline and brain function deficits, has not been quantified. We examined the cross-sectional estimates of the "rate of decline" in cognitive performance and psychophysiological measures of brain function over age in AD, preclinical (subjective memory complaint-SMC, Mild Cognitive Impairment-MCI) and healthy groups. Correlations between memory performance and indices of brain function were also conducted. The rate of cognitive decline increased between groups: AD showed advanced decline, and SMC/MCI groups represented intermediate stages of decline relative to normal aging expectations. In AD, advanced EEG alterations (excessive slow-wave/reduced fast-wave EEG, decreased working memory P450 component) were observed over age, which were coupled with memory decline. By contrast, MCI group showed less severe cognitive changes but specific decreases in the working memory N300 component and slow-wave (delta) EEG, associated with decline in memory. DISCUSSION AND INTEGRATIVE SIGNIFICANCE: While the cognitive data suggests a continuum of deterioration associated with increasing symptom severity across groups, integration with brain function measures points to possible distinct compensatory strategies in MCI and AD groups. An integrative approach offers the potential for objective markers of the critical turning point, with age as a potential factor, from mild memory problems to disease.
 
Electrophysiological data analysis.
This paper presents a small part of a larger interdisciplinary study that investigates brain activity (using event related potential methodology) of male adolescents when solving mathematical problems of different types. The study design links mathematics education research with neurocognitive studies. In this paper we performed a comparative analysis of brain activity associated with the translation from visual to symbolic representations of mathematical objects in algebra and geometry. Algebraic tasks require translation from graphical to symbolic representation of a function, whereas tasks in geometry require translation from a drawing of a geometric figure to a symbolic representation of its property. The findings demonstrate that electrical activity associated with the performance of geometrical tasks is stronger than that associated with solving algebraic tasks. Additionally, we found different scalp topography of the brain activity associated with algebraic and geometric tasks. Based on these results, we argue that problem solving in algebra and geometry is associated with different patterns of brain activity.
 
Computational morphological analysis comprises the development of measures (indicators) that describe different form attributes of a neuron and provides additional parameters for classification algorithms. Our work addressed the problem of small group sizes often encountered in neuromorphological and neurophysiological research, automated classification tasks (unsupervised learning) and introduced a new morphological measure: the wavelet statistical moment. We analysed cat alpha/Y, beta/X and delta Golgi-stained retinal ganglion cells using six different shape features (circularity, 2(nd) statistical moment and entropy of Gaussian blurred images, wavelet statistical moment, number of terminations and the fractal dimension). This allowed us to compare the sensitivity of the methods in uniquely describing morphological attributes of these cells.
 
Since their discovery in the late 19th century our conception of motoneurons has steadily evolved. Motoneurons share the same general function: they drive the contraction of muscle fibers and are the final common pathway, i.e., the seat of convergence of all the central and peripheral pathways involved in motricity. However, motoneurons innervate different types of muscular targets. Ordinary muscle fibers are subdivided into three main subtypes according to their structural and mechanical properties. Intrafusal muscle fibers located within spindles can elicit either a dynamic, or a static, action on the spindle sensory endings. No less than seven categories of motoneurons have thereby been identified on the basis of their innervation pattern. This functional diversity has hinted at a similar diversity in the inputs each motoneuron receives, as well as in the electrical, or cellular, properties of the motoneurons that match the properties of their muscle targets. The notion of the diverse properties of motoneurons has been well established by the work of many prominent neuroscientists. But in today's scientific literature, it tends to fade and motoneurons are often thought of as a homogenous group, which develop from a given population of precursor cells, and which express a common set of molecules. We first present here the historical milestones that led to the recognition of the functional diversity of motoneurons. We then review how the intrinsic electrical properties of motoneurons are precisely tuned in each category of motoneurons in order to produce an output that is adapted to the contractile properties of their specific targets.
 
The objective of this study is to investigate the relative contributions of maturation to the dynamic behavior of respiration during ontogeny in the neonate. The phrenic neurogram, an output of the respiratory network, was recorded during eupnea at three postnatal ages (3-7, 12-19, and 26-31 days) in decerebrate piglets. The inter-breath interval (IBI) time series were reconstructed from phrenic neurograms for each piglet and analyzed using the approximate entropy (ApEn) method. The mean values of the approximate entropy were high during the first seven days of the postnatal age [1.02 +/- 0.02 (standard error)] and decreased for the 12-19 days (0.67 +/- 0.008) and increased during subsequent maturation [the 26-31 days age group (0.92 +/- 0.015)]. The mean approximate entropy values for the 3-7 days age group was significantly different from those of the 12-19 days age groups (p < 0.05) using the nonparametric statistical test. The complexity values for the 3-7 days age group were slightly higher than those of the 26-31 days age group, but these differences were not statistically significant (p > 0.05). Therefore, these findings suggest that a decrease in the complexity values is unique to the 12-19 days age groups. This could be due to a reduction in the number of dendritic terminals per cell for the 12-19 days age groups. The results of these preliminary experiments also indicate that the behavior of the respiratory pattern generator in the neonate fluctuates during the early maturation period.
 
The proposed pathogenesis of OSA-related neurocognitive decline. The augmented neuroin°ammatory processes negatively a®ect the neuronal, glial and vascular endothelial cells (Kim et al. , 2006; Zhang et al. , 2000). The intermittent hypoxia and related oxidative challenge results in the NTS and hypoglossal nucleus in°ammation and dysfunction (Kaur et al. , 2011). This would cause diminished genioglossal tonicity and results in pharyngeal collapse (Boyd et al. , 2004; Svanborg, 2005). Snoring, apneas and resultant hypoxia will then arise. Therefore, sleep apnea-induced neuroin°ammation is considered as a key contributor to neuronal degeneration and provoked cognitive dysfunctions (Daulatzai, 2012; Grigg-Damberger & Ralls, 2012). Note : NTS: Nucleus Tractus Solitarius, OSA: Obstructive Sleep Apnea. 
(Color online) Brain mapping which represents respiratory-related microarousals. This short segment of sleep EEG is extracted from full-night PSG test in a patient with OSAS, showing a typical microarousal in stage 2 of NREM sleep (N2). The color-coded brain mapping images in the right panel are the QEEG maps using FFT to isolate beta-frequency intrusions during NREM sleep. Hot colors represent fast frequencies intruded into NREM sleep resulting in micro-arousals concurrently occurred with an apnea event. In NREM sleep, the EEG is generally dominated by alpha activity which is often interpreted as light sleep by the neural network. The left panel shows a 19-second EEG segment and the corresponding output during a microarousal event in this patient. The start and end of the event, as marked by an expert polysomnography scorer, are shown by vertical dashed lines. The wakefulness minus deep-sleep output [P(W) – P(S)] is approaching 1 (wakefulness) in many instances during the microarousal event (the red box). 
Main cognitive domains studied in OSAS and the related testing batteries. Studies have revealed that sustained attention and executive functions
The present review attempts to put together the available evidence and potential research paradigms at the interface of obstructive sleep apnea syndrome (OSAS), sleep micro- and macrostructure, cerebral vasoreactivity and cognitive neuroscience. Besides the significant health-related consequences of OSAS including hypertension, increased risk of cardio- and cerebrovascular events, notable neurocognitive lapses and excessive daytime somnolence are considered as potential burdens. The intermittent nocturnal hypoxia and hypercapnia which occur in OSAS are known to affect cerebral circulation and result in brain hypoperfusion. Arousal instability is then resulted from altered cyclic alternating patterns (CAPs) reflected in sleep EEG. In chronic state, some pathological loss of gray matter may be resulted from obstructive sleep apnea. This is proposed to be related to an upregulated proinflammatory state which may potentially result in apoptotic cell loss in the brain. On this basis, a pragmatic framework of the possible neural mechanisms which underpin obstructive sleep apnea-related neurcognitive decline has been discussed in this review. In addition, the impact of OSAS on cerebral autoregulation and sleep microstructure has been articulated.
 
Long-term potentiation (LTP) of synaptic transmission is a widely accepted model of learning and memory. In vitro brain slice techniques were used to investigate the effects of cortical-spreading depression and picrotoxin, an antagonist of the gamma-aminobutyric acid A (GABA(A)) receptor, on the tetanus-induced long-term potentiation of field excitatory postsynaptic potentials. Cortical-spreading depression is involved in glutamate desensitization; on the other hand, GABA(A) antagonists could increase postsynaptic excitability. This study shows that picrotoxin effectively induced long-term potentiation with 142.25 ± 4.18% of the baseline in the picrotoxin group (n = 8) versus 134.36 ± 2.35% of the baseline in the control group (n = 10). In group with picrotoxin applied to CSD, we obtained the smallest magnitude of LTP (120.15 ± 3.73% of the baseline, n = 8). These results suggest that picrotoxin could increase hippocampal activity and LTP; on the contrary, CSD reduced LTP magnitude. In addition, the results also suggest that the decay rate of post-tetanic potentiation has a direct relationship with LTP. Moreover, data were interpreted by nonlinear least squares quantifying, and LTP could also be quantified. The nonlinear attribute of LTP had an influence on the fitting, with respect to increasing the accuracy of the parameters and the compatibility of combination of stimuli that produce LTP.
 
Top-cited authors
Leanne M Williams
  • Stanford University
Evian Gordon
  • The Brain Resource Company
C. Richard Clark
  • Emeritus Professor
Nicholas James Cooper
  • University of Cambridge, Diabetes and Inflammation Laboratory
Martijn Arns
  • Brainclinics Foundation