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ABSTRACT: A new remote-controlled interface-type chamber was designed in order to conduct experiments in brain slices involving gas, fluid, and temperature changes with as little tissue manipulation as possible. The chamber allows for extremely quick changes between different fluid and/or gaseous phases and for active cooling as well as heating by using a set of electromechanical valves and Peltier elements. The design drawings are complemented by exemplary tests of temperature and gas changes, and electrophysiological recordings of slices manipulated with gas and fluid alterations were used to test the efficacy and accuracy of the design. Changing between normoxia and anoxia needs less than 30 s, while the readjustment of the chamber to a new, preset temperature is accomplished in about 1 min. Supplementary data provide a proposal for the electronic circuit diagram. This chamber design should simplify data acquisition in interface environments.
Journal of neuroscience methods 10/2010; 193(1):77-81. · 2.30 Impact Factor
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ABSTRACT: We studied auditory thalamocortical interactions in vitro, using an auditory thalamocortical brain slice preparation. Cortical activity evoked by electrical stimulation of the medial geniculate nucleus (MGN) was investigated through field potential recordings and voltage sensitive dyes. Experiments were performed in slices obtained from adult mice (9-14 weeks). Stimulus evoked activity was detected in the granular and supragranular layers after a short latency (5-6 ms). In 9-14 weeks old mice infragranular activity was detected in 10 of 24 preparations and was found to be increased in younger mice (p 31-64). In 14 of 24 slices a prominent horizontal spread was observed, which extended into cortical areas lateral to A1. In these experiments, the shortest onset latencies and largest signal amplitudes were located in the supragranular layers of A1. In areas lateral to A1, shortest onset latencies were located in the granular layer, while largest signal amplitudes were found in the supragranular layers. Evoked cortical activity was sensitive to removal of extracellular Ca(2+) or application of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM). Short repetitive stimulation, resembling thalamic burst activity (three pulses at 100 Hz), resulted in an increase of signal amplitude and excited area by approximately 25%, without changing the overall spatiotemporal activity profile. Blockade of N-methyl-D-aspartate receptors by 2-amino-5-phosphonopentanoate (AP5, 50 microM) reduced amplitudes and excited area by approximately 15-30%, irrespective of stimulation frequency. Application of bicuculline (10 microM) greatly increased cortical responses to thalamic stimulation. Under these conditions, evoked activity displayed a pronounced horizontal spread in combination with a 2-3-fold increase in amplitude. In conclusion, afferent thalamic inputs primarily activate supragranular and granular layers in the auditory cortex of adult mice. This activation is predominantly mediated by non-NMDA receptors, while GABA(A) receptor-mediated inhibition limits the horizontal and vertical spread of activity.
Neuroscience 10/2009; 165(2):371-85. · 3.38 Impact Factor
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ABSTRACT: While the vasomotor effects of pCO(2) modulation are well documented, the influence of the carbon dioxide-bicarbonate system on the ischemia tolerance of brain tissue itself is controversial. Guinea-pig hippocampal tissue was subjected to ischemia simulation in an interface environment and examined electrophysiologically. Characteristics of anoxic depolarization as well as the postischemic recovery of evoked potentials were registered. During ischemia simulation, pH was changed and afterwards restored to 7.4. pH of 7.6 (n=6), and 7.8 (n=6) were adjusted by increasing bicarbonate concentration without changing pCO(2), while pH 8.2 was reached either with normal pCO(2) (n=8) or with zero CO(2) (n=9). pH 7.1 was created by doubling pCO(2) (n=22) or reducing bicarbonate (n=21), while acid pH of 6.9 (high pCO(2) and low bicarbonate) led to erratic measurements in the interface setup. Alkalotic conditions did not improve electrophysiological stability of the tissue, and pH 8.2 impeded the recovery of evoked potentials. Hypercarbic pH 7.1 led to significantly longer latency of depolarization while the same pH with lowered bicarbonate did not. Evoked potentials, however, recovered only partially after ischemia at hypercarbic pH 7.1. Once the tissue had recovered from anoxic depolarization at control pH, hypercarbic acidosis did not have any further protective effect when ischemia simulation was repeated (n=12). These results do not strengthen the concept of hyperventilation in intensive care, while they suggest a potential of hypercarbia within broader strategies delaying the onset of secondary brain damage.
Neuroscience 11/2008; 158(2):617-22. · 3.38 Impact Factor
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ABSTRACT: Cortical spreading depression (CSD) plays a role in migraine with aura. However, studies of the neuronal effects of CSD in human cortex are scarce. Therefore, in the present study, the effects of CSD on the field excitatory postsynaptic potentials (fEPSP) and the induction of long-term potentiation (LTP) were investigated in human neocortical slices obtained during epilepsy surgery. CSD significantly enhanced the amplitude of fEPSP following a transient suppressive period and increased the induction of LTP in the third layer of neocortical tissues. These results indicate that CSD facilitates synaptic excitability and efficacy in human neocortical tissues, which can be assumed to contribute to hyperexcitability of neocortical tissues in patients suffering from migraine.
Cephalalgia 06/2008; 28(5):558-62. · 3.43 Impact Factor
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ABSTRACT: Adenosine is an inhibitory modulator of brain activity with neuroprotective and anticonvulsant properties. To investigate the distribution of bioelectric activities under application of adenosine, rat hippocampal and neocortical slices were incubated with the voltage-sensitive dye RH795 and neuronal activity was monitored using a fast-imaging photodiode array combined with standard field potential recordings. The effects of adenosine (1-50 micromol/l) on the spatial distribution of stimulus-induced activities were studied in non-epileptiform as well as epileptiform conditions. Epileptiform activity was induced by omission of Mg(2+) from the bath medium. The adenosine's inhibitory effects on the amplitude and spatial extent of stimulus-induced bioelectric activity in the hippocampus were most prominent in strata radiatum and pyramidale in both control and epileptic mediums. Adenosine's inhibitory actions were different on various layers of neocortical tissues in non-epileptiform and epileptiform conditions. Layers II and III showed the most inhibition by application of adenosine in control slices. In epileptiform medium, however, adenosine exerts significant suppressive effects only in layer I of neocortical slices. The data demonstrate a region-specific modulatory potential of adenosine on neuronal network excitability in the hippocampus and neocortex. This may be important in local adenosine therapy in epilepsy.
Neuroscience 04/2008; 152(2):547-57. · 3.38 Impact Factor
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ABSTRACT: Eugenol, an aromatic molecule derived from several plants, has been receiving examination for clinical relevance in epilepsy and headache. To investigate the neurophysiologic properties of the action of eugenol, its effects on epileptiform field potentials elicited by omission of extracellular Mg2+, spreading depression induced by KCl microinjection, electrically evoked field potentials, and long-term potentiation were tested in rat neocortical and hippocampal tissues. Eugenol (10-100 micromol/l) dose-dependently and reversibly suppressed both epileptiform field potentials and spreading depression Eugenol also reversibly decreased the amplitude of the field postsynaptic potentials evoked in CA1 area of hippocampus and the third layer of neocortex. Eugenol significantly reduced the long-term potentiation by approximately 30% compared with controls. Thus, eugenol can suppress epileptiform field potentials and spreading depression, likely via inhibition of synaptic plasticity. The results indicate the potential for eugenol to use in the treatment of epilepsy and cephalic pain.
Neuroscience 07/2006; 140(2):743-51. · 3.38 Impact Factor
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ABSTRACT: Recent advances in our understanding of the basic mechanisms of epilepsy have derived, to a large extent, from increasing ability to carry out detailed studies on patients surgically treated for intractable epilepsy. Clinical and experimental perioperative studies divide into three different phases: before the surgical intervention (preoperative studies), on the intervention itself (intraoperative studies), and on the period when the part of the brain that has to be removed is available for further investigations (postoperative studies). Before surgery, both structural and functional neuroimaging techniques, in addition to their diagnostic roles, could be used to investigate the pathophysiological mechanisms of seizure attacks in epileptic patients. During epilepsy surgery, it is possible to insert microdialysis catheters and electroencephalogram electrodes into the brain tissues in order to measure constituents of extracellular fluid and record the bioelectrical activity. Subsequent surgical resection provides tissue that can be used for electrophysiological, morphological, and molecular biological investigations. To take full advantage of these opportunities, carefully designed experimental protocols are necessary to compare the data from different phases and characterize abnormalities in the human epileptic brain.
Anatomy and Embryology 01/2006; 210(5-6):525-37. · 1.42 Impact Factor
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ABSTRACT: Editing and alternative splicing of mRNA are posttranscriptional steps probably involved in pathophysiological aspects of epilepsy. The present study analyses the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptor subunit GluR2 with respect to the expression of (i) editing at the R/G site and (ii) flip-flop cassettes. Nervous tissue from patients with temporal lobe epilepsy was analysed by RT-PCR followed by restriction enzyme assays. Human autoptic tissue served as control. R/G editing status: the relative amount of edited RNA was significantly increased in the hippocampal tissue, whereas no changes were found in neocortical tissues. Flip-flop expression: no significant alterations were found in relative abundance of spliced variants containing the flip exon. The increased editing at the R/G site in the hippocampal tissue of epilepsy patients may enhance responses to glutamate, resulting in a synapse operating at an increased gain.
Neurobiology of Disease 04/2004; 15(2):371-9. · 5.40 Impact Factor
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C Rüschenschmidt,
R Köhling,
M Schwarz,
H Straub,
A Gorji,
E Siep,
A Ebner,
H W Pannek,
I Tuxhorn,
P Wolf, E-J Speckmann
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ABSTRACT: A-type currents powerfully modulate discharge behavior and have been described in a large number of different species and cell types. However, data on A-type currents in human brain tissue are scarce. Here we have examined the properties of a fast transient outward current in acutely dissociated human neocortical neurons from the temporal lobe of epilepsy patients by using the whole-cell voltage-clamp technique. The A-type current was isolated with a subtraction protocol. In addition, delayed potassium currents were reduced pharmacologically with 10 mM tetraethylammonium chloride. The current displayed an activation threshold of about -70 mV. The voltage-dependent activation was fitted with a Boltzmann function, with a half-maximal conductance at -14.8 +/- 1.8 mV (n = 5) and a slope factor of 17.0 +/- 0.5 mV (n = 5). The voltage of half-maximal steady-state inactivation was -98.9 +/- 8.3 mV (n = 5), with a slope factor of -6.6 +/- 1.9 mV (n = 5). Recovery from inactivation could be fitted monoexponentially with a time constant of 18.2 +/- 7.5 msec (n = 5). At a command potential of +30 mV, application of 5 mM 4-aminopyridine or 100 microM flecainide resulted in a reduction of A-type current amplitude by 35% or 22%, respectively. In addition, flecainide markedly accelerated inactivation. Current amplitude was reduced by 31% with application of 500 microM cadmium. All drug effects were reversible. In conclusion, neocortical neurons from epilepsy patients express an A-type current with properties similar to those described for animal tissues.
Journal of Neuroscience Research 04/2004; 75(6):807-16. · 2.74 Impact Factor
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ABSTRACT: Cortical spreading depression (CSD) has been suggested to underlie some neurological disorders such as migraine. Despite the intensity with which many investigators have studied SD in the brain, only a few studies have aimed to identify SD in the spinal cord. Here we described the main characteristic features of SD in the spinal cord induced by different methods including various spinal cord injury models and demonstrated that SD enhances the spinal cord activity following a transient suppressive period. These findings suggest that SD may play a role in the mechanisms of spinal neurogenic shock, spinal cord injury, and pain. Furthermore, we studied the effect of CSD on the neuronal activity of the spinal cord. CSD was induced via cortical pinprick injury or KCl injection in the somatosensory cortex. CSD did not propagate into the cervical spinal cord. However, intracellular recordings of the neurons in the dorsal horn of C2 segment, ipsilateral to the hemisphere in which CSD was evoked, showed a transient suppression of spontaneous burst discharges, followed by a significant enhancement of the neuronal activity. This indicates a link between a putative cause of the neurological symptoms and the subsequent pain of migraine.
Neurobiology of Disease 03/2004; 15(1):70-9. · 5.40 Impact Factor
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ABSTRACT: Spreading depression (SD) is characterized by a transient breakdown of neuronal function concomitant with a massive failure of ion homeostasis. It is a phenomenon that can be induced in neocortical tissue by raising excitability, e.g. injection of K(+), application of glutamatergic agonists, or blocking Na(+)/K(+) ATPase. Here we report a novel method of SD induction using minimal disinhibition with application of low concentrations (5 microM) of the GABA(A) receptor blocker bicuculline. This procedure-while subthreshold for epileptiform activity-readily induced spontaneous SDs in native rat neocortical slices, accompanied by typical depolarizations of neurons and glial cells. In contrast, in human neocortical preparations obtained from epilepsy surgery, in approximately 20% of the slices spontaneous epileptiform activity appeared with this bicuculline dosage without SDs. Raising the concentration of bicuculline to an epileptogenic dose (10 microM) in human tissue also resulted in the generation of epileptiform activity only. Likewise, in slices from pilocarpine-treated, chronically epileptic rats, bicuculline also only induced epileptiform activity without eliciting SDs. The experiments indicate that chronic epilepsy causes a differential sensitivity to partial GABA(A) receptor blockade with regard to induction of SD.
Brain Research 07/2003; 975(1-2):129-34. · 2.73 Impact Factor
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ABSTRACT: In vitro and in vivo brain slice techniques were used to examine phencyclidine (PCP) effects on the lateral propagation of epileptiform field potentials (EFP) across adjacent areas of rat frontal neocortex. Epileptiform activity was induced by perfusing slices with Mg 2+-free artificial cerebrospinal fluid. Simultaneous field potential recordings of EFP were obtained from four microelectrodes placed 2-3 mm apart across coronal slices in the third layer. PCP, applied focally between recording sites, blocked rapid propagation across treated areas and resulted in the emergence of spatially separate, independent pacemakers. The characteristics of paroxysmal depolarization shifts did not change significantly by the blockade of lateral propagation of EFP. The same asynchronized pattern of EFP conduction was observed after local application of the N-methyl-D-aspartate (NMDA)-receptor antagonist DL-2-amino-5-phosphono-valeric acid. Local administration of haloperidol as well as NMDA before PCP application reversibly prevented appearance of multiple pacemakers. Focal application of dopamine produced an abnormal pattern of lateral conduction of EFP in 50 % of tested slices. Pacemaker failure as an indicator of functional impairment of cortical integration is the proposed mechanism for developing of schizophrenia-like psychosis associated with epilepsy. Abbreviations. APV: DL-2-amino-5-phosphono-valeric acid EEG:electroencephalogram EFP:epileptiform field potentials NMDA:N-methyl-D-aspartate PCP:phencyclidine SLPE:Schizophrenialike psychosis associated with epilepsy
Pharmacopsychiatry 06/2003; 36(3):113-20. · 2.07 Impact Factor
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ABSTRACT: Potassium- and calcium conductances regulate neuronal excitability and epileptiform activity. In this study, the effects of different extracellular potassium concentrations ([K(+)](o)) were investigated on the modulatory effect of the L-type transmembranous calcium currents on epileptiform discharges. The in vitro brain slice technique was used to examine the effects of calcium channel blockers, verapamil and nifedipine, on the repetition rate, amplitude, and duration of epileptiform field potentials (EFP) in the presence of low, physiological, and high background [K(+)](o) in guinea pig hippocampal slices. Epileptiform activity was induced by omission of Mg(2+) from artificial cerebrospinal fluid contained 2, 4, and 8 mM [K(+)](o). Both verapamil and nifedipine suppressed EFP after a transient increase in repetition rate. The extent of EFP frequency rate acceleration significantly increased with reduction of [K(+)](o). The increase in EFP frequency rate induced by application of verapamil and nifedipine was accompanied by a reduction in the EFP amplitude and a reversible increase in the burst discharge duration. The extent of burst discharge prolongation was also significantly higher with decreasing [K(+)](o). Further application of verapamil and nifedipine suppressed the epileptiform burst activity in the presence of different [K(+)](o). The latency of EFP depression was significantly diminished both with increased and decreased background potassium concentrations. The data indicate the importance of the effect of the L-type transmembranous calcium currents on the regulatory effect of background [K(+)](o) on epileptiform burst discharge frequency and duration.
Brain Research 02/2003; 959(1):149-59. · 2.73 Impact Factor
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ABSTRACT: Intra- and extracellular recording techniques were used to study the epileptiform activity generated by guinea pig hippocampal slices perfused with free-magnesium artificial cerebrospinal fluid in the presence of physiologic (4 mM), reduced (2 mM) or elevated (8 mM) extracellular potassium concentrations ([K(+)](o)). Extracellular field potentials along with intracellular recordings were recorded in CA1 or CA3 region. Reduction of [K(+)](o) significantly increased the latency of epileptiform field potential (EFP) appearance as well as burst discharge duration and decreased EFP repetition rate. Depending on different background [K(+)](o), epileptiform burst discharges appeared in different patterns including varied types of paroxysmal depolarisation shifts and burst activity in CA1 and CA3 subfields. Comparison with physiological and increased [K(+)](o,) reduction of [K(+)](o) significantly increased the mean duration of bursts, mean amplitude of depolarisation, mean after-hyperpolarisation duration, and inter-spike intervals in both CA1 and CA3 areas. Three distinct patterns were distinguished on the basis of their evoked firing pattern in response to application of depolarising current pulses in the interval of epileptiform burst discharges. Neurons superfused with 2 mM [K(+)](o) presented fast adapting pattern while cells washed with 4 or 8 mM [K(+)](o) exhibited intrinsically bursting or slow adapting patterns. Comparing the groups with different background [K(+)](o), there is a more severe form of discharges in low K(+) and a subtle difference between 4 and 8 mM K(+). The data indicate the importance of background [K(+)](o) on epileptiform burst discharge pattern and characteristics.
Brain Research 02/2003; 959(1):135-48. · 2.73 Impact Factor
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H Straub,
U Kuhnt,
J-M Höhling,
R Köhling,
A Gorji,
D Kuhlmann,
I Tuxhorn,
A Ebner,
P Wolf,
H-W Pannek,
R Lahl, E-J Speckmann
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ABSTRACT: Stimulus-induced pattern of bioelectric activity in human neocortical tissue was investigated by use of the voltage sensitive dye RH795 and a fast optical recording system. During control conditions stimulation of layer I evoked activity predominantly in supragranular layers showing a spatial extent of up to 3000 microm along layer III. Stimulation in white matter evoked distinct activity in infragranular layers with a spatial extent of up to 3000 microm measured along layer V. The mean amplitude of optical signals close to the stimulated sites in layer I and white matter determined 25 ms following the stimulus, decreased by 50% at a lateral distance of approximately 900 microm and 1200 microm, respectively. Velocity of spread along the vertical stimulation axis reached 0.24 m/s in the supragranular layers (layers I to III) and then decreased to 0.09 m/s following layer I activation; stimulation of white matter induced a velocity of spread in layer V of 0.38 m/s, which slowed down to 0.12 m/s when passing the lower border of lamina IV. The horizontal velocities of spread determined from the stimulation site to a lateral distance of 500 microm reached 0.26-0.28 m/s and 0.28-0.35 m/s for layer I and white matter stimulation, respectively. At larger distances velocity of spread decreased. Increased excitability (Mg(2+)-free solution) had no significant effect on the spatio-temporal distribution of evoked activity as compared with control conditions. There were also no obvious differences between the results obtained in slices, which generated spontaneously sharp waves and those which were not spontaneously active. About 30% of the slices (n=7) displayed a greatly different response pattern, which seemed not to be related in a simple way to the stimulation as was the case in the majority of the investigated slices. The activity pattern of those slices appeared atypical in regard to their deviations of the vertical and horizontal extent of activity, to their reduced spatial extent of activity during increased excitability, to their layer-related distribution of activity, and to the appearance of afterdischarges.Concluding, in 30% of the human temporal lobe slices atypical activity pattern occurred which obviously reflect intrinsic epileptiform properties of the resected tissue. The majority of slices showed stereotyped activity pattern without evidence for increased excitability.
Neuroscience 01/2003; 121(3):587-604. · 3.38 Impact Factor
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ABSTRACT: Dystonic mutant dt(sz) hamsters are a model for paroxysmal dystonia. Handling/stress provoke the dystonic attacks. This phenomenon subsedes with maturation, but can be reinvoked when these animals receive sodium channel blockers such as lamotrigine, suggesting a dysfunction of striatal sodium channels. Voltage-gated fast sodium currents (I(Na(+))) were studied in acutely isolated striatal neurons from healthy and dt(sz) hamsters in whole-cell voltage clamp recordings. The action of lamotrigine was tested on (a) current/voltage relationship, (b) kinetics, and (c) steady-state inactivation and activation. Under control conditions, properties of I(Na(+)) were not different between healthy and dt(sz) neurons. With lamotrigine, however, (a) peak currents were significantly less depressed by the drug in neurons from dt(sz) hamsters as compared to healthy cells, and (b) the steady-state inactivation curve shift of I(Na(+)) was less pronounced in dt(sz) neurons. The results suggest that in dt(sz) hamsters, fast sodium currents in striatal neurons are more resistant to blockade. This sodium channel alteration might be causal for a functional imbalance between input and output structures of the basal ganglia under conditions of compromised I(+)(Na).
Neurobiology of Disease 04/2002; 9(2):258-68. · 5.40 Impact Factor
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ABSTRACT: About 20-30% of patients with epilepsy continue to have seizures despite carefully monitored treatment with antiepileptic drugs. The mechanisms explaining why some patients' respond and others prove resistant to antiepileptic drugs are poorly understood. It has been proposed that pharmacoresistance is related to reduced sensitivity of sodium channels in hippocampal neurons to antiepileptic drugs such as carbamazepine or phenytoin. In line with this proposal, a reduced effect of carbamazepine on sodium currents in hippocampal CA1 neurons was found in the rat kindling model of temporal lobe epilepsy (TLE), i.e. a form of epilepsy with the poorest prognosis of all epilepsy types in adult patients. To address directly the possibility that neuronal sodium currents in the hippocampus play a crucial role in the pharmacoresistance of TLE, we selected amygdala-kindled rats with respect to their in vivo anticonvulsant response to phenytoin into responders and nonresponders and then compared phenytoin's effect on voltage-activated sodium currents in CA1 neurons. Furthermore, in view of the potential role of calcium current modulation in the anticonvulsant action of phenytoin, the effect of phenytoin on high-voltage-activated calcium currents was studied in CA1 neurons. Electrode-implanted but not kindled rats were used as sham controls for comparison with the kindled rats. In all experiments, the interval between last kindled seizure and ion channel measurements was at least 5 weeks. In kindled rats with in vivo resistance to the anticonvulsant effect of phenytoin (phenytoin nonresponders), in vitro modulation of sodium and calcium currents by phenytoin in hippocampal CA1 neurons did not significantly differ from respective data obtained in phenytoin responders, i.e. phenytoin resistance was not associated with a changed modulation of the sodium or calcium currents by this drug. Compared to sham controls, phenytoin's inhibitory effect on sodium currents was significantly reduced by kindling without difference between the responder and nonresponder subgroups. Further studies in phenytoin-resistant kindled rats may help to elucidate the mechanisms that can explain therapy resistance.
Neuropharmacology 02/2002; 42(1):107-16. · 4.81 Impact Factor
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ABSTRACT: Cyclosporine A (CsA) neurotoxicity is a common cause of seizures in transplant patients and others receiving immunosuppressive therapy. CsA at concentrations higher than the levels estimated for cerebrospinal fluid of the patients suffering from seizure attacks was ineffective to induce epileptiform field potentials (EFP) in in vitro brain-slice preparation. The aim of this study was to test the effect of CsA at lower concentrations on neuronal activity. Guinea-pig hippocampal slices were exposed to artificial cerebrospinal fluid containing CsA (0.1-2 microM). Furthermore, the effects of CsA (0.25-10 microM) were tested on EFP elicited by omission of Mg2+ from superfusate. Low concentrations of CsA (0.1-0.25 microM) induced EFP while higher doses (0.5-2 microM) failed to decrease the seizure threshold. CsA at concentrations of 0.25 and 1 microM had no significant effect on the low Mg2+-induced EFP. Higher CsA concentration (10 microM) strongly suppressed EFP. The results indicate that CsA at doses that are probably clinically relevant increases the neuronal excitability.
Neuroscience 02/2002; 115(4):993-7. · 3.38 Impact Factor
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ABSTRACT: Optical imaging of neuronal network activity yields information of spatial dynamics which generally is analyzed visually. The transient appearance of spatial activity patterns is difficult to gauge in a quantifiable manner, or may even altogether escape detection. Here, we employ geometric shape matching using Fréchet distances or straight skeletons to search for pre-selected patterns in optical imaging data with adjustable degrees of tolerance. Data were sampled from fluorescence changes of a voltage-sensitive dye recorded with a 464-photodiode array. Fluorescence was monitored in a neuronal network in vitro. Neuronal activity prompting fluorescence fluctuations consisted of spontaneous epileptiform discharges in neocortical slices from patients undergoing epilepsy surgery. The experiments show that: (a) spatial activity patterns can be detected in optical imaging data; (b) shapes such as "mini-foci" appear in close correlation to bioelectric discharges monitored with field potential electrodes in a reproducible manner; (c) Fréchet distances yield more conservative matches regarding rectangular, and less conservative hits with respect to radially symmetric shapes than the straight skeleton approach; and (d) tolerances of 0.03-0.1 are suited to detect faithful images of pre-selected shapes, whereas values >0.8 will report matches with any polygonal pattern. In conclusion, the methods reported here are suited to detect and analyze spatial, geometric dynamics in optical imaging data.
Journal of Neuroscience Methods 02/2002; 114(1):17-23. · 1.98 Impact Factor
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ABSTRACT: The specific mechanisms by which low concentrations of cyclosporine induce seizures and low concentrations of phencyclidine provoke behavioral excitation remain to be elucidated. Both compounds block N-methyl-d-aspartate (NMDA) receptors. The aim of this study was to determine if low concentrations of the NMDA-receptor blockers increase the seizure susceptibility.
Guinea pig hippocampal slices were exposed to artificial cerebrospinal fluid containing the NMDA blocker dl-2-amino-5-phosphono-valerate (APV; 0.1-10 microM). Extracellular field potentials were recorded from CA1 and CA3 regions.
Low concentrations of APV induced epileptiform burst discharges (0.1-0.25 microM), whereas higher doses failed to decrease the seizure threshold (1-10 microM).
The results indicate that the excitatory effect of low concentrations NMDA blockers may play a role in the neurotoxicity of aforementioned substances.
Epilepsia 11/2001; 42(10):1228-30. · 3.96 Impact Factor
