Vasily Vorobyov

Cardiff University, Cardiff, Wales, United Kingdom

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Publications (25)99.14 Total impact

  • Vasily Vorobyov
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    ABSTRACT: An association of the detrimental effect of monocular deprivation on binocular vision with reduced reliability of neuronal responses in the primary visual cortex has been shown on randomly presented binocular stimuli [V. Vorobyov et al. (2007) Eur J Neurosci. 26(12), 3553-3563]. To examine this effect on biologically relevant signals, binocular gratings of varying relative phase disparity were presented in sequential order, simulating motion, to 55 cats with various types of daily visual experience. During sequential stimulation, the proportions of 'unstable' cells (with phase differences exceeding 22.5 ° between peak binocular responses in two consecutive trials) were similar in cats with exclusively binocular experience and with short periods of daily monocular vision (≤ 3.25 h), in mixed binocular-monocular conditions. In contrast, random stimulation was characterized by a significantly enlarged population of 'unstable' cells in the latter. After a longer period of monocular vision (6.5 h) or exclusively discordant binocular experience (strabismus), sequential stimulation was accompanied by a significant increase of this population, whereas during randomized stimulation it was very similar to that in cats with short periods of daily monocular vision. Finally, there were no differences in populations of 'unstable' cells in cats with long monocular or strabismic vision and those with exclusive monocular experience during sequential stimulation, in contrast with a significant increase in the latter during randomized stimulation. I propose that the detrimental effect of abnormal binocular experience on binocular processing in the primary visual cortex is associated with a disruption of the mechanisms involved in both discrimination of binocular disparity signals and evaluation of their temporal profiles.
    European Journal of Neuroscience 02/2013; · 3.75 Impact Factor
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    ABSTRACT: Monocular deprivation (MD) during a critical period of postnatal development produces significant changes in the anatomy and physiology of the visual cortex, and the deprived eye becomes amblyopic. Extracellular matrix molecules have a major role in restricting plasticity such that the ability to recover from MD decreases with age. Chondroitin sulfate proteoglycans (CSPGs) act as barriers to cell migration and axon growth. Previous studies showing that degradation of CSPGs by the bacterial enzyme chondroitinase can restore plasticity in the adult rat visual cortex suggest a potential treatment for amblyopia. Here MD was imposed in cats from the start of the critical period until 3.5 months of age. The deprived eye was reopened, the functional architecture of the visual cortex was assessed by optical imaging of intrinsic signals, and chondroitinase was injected into one hemisphere. Imaging was repeated 1 and 2 weeks postinjection, and visually evoked potentials (VEPs) and single-cell activity were recorded. Immunohistochemistry showed that digestion of CSPGs had been successful. After 2 weeks of binocular exposure, some recovery of deprived-eye responses occurred when chondroitinase had been injected into the hemisphere contralateral to that eye; when injected into the ipsilateral hemisphere, no recovery was seen. Deprived-eye VEPs were no larger in the injected hemisphere than in the opposite hemisphere. The small number of neurons dominated by the deprived eye exhibited poor tuning characteristics. These results suggest that despite structural effects of chondroitinase in adult cat V1, plasticity was not sufficiently restored to enable significant functional recovery of the deprived eye.
    Journal of Neuroscience 01/2013; 33(1):234-43. · 6.91 Impact Factor
  • Sajjida Jaffer, Vasily Vorobyov, Frank Sengpiel
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    ABSTRACT: Monocular deprivation (MD) by lid suture is one of the classic paradigms for the study of developmental plasticity in the cerebral cortex, and we have detailed knowledge of its anatomical and physiological consequences as well as underlying molecular and cellular mechanisms. However, the effects of other forms of manipulating visual input through one eye on the functional architecture of the primary visual cortex (V1) have not yet been examined directly. We compared MD by lid suture with the effects of daily monocular lens wear using either a frosted lens or a neutral density (ND) filter. We used optical imaging of intrinsic signals and visually evoked potentials (VEPs) to assess responses in V1 to monocular stimulation. We found that loss of stimulus contrast through monocular frosted lens wear resulted in marked takeover of cortical territory by the nondeprived eye (NDE) similar to that caused by classic MD, and in virtual absence of orientation-selective responses following stimulation of the deprived eye (DE). Furthermore, amplitudes of VEPs in response to gratings of a range of spatial frequencies were significantly reduced in the DE compared to the NDE. In contrast, differences in luminance between two eyes caused by an ND filter in front of one eye did not affect ocular dominance and orientation maps, and there was no significant difference in the amplitude of VEPs elicited through the two eyes. Our results are consistent with previous electrophysiological studies in demonstrating that binocular pattern information is necessary to maintain normal functional maps in both eyes, while reduced luminance in one eye has little effect on the overall functional architecture and visual responses in V1.
    Visual Neuroscience 08/2012; 29(4-5):247-53. · 1.48 Impact Factor
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    ABSTRACT: Although the basis of our knowledge of experience-dependent plasticity comes from studies on carnivores and primates, studies examining the physiological and molecular mechanisms that underlie development and plasticity have increasingly employed mice. We have used several common rearing paradigms, such as dark-rearing and monocular deprivation (MD), to examine the timing of the physiological and molecular changes to altered experience in the cat primary visual cortex. Dark-rearing from birth or for 1 week starting at 4 weeks of age produced a similar reduction in the amplitude of responses measured through intrinsic signal imaging and a reduction in orientation selectivity. One week of visual experience following dark-rearing until 4 weeks of age yielded normal responses in both amplitude and orientation selectivity. The depression of deprived-eye responses was similar in magnitude after 2 and 7 days of MD. In contrast, non-deprived-eye responses almost doubled in magnitude after 7 days compared with 2 days of MD. These changes in the functional properties of primary visual cortex neurons were mirrored by specific changes in synaptic protein expression. Changes in proteins such as the NR2A and NR2B subunits of the N-methyl-D-aspartate receptor, postsynaptic density protein 95, alpha-CA(2+) /calmodulin-dependent protein kinase II (αCaMKII), and GABA(A) α1a indicated that the levels of sensory activity regulated mechanisms associated with both excitatory (NR2A and NR2B) and inhibitory (GABA(A) α1a) transmission so as to maintain response homeostasis. Additionally, we found that MD regulated the AMPA receptor glutamate (GluR1) subunit as well as signalling molecules (αCaMKII and synaptic Ras GTPase activating protein, SynGAP) downstream of N-methyl-D-aspartate receptors. Proteins in a common signalling pathway appeared to have similar developmental expression profiles that were broadly similar between cats and rodents.
    European Journal of Neuroscience 04/2012; 35(8):1281-94. · 3.75 Impact Factor
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    ABSTRACT: To study the effects of acute and repeated injections of nootropics and to learn how glutamate receptors might be involved in their mediation, the frequency spectra of cortical and hippocampal electroencephalogram (EEG) were analyzed in non-narcotized rats subcutaneously injected repeatedly with Piracetam (400mg/kg) or its analogue, Noopept (0.2mg/kg), after intracerebroventricular infusions of saline (5 μl) or the antagonists of NMDA and quisqualate/AMPA receptors: CPP (0.1 nmol) and GDEE (1 μmol), respectively. Piracetam increased alpha/beta1 EEG activity in the left frontal cortex, and alpha activity in both the right cortex and hippocampus, with a 10-min latency and 40-min duration. Noopept increased alpha/beta1 activity, with 30-min latency and 40-min duration in all brain areas. CPP pretreatment eliminated Piracetam EEG effects; reduced Noopept effects in the cortex and completely suppressed them in the hippocampus. After four injections of Piracetam, EEG effects were very small in the cortex, and completely lacking in the hippocampus, while GDEE pretreatment partially recovered them. The effect of Noopept in the alpha/beta1 ranges was replaced by increased beta2 activity after the eighth injection, while no effects were observed after the ninth one. GDEE pretreatment restored the effect of Noopept in the beta2 frequency range. These results demonstrate similarities in EEG effects and their mediatory mechanisms for Piracetam and its much more effective analogue, Noopept. Activation of NMDA receptors is involved in the effects of a single injection of the nootropics, whereas activation of quisqualate/AMPA receptors is associated with the decrease in their efficacy after repeated use.
    Brain research bulletin 03/2011; 85(3-4):123-32. · 2.97 Impact Factor
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    ABSTRACT: To analyze mediatory mechanisms underlying attention-deficit hyperactivity disorder (ADHD) and their association with epilepsy, the electroencephalogram (EEG) responses to various centrally applied neurotransmitter agonists were studied in spontaneously hypertensive (SH), kainate-treated (KA), and normotensive (control) rats, with chronically implanted electrodes into the frontal cortex and hippocampus and a cannula into the lateral cerebral ventricle. In SH rats, the baseline EEG showed increased delta and beta2 activity in the hippocampus and decreased alpha/beta1 activity in both brain areas. In KA rats, these delta and alpha/beta1 effects were observed 2 weeks post-kainate, while the beta2 activity increase occurred after 5 weeks in the hippocampus and, to a greater extent, 9 weeks post-injection in both brain areas. In SH rats, NMDA increased delta and decreased alpha/beta1 activity, similar to KA rats 5 weeks post-injection. In SH rats, clonidine augmented theta/beta2 increase in the cortex and alpha suppression in both brain areas, in parallel with induction of beta2 activity in the hippocampus. These beta2 effects were observed 5 and 9 weeks post-kainate. In SH rats, baclofen produced robust delta/theta enhancement and alpha/beta1 suppression in both brain areas, with additional beta2 activity increase in the hippocampus, while muscimol was ineffective in both groups of rats. In KA rats, EEG responses to GABA agonists were similar to those in control. Our results demonstrate sensitization of NMDA receptors and α2-adrenoceptors both in SH and KA rats and that of GABAb receptors specifically in SH rats.
    Brain research 02/2011; 1383:154-68. · 2.46 Impact Factor
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    ABSTRACT: To compare the effects of repeated exposure to extremely low frequency-modulated microwaves (ELF-MW) on cortical and hypothalamic electroencephalograms (EEG). In 10 freely moving rats with carbon electrodes implanted into the cortex and dorsomedial hypothalamus, averaged frequency spectra (0.5-30 Hz) of the EEG were studied for five consecutive days either under sham exposures (five rats) or under mixed sham/MW-exposures (five rats). The rats were exposed to ELF-MW (915 MHz, 20-ms pulse duration, approximately 0.3 mW/cm(2), 4 Hz) intermittently (1-min 'On', 1-min 'Off') for 10 min (specific absorption rate, SAR, approximately 0.7 mW/g on average) several times per day, with 10-min pre- and post-exposure periods. In baseline EEG, the activities of 3.2-6.0 Hz and 17.8-30.5 Hz dominated in the cortex and of 6.0-17.8 Hz in the hypothalamus. This cortical-hypothalamic imbalance was relatively stable at sham-exposures and insensitive to ELF-MW in all frequency ranges but one. ELF-MW increased the beta(2) (17.8-30.5 Hz) level in the hypothalamus to a greater extent than in the cortex, causing significant diminishing of the initial EEG bias between them. Moreover, a cumulative phenomenon under repeated exposures to ELF-MW was revealed. These results are in line with evidence that repeated low-level exposure to ELF-MW affects brain functioning and provide an additional approach when analysing underlying mechanisms.
    International Journal of Radiation Biology 05/2010; 86(5):376-83. · 1.84 Impact Factor
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    ABSTRACT: To learn whether the low flux density combined magnetic field (CMF) can affect rats pretreated with a dopamine agonist, the frequency spectra of cortical and hippocampal EEG were studied after intraperitoneal injection of agroclavine (50 microg/kg, Day 1) either alone (N=5) or combined with 30-min exposure to CMF (B(AC)=50 microT, f(AC)=20.9Hz, B(DC)=27.3 microT) (N=5) an hour post-injection. The CMF caused an immediate and robust increase in the hippocampal beta(2) activity (22.5-30.5Hz) vs. its value in the pre-exposure period. This effect persisted during 30-min post-exposure period. After vehicle injection (0.1% ethanol) on Day 10, the beta(2) activity increased gradually during the exposure to CMF and was at the pre-exposure level during the post-exposure period. In two rats, pretreated with the vehicle on Day 1, CMF increased a hippocampal beta(2) level. The effect was about half the amplitude and shorter in duration than that after agroclavine, with no effects in the post-exposure period. However, during the 2nd exposure to CMF, started 30 min later, cortical and hippocampal beta activity was significantly greater than that during the 1st. On Day 10, the 1st exposure was completely ineffective, while during the 2nd, the hippocampal beta(2) activity was increased gradually. These results demonstrate that dopaminergic activation can potentiate CMF-evoked EEG effects in the hippocampal beta(2) frequency band.
    Brain research bulletin 07/2009; 80(1-2):1-8. · 2.97 Impact Factor
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    ABSTRACT: Visual activity after eye-opening influences feature map structure in primary visual cortex (V1). For instance, rearing cats in an environment of stripes of one orientation yields an over-representation of that orientation in V1. However, whether such changes also affect the higher-order statistics of orientation maps is unknown. A statistical bias of orientation maps in normally raised animals is that the probability of the angular difference in orientation preference between each pair of points in the cortex depends on the angle of the line joining those points relative to a fixed but arbitrary set of axes. Natural images show an analogous statistical bias; however, whether this drives the development of comparable structure in V1 is unknown. We examined these statistics for normal, stripe-reared and dark-reared cats, and found that the biases present were not consistently related to those present in the input, or to genetic relationships. We compared these results with two computational models of orientation map development, an analytical model and a Hebbian model. The analytical model failed to reproduce the experimentally observed statistics. In the Hebbian model, while orientation difference statistics could be strongly driven by the input, statistics similar to those seen in experimental maps arose only when symmetry breaking was allowed to occur spontaneously. These results suggest that these statistical biases of orientation maps arise primarily spontaneously, rather than being governed by either input statistics or genetic mechanisms.
    NeuroImage 05/2009; 47(1):157-72. · 6.25 Impact Factor
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    ABSTRACT: Prolonged viewing of an unchanging pattern causes adaptation, which can be demonstrated by visual aftereffects such as the tilt and waterfall illusions. In normal observers, these typically exhibit interocular transfer (IOT), being observed when the adapting and test stimuli are shown to different eyes. Convergence of inputs from both eyes upon binocular neurons only occurs in the primary visual cortex (V1), and adaptation is substantially a cortical phenomenon. However, little is known about a physiological substrate of IOT in V1 and how it relates to the binocularity of neurons and local ocular dominance (OD) column architecture. We employed optical imaging to obtain OD maps in cat V1 and recorded from single neurons at targeted penetration sites to quantify their adaptation by drifting gratings when adapter and test stimulus were presented either to the same or to the opposite eyes. In contrast to earlier reports, clear IOT of adaptation was observed for binocular as well as monocular neurons; at population level, its strength amounted to 55%. Moreover, the position of the cells with respect to OD column borders had no significant effect on the strength of IOT. IOT does not appear to strongly depend on conventional binocularity of neurons.
    Cerebral Cortex 12/2008; 19(8):1835-43. · 8.31 Impact Factor
  • Vasily Vorobyov, Frank Sengpiel
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    ABSTRACT: In the 6-hydroxydopamine (6-OHDA) rat model of Parkinson's disease (PD), the frequency spectra of EEG in the cortex and the striatum were studied following injection of the dopamine agonist, apomorphine (APO) alone or in combination with the NMDA antagonist, MK-801. In control rats, APO produced long-lasting (1 h) suppression of alpha activity, significantly greater in the cortex than in the striatum. In 6-OHDA rats, an even larger suppressive effect was observed in the beta frequency range, again significantly more pronounced in the cortex than in the striatum. In these animals, alpha suppression was similar in cortex and striatum in the first hour after APO injection, but alpha activity level was significantly higher in the striatum than in the cortex in the second hour. Pretreatment with MK-801 in 6-OHDA rats eliminated the APO-induced difference between cortex and striatum in the beta range, inversed the effect in the alpha range, and intensified delta activity stronger in the striatum than in the cortex. Thus, frequency-dependent differences in EEG power between cortex and striatum may be involved in dopaminergic treatment of PD and, at least in part, be mediated through NMDA receptors.
    Experimental Brain Research 09/2008; 191(3):277-87. · 2.22 Impact Factor
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    ABSTRACT: Alterations in electroencephalogram (EEG) asymmetry and deficits in interhemispheric integration of information have been shown in patients with Alzheimer's disease (AD). However, no direct evidence of an association between EEG asymmetry, morphological markers in the brain, and cognition was found either in AD patients or in AD models. In this study we used rats with bilateral olfactory bulbectomy (OBX) as one of the AD models and measured their learning/memory abilities, brain beta-amyloid levels and EEG spectra in symmetrical frontal and occipital cortices. One year after OBX or sham-surgery, the rats were tested with the Morris water paradigm and assigned to three groups: sham-operated rats, SO, and OBX rats with virtually normal, OBX(+), or abnormal, OBX(-), learning (memory) abilities. In OBX vs. SO, the theta EEG activity was enhanced to a higher extent in the right frontal cortex and in the left occipital cortex. This produced significant interhemispheric differences in the frontal cortex of the OBX(-) rats and in the occipital cortex of both OBX groups. The beta1 EEG asymmetry in SO was attenuated in OBX(+) and completely eliminated in OBX(-). OBX produced highly significant beta2 EEG decline in the right frontal cortex, with OBX(-)>OBX(+) rank order of strength. The beta-amyloid level, examined by post-mortem immunological DOT-analysis in the cortex-hippocampus samples, was about six-fold higher in OBX(-) than in SO, but significantly less (enhanced by 82% vs. SO) in OBX(+) than in OBX(-). The involvement of the brain mediatory systems in the observed EEG asymmetry differences is discussed.
    Brain Research 09/2008; 1232:185-94. · 2.88 Impact Factor
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    ABSTRACT: While continuous monocular deprivation (MD) of patterned vision causes severe loss of visual cortical responses and visual acuity in the affected eye, these effects can be avoided by providing brief daily periods of binocular exposure [BE; D.E. Mitchell et al. (2003) Curr. Biol., 8, 1179-1182; D.E. Mitchell et al. (2006) Eur. J. Neurosci., 23, 2458-2466; D.S. Schwarzkopf et al. (2007) Eur. J. Neurosci., 25, 270-280]. In order to analyse binocular mechanisms involved in this phenomenon, we studied neuronal responses in primary visual cortex to binocular disparity stimuli in cats that had experienced mixed daily visual exposure (i.e. different amounts of daily binocular and monocular exposure). To examine whether binocular responses are as reliable in MD as in normal animals, we analysed single-trial responses to spatial phase disparity stimuli. In cats with various amounts of daily binocular experience (3.5 h, 7 h or 12 h) alone, about half of neurons (47.9%) showed reliable phase-specific binocular responses in two consecutive trials. The percentage of phase-selective cells was reduced in cats with mixed visual exposure with a decrease in the duration of daily BE. Within these neurons, a 'stable' cell population, i.e. with identical relative phases eliciting the strongest and weakest responses in two trials, was also reduced. In other words, the responses of neurons recorded from deprived animals were more likely to show different preferred phases on successive trials, although their amplitude ratios in both trials were about equal. We suggest that the detrimental effect of MD on binocular vision may begin, at least in part, with a subtle disruption of the mechanism involved in discrimination of binocular disparity signals.
    European Journal of Neuroscience 01/2008; 26(12):3553-63. · 3.75 Impact Factor
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    ABSTRACT: Even short periods of early monocular deprivation result in reduced cortical representation and visual acuity of the deprived eye. However, we have shown recently that the dramatic deprivation effects on vision can be prevented entirely if the animal receives a brief period of concordant binocular vision each day. We examine here the extent to which the cortical deprivation effects can be counteracted by daily periods of normal experience. Cats received variable daily regimens of monocular deprivation (by wearing a mask) and binocular vision. We subsequently assessed visual cortex function with optical imaging of intrinsic signals and visually evoked potential recordings. Regardless of the overall length of visual experience, daily binocular vision for as little as 30 min, but no less, allowed normal ocular dominance and visual responses to be maintained despite several times longer periods of deprivation. Thus, the absolute amount of daily binocular vision rather than its relative share of the daily exposure determined the outcome. When 30 min of binocular exposure was broken up into two 15-min blocks flanking the deprivation period, ocular dominance resembled that of animals with only 15 min of binocular vision, suggesting that binocular experience must be continuous to be most effective. Our results demonstrate that normal experience is clearly more efficacious in maintaining normal functional architecture of the visual cortex than abnormal experience is in altering it. The beneficial effects of very short periods of binocular vision may prevent any long-term effects (amblyopia) from brief periods of compromised vision through injury or infection during development.
    European Journal of Neuroscience 02/2007; 25(1):270-80. · 3.75 Impact Factor
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    ABSTRACT: Most strabismic observers do not suffer from double vision because of suppression from conscious perception of 1 of the 2 eyes' conflicting views. Direct evidence for the site and neural substrate of strabismic suppression has not been available so far, although psychophysical data suggest a cortical origin. On the other hand, cross-orientation suppression among conflicting stimuli presented monocularly has recently been shown to have a strong thalamic component. Here we present evidence, using both visual stimulation and pharmacological techniques, that strabismic suppression occurs in the primary visual cortex and involves gamma-amino butyric acid (GABA)-mediated inhibition. We show that its dependency on the drift rate of the suppressing stimulus is consistent with a cortical origin; unlike monocular cross-orientation suppression, it cannot be evoked by very fast-moving stimuli. Furthermore, strabismic suppression is greatly reduced when GABAergic inhibition is locally blocked by the GABA(A) antagonist bicuculline.
    Cerebral Cortex 01/2007; 16(12):1750-8. · 8.31 Impact Factor
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    Stuart D Faulkner, Vasily Vorobyov, Frank Sengpiel
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    ABSTRACT: The effects of early monocular deprivation on visual acuity and visual cortical responses can be reversed quickly if vision is restored to the deprived eye and the other eye is deprived instead, a procedure known as reverse occlusion. However, recovery of vision through the originally deprived eye (ODE) is not stable. Following re-opening of the recently deprived (originally nondeprived) eye (ONDE), vision in the ODE typically deteriorates rapidly, possibly because of competitive interactions, whereas vision in the ONDE also remains compromised, resulting in bilateral amblyopia, the reasons for which are unknown. Here we monitor the physiological changes in the visual cortex during recovery from reverse occlusion in a longitudinal study, using optical imaging of intrinsic signals and single-cell recording in anesthetized cats. We show that a brief period of just 4 days of concordant binocular vision intercalated between the two periods of monocular experience allows close to equal responses to develop through both eyes, both in terms of cortical territory and orientation selectivity. In contrast, with no binocular vision or discordant binocular experience, cortical territory dominated by the ONDE is significantly reduced, and orientation tuning of cells dominated by the ODE is wider than that of cells dominated by the ONDE. These results support the notion that a brief period of binocular vision is sufficient to prevent bilateral acuity loss caused by reverse occlusion.
    Journal of Neurophysiology 04/2006; 95(3):1718-26. · 3.30 Impact Factor
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    ABSTRACT: The effects of chronic (7 days) exposure to an extremely low frequency magnetic field (ELF-MF, 50 Hz, 0.5 mT) on spontaneous and amphetamine-induced (1.5mg/kg, i.p.) locomotor and stereotypic activities in adult rats were examined by open field test for 2h on exposure days 1, 3, and 7. After 1 day of exposure to ELF-MF, the spontaneous locomotor activity was increased clearly at the first hour of observation and significantly at the second one as compared to the corresponding values in other series with ELF-MF and sham-exposed animals. After 7 days of exposure to ELF-MF, an amphetamine enhancing effect on the locomotor activity was significantly reduced at the second hour of observation as compared to that in 1-day- and sham-exposed rats treated with amphetamine. In contrast to the locomotor activity, the amphetamine-induced stereotypic behaviour in 7-day pre-exposed rats was significantly reduced at the first hour versus sham-exposed rats. While at the second hour of observation this effect was significant as compared to 1- and 3-day exposed animals (but not sham-exposed rats). Our results indicate that an extremely low frequency magnetic field is able to affect differently two types of behaviour, which are dependent on both the time course of exposure and the imbalance in the brain mediatory systems.
    Brain Research Bulletin 12/2005; 67(6):498-503. · 2.94 Impact Factor
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    Stuart D Faulkner, Vasily Vorobyov, Frank Sengpiel
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    ABSTRACT: Competition between the two eyes for synaptic space is thought to play a crucial role in the developmental plasticity of ocular dominance in the primary visual cortex. This competition should be disrupted if geniculocortical afferents from the two eyes are spatially segregated. In kittens, strabismus was induced in one eye before the onset of the critical period; the effects of a brief period of monocular deprivation (MD) at the height of the critical period and subsequent recovery were assessed in a longitudinal study employing optical imaging of intrinsic signals. Results were compared with those from a control group without strabismus. MD caused a substantial loss of cortical territory dominated by the deprived eye in all animals. However, in the strabismic animals this loss was smaller than in the control group for the hemisphere contralateral to the deprived eye. When the deprived eye was reopened, recovery of cortical territory was remarkably rapid in all kittens, and close to pre-deprivation responses were attained within 3-4 days of reopening. However, kittens without strabismus exhibited a greater rate of recovery from MD. Moreover, recovery of visual acuity, as assessed by visually evoked potential (VEP) measurements, was slower and less complete in animals with strabismus prior to MD. Therefore, strabismus does not provide lasting protection against the effects of MD.
    Cerebral Cortex 12/2005; 15(11):1822-33. · 8.31 Impact Factor
  • Frank Sengpiel, Vasily Vorobyov
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    ABSTRACT: The response of neurons in the primary visual cortex to an optimally oriented grating is usually suppressed quite dramatically when a second grating of, for example, orthogonal orientation is superimposed. Such "cross-orientation suppression" has been implicated in the generation of cortical orientation selectivity and local response normalization. Until recently, little experimental evidence was available concerning the neurophysiological substrate of this phenomenon, although an involvement of intracortical inhibition was commonly assumed. However, Freeman et al. (2002) proposed that cortical cross-orientation suppression is caused by suppression in the thalamus and depression at geniculocortical synapses. Here, we examine a dichoptic form of cross-orientation suppression, termed interocular suppression and thought to be involved in binocular rivalry (Sengpiel et al., 1995a). We show that its dependency on the drift rate of the suppressing stimulus is consistent with a cortical origin; unlike monocular cross-orientation suppression, it cannot be evoked by very fast-moving stimuli. Moreover, we find that previous adaptation to the orthogonal stimulus essentially eliminates interocular suppression. Because adaptation is a cortical phenomenon, this result also argues in favor of a cortical locus of suppression, again unlike monocular cross-orientation suppression, which is not affected by adaptation to the suppressor (Freeman et al., 2002). Finally, interocular suppression is greatly reduced in the presence of the GABA antagonist bicuculline. Together, our study demonstrates that interocular suppression is substantially different from monocular cross-orientation suppression and is mediated by inhibitory circuitry within the visual cortex.
    Journal of Neuroscience 08/2005; 25(27):6394-400. · 6.91 Impact Factor
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    ABSTRACT: We used systemic kainic acid (KA) injection to investigate how the development of temporal lobe epilepsy and the associated network reorganization affect the electrocorticogram (ECoG) responses to various neurotransmitter agonists. Unrestrained rats chronically implanted with electrodes over somatosensory cortex and dorsal hippocampus and a cannula into the right lateral ventricle were used to investigate the ECoG frequency responses of intracerebroventricularly applied agonists (NMDA, clonidine, muscimol, and baclofen) at several types of receptors [NMDA, alpha2-adrenergic (NE), GABAA, and GABAB, respectively] in KA-treated versus naïve animals. The ECoG was analyzed 2, 5, and 9 weeks after intraperitoneal injection of KA alone or in combination with basic fibroblast growth factor (bFGF, intracerebroventricularly). Within the first 5 weeks of KA injection, the ECoG power shifted towards the lower-frequency range. Concurrently, the electrographic responses to NMDA and clonidine were potentiated, whereas the ECoG effects mediated by GABAA and GABAB receptors remained largely unaffected. In control rats, bFGF strongly enhanced the electrographic NMDA responses. In sharp contrast, bFGF potently mitigated the abnormally increased NMDA sensitivity of epileptic rats, if applied 4 weeks post KA injection. These data suggest that upregulation and downregulation of the NMDA receptor-mediated effects on cortical activity might be a prominent feature of bFGF signaling in the intact and the damaged brain, respectively.
    Brain Research 08/2005; 1051(1-2):123-36. · 2.88 Impact Factor

Publication Stats

193 Citations
99.14 Total Impact Points

Institutions

  • 2005–2013
    • Cardiff University
      • School of Biosciences
      Cardiff, Wales, United Kingdom
  • 2002–2011
    • Russian Academy of Sciences
      • Institute of Cell Biophysics
      Moscow, Moscow, Russia