Spontaneous interictal-like activity originates in multiple areas of the CA2-CA3 region of hippocampal slices

1994 ◽  
Vol 71 (4) ◽  
pp. 1574-1585 ◽  
Author(s):  
L. V. Colom ◽  
P. Saggau
Keyword(s):  
Guinea Pig ◽  
Epileptiform Activity ◽  
Hippocampal Slices ◽  
Optical Recording ◽  
Objective Lens ◽  
Gamma Aminobutyric Acid ◽  
Subsequent Increase ◽  
Epileptiform Discharges ◽  
High K ◽  
Ca3 Region

1. The sites of origin of spontaneous interictal-like epileptiform activity in hippocampal slices from guinea pig, mouse, and rat were determined. A multisite fast optical recording technique using voltage-sensitive dyes and an array of 100 photodiodes was employed. The use of a low-magnification objective lens allowed the visualization of almost the entire transverse hippocampal slice. Three in vitro models of epilepsy were employed, utilizing different manipulations of the bath perfusion medium to induce epileptiform activity: 1) raising the external potassium (K+) concentration, 2) adding the potassium channel blocker 4-aminopyridine (4-AP), and 3) adding antagonists of gamma-aminobutyric acid-A (GABAA) receptors (bicuculline and picrotoxin, BIC-PTX). 2. Spontaneous epileptiform discharges were detected in each subfield of cornu ammonis (CA) but not in the dentate gyrus (DG) of each studied species. Preliminary experiments confirmed that interictal-like epileptiform activity originated in the CA2-CA3 region. Ictal-like activity was never observed in our experiments. 3. In the guinea pig, when GABAA antagonists were employed, the site of origin of spontaneous epileptiform discharges was consistently located in the CA2-CA3a region. When high K+ or 4-AP was used, this region was the most frequent site of origin. Subsequent epileptiform discharges with similar sites of origin occasionally invaded different areas of the CA2-CA3 region, revealing a variable area of occupance of epileptiform discharges. 4. In the mouse and rat, the site of origin of spontaneous discharges was invariably located in the CA3b-CA3c region independent of the epilepsy model. 5. In both the guinea pig and rat, when the CA2-CA3a region was surgically separated from the CA3b-CA3c region, independent discharges were observed in both regions. Areas that could generate discharges only under certain epileptogenic conditions were found in these species (potential sites of origin). Two independent sites of origin with different propagation patterns and area of occupance were occasionally observed within the CA2-CA3a region. 6. In the guinea pig, such lesions demonstrated that both regions can independently generate epileptiform discharges at different frequencies. When high K+ or 4-AP was employed, epileptiform activity was observed in both regions. Although BIC-PTX only generated discharges in the CA2-CA3a region, a subsequent increase in K+ induced additional discharges in the CA3b-CA3c region, revealing a potential site of origin. 7. In rat hippocampal slices with such lesions, spontaneous epileptiform discharges were observed in both CA2-CA3a and CA3b-CA3c region when 4-AP was employed.(ABSTRACT TRUNCATED AT 400 WORDS)

Ictal Epileptiform Activity in the CA3 Region of Hippocampal Slices Produced by Pilocarpine

1998 ◽  
Vol 79 (6) ◽  
pp. 3019-3029 ◽  
Author(s):  
Paul A. Rutecki ◽  
Yili Yang
Keyword(s):  
Epileptiform Activity ◽  
Hippocampal Slices ◽  
Reversal Potential ◽  
Extracellular Potassium ◽  
Muscarinic Agonist ◽  
Epileptiform Discharges ◽  
Artificial Cerebrospinal Fluid ◽  
Discharge Duration ◽  
Interictal Discharges ◽  
Ca3 Region

Rutecki, Paul A. and Yili Yang. Ictal epileptiform activity in the CA3 region of hippocampal slices produced by pilocarpine. J. Neurophysiol. 79: 3019–3029, 1998. Pilocarpine, a muscarinic agonist, produces status epilepticus that is associated with the later development of chronic recurrent seizures. When applied to rat hippocampal slices, pilocarpine (10 μM) produced brief (<200 ms) epileptiform discharges that resembled interictal activity that occurs between seizures, as well as more prolonged synchronous neuronal activation that lasted seconds (3–20 s), and was comparable to ictal or seizures-like discharges. We assessed the factors that favored ictal patterns of activity and determined the biophysical properties of the ictal discharge. The probability of observing ictal discharges was increased when extracellular potassium ([K+]o) was increased from 5 to 7.5 mM. Raising [K+]o to 10 mM resulted in loss of ictal patterns and, in 20 of 34 slices, desynchronization of epileptiform activity. Making the artificial cerebrospinal fluid (ACSF) hyposmotic favored ictal discharges at 5 mM [K+]o, but shifted 7.5 mM [K+]o ACSF patterns to interictal discharges or desynchronized activity. Conversely, increasing osmolality suppressed ictal patterns. The pilocarpine-induced ictal discharges were blocked by atropine (1 μM, n = 5), a muscarinic antagonist, and pirenzepine (1 μM, n = 6), a selective M1 receptor antagonist. Kainate/α-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid receptor blockade stopped all epileptiform activity ( n = 8). The N-methyl-d-aspartate antagonist d,l-2-amino-5-phosphonovaleric acid (100 μM, n = 34) did not change the pattern of epileptiform activity but significantly increased the rate of interictal discharges and prolonged the duration of ictal discharges. The ictal discharge was characterized intracellularly by a depolarization that was associated with action potential generation and persisted as a membrane oscillation of 4–10 Hz. The ictal oscillations reversed in polarity at −22.7 ± 2.2 mV ( n = 11) with current-clamp recordings and −20.9 ± 3.1 mV ( n = 7) with voltage-clamp recordings. The reversal potential of the ictal discharge in the presence of the γ-aminobutyric acid-A blocker bicuculline (10 μM, n = 6) was −2.2 ± 2.6 mV and was significantly different from that measured without bicuculline. Bicuculline added to 7.5 mM [K+]o and 10 μM pilocarpine did not cause epileptiform activity to change pattern but significantly increased the rate of interictal discharges and prolonged the ictal discharge duration. Both synaptic and nonsynaptic mechanisms are important for the generation of ictal patterns of epileptiform activity. Although the synchronous epileptiform activity produced by pilocarpine required fast glutamate-mediated synaptic transmission, the transition from an interictal to ictal pattern of activity depended on [K+]o and could be influenced by extracellular space.

scholarly journals Voltage Imaging Reveals the CA1 Region at the CA2 Border as a Focus for Epileptiform Discharges and Long-Term Potentiation in Hippocampal Slices

2007 ◽  
Vol 98 (3) ◽  
pp. 1309-1322 ◽  
Author(s):  
Payne Y. Chang ◽  
Portia E. Taylor ◽  
Meyer B. Jackson
Keyword(s):  
Epileptiform Activity ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Voltage Imaging ◽  
Ca1 Region ◽  
Epileptiform Discharges ◽  
Term Potentiation ◽  
Electrical Shocks ◽  
Ca3 Region

Voltage-sensitive-dye imaging was used to study the initiation and propagation of epileptiform activity in transverse hippocampal slices. A portion of the slices tested generated epileptiform discharges in response to electrical shocks under normal physiological conditions. The fraction of slices showing epileptiform responses increased from 44 to 86% when bathing [K+] increased from 3.2 to 4 mM. Regardless of stimulation site in the dentate gyrus and hippocampus, discharges generally initiated in the CA3 region. After onset, discharges abruptly appeared in the CA1 region, right at the CA2 border. This spread from the CA3 region to the CA1 region was saltatory, occurring before detectable activity in the intervening CA2 and CA3 regions. Discharges did eventually propagate smoothly through the intervening CA3 region into the CA2 region, but on a slower timescale. The surge in the CA1 region did not spread back into the CA2 region, but spread through the CA1 region toward the subiculum. Tetanic stimulation, theta bursts, and GABAA receptor antagonists failed to alter this characteristic pattern, but did reduce the latency of discharge onset. The part of the CA1 region at the CA2 border, where epileptic responses emerged with relatively short latency, also expressed stronger long-term potentiation (LTP) than the rest of the CA1 region. The CA2 region, where discharges had long latencies and low amplitudes, expressed weaker LTP. Thus the CA1 region at the CA2 border has unique properties, which make this part of the hippocampus an important locus for both epileptiform activity and plasticity.

Enhanced NMDAR-dependent epileptiform activity is controlled by oxidizing agents in a chronic model of temporal lobe epilepsy

1996 ◽  
Vol 76 (6) ◽  
pp. 4185-4189 ◽  
Author(s):  
J. C. Hirsch ◽  
O. Quesada ◽  
M. Esclapez ◽  
H. Gozlan ◽  
Y. Ben-Ari ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Ex Vivo ◽  
Epileptiform Activity ◽  
Hippocampal Slices ◽  
Nmda Antagonist ◽  
Pyramidal Cells ◽  
Resting Membrane Potential ◽  
Postsynaptic Potentials ◽  
Epileptiform Discharges ◽  
Late Part

1. Graded N-methyl-D-aspartate receptor (NMDAR)-dependent epileptiform discharges were recorded from ex vivo hippocampal slices obtained from rats injected a week earlier with an intracerebroventricular dose of kainic acid. Intracellular recordings from pyramidal cells of the CA1 area showed that glutamate NMDAR actively participated in synaptic transmission, even at resting membrane potential. When NMDAR were pharmacologically isolated, graded burst discharges could still be evoked. 2. The oxidizing reagent 5,5'-dithiobis(2-nitrobenzoic acid) (DTNB, 200 microM, 15 min) suppressed the late part of the epileptiform burst that did not recover after wash but could be reinstated by the reducing agent tris (2-carboxyethyl) phosphine (TCEP, 200 microM, 15 min) and again abolished with the NMDA antagonist D-2-amino-5-phosphonovaleric acid (D-APV). 3. Pharmacologically isolated NMDAR-mediated responses were decreased by DTNB (56 +/- 10%, mean +/- SD, n = 6), an effect reversed by TCEP. 4. When only the fast glutamateric synaptic component was blocked, NMDA-dependent excitatory postsynaptic potentials (EPSPs) could be evoked despite the presence of underlying fast and slow inhibitory postsynaptic potentials (IPSPs). DTNB decreased EPSPs to 48 +/- 12% (n = 5) of control. 5. Since a decrease of the NMDAR-mediated response by +/- 50% is sufficient to suppress the late part of the burst, we suggest that epileptiform activity can be controlled by manipulation of the redox sites of NMDAR. Our observations raise the possibility of developing new anticonvulsant drugs that would spare alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-R (AMPAR)-mediated synaptic responses and decrease NMDAR-mediated synaptic transmission without blocking it completely.

Effect of exposure in vitro to ethanol and hypoxia on gamma-aminobutyric acid efflux in the hippocampus of the fetal and adult guinea-pig

1995 ◽  
Vol 7 (5) ◽  
pp. 1339 ◽  
Author(s):  
MC Catlin ◽  
DH Penning ◽  
JF Brien
Keyword(s):  
Guinea Pig ◽  
Hippocampal Slices ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Gaba System ◽  
Direct Exposure ◽  
Interface System ◽  
Near Term ◽  
Co2 Environment

The objective of this study was to determine the effects of acute direct exposure to ethanol, hypoxia or ethanol plus hypoxia on K+-stimulated gamma-aminobutyric acid (GABA) efflux (neuronal release minus uptake) in the hippocampus of the near-term fetal and adult guinea-pig. Transverse hippocampal slices were studied in a static-interface system. Exposure in vitro to ethanol or hypoxia involved 10-min incubation with 50 mM ethanol or 10-min incubation in a 95% N2/5% CO2 environment. GABA was quantitated by HPLC. Ethanol did not alter K+-stimulated GABA efflux; hypoxia augmented K+-stimulated GABA efflux three-fold in the near-term fetus and seven-fold in the adult; concurrent exposure to ethanol did not alter the effect of hypoxia. The data demonstrate that, for acute direct exposure to hypoxia and/or ethanol, only hypoxia increases K+-stimulated GABA efflux, the magnitude of which is dependent on the extent of development of the GABA system.

Cesium Induces Spontaneous Epileptiform Activity Without Changing Extracellular Potassium Regulation in Rat Hippocampus

1999 ◽  
Vol 82 (6) ◽  
pp. 3339-3346 ◽  
Author(s):  
Zhi-Qi Xiong ◽  
Janet L. Stringer
Keyword(s):  
Nmda Receptor ◽  
Dentate Gyrus ◽  
Extracellular Space ◽  
Hippocampal Neurons ◽  
Epileptiform Activity ◽  
Hippocampal Slices ◽  
Nmda Receptor Antagonist ◽  
Extracellular Potassium ◽  
Epileptiform Discharges ◽  
Cultured Hippocampal Neurons

Cesium has been widely used to study the roles of the hyperpolarization-activated (Ih) and inwardly rectifying potassium (KIR) channels in many neuronal and nonneuronal cell types. Recently, extracellular application of cesium has been shown to produce epileptiform activity in brain slices, but the mechanisms for this are not known. It has been proposed that cesium blocks the KIR in glia, resulting in an abnormal accumulation of potassium in the extracellular space and inducing epileptiform activity. This hypothesis has been tested in hippocampal slices and cultured hippocampal neurons using potassium-sensitive microelectrodes. In the present study, application of cesium produced spontaneous epileptiform discharges at physiological extracellular potassium concentration ([K+]o) in the CA1 and CA3 regions of hippocampal slices. This epileptiform activity was not mimicked by increasing the [K+]o. The epileptiform discharges induced by cesium were not blocked by the N-methyl-d- aspartate (NMDA) receptor antagonist AP-5, but were blocked by the non-NMDA receptor antagonist CNQX. In the dentate gyrus, cesium induced the appearance of spontaneous nonsynaptic field bursts in 0 added calcium and 3 mM potassium. Moreover, cesium increased the frequency of field bursts already present. In contrast, ZD-7288, a specific Ihblocker, did not cause spontaneous epileptiform activity in CA1 and CA3, nor did it affect the field bursts in the dentate gyrus, suggesting that cesium induced epileptiform activity is not directly related to blockade of the Ih. When potassium-sensitive microelectrodes were used to measure [K+]o, there was no significant increase in [K+]o in CA1 and CA3 after cesium application. In the dentate gyrus, cesium did not change the baseline level of [K+]o or the rate of [K+]o clearance after the field bursts. In cultured hippocampal neurons, which have a large and relatively unrestricted extracellular space, cesium also produced cellular burst activity without significantly changing the resting membrane potential, which might indicate an increase in [K+]o. Our results suggest that cesium causes epileptiform activity by a mechanism unrelated to an alteration in [K+]o regulation.

Spread of synchronous firing in longitudinal slices from the CA3 region of the hippocampus

1988 ◽  
Vol 60 (4) ◽  
pp. 1481-1496 ◽  
Author(s):  
R. Miles ◽  
R. D. Traub ◽  
R. K. Wong
Keyword(s):  
Epileptiform Activity ◽  
Hippocampal Slices ◽  
Neuronal Firing ◽  
Burst Firing ◽  
Stratum Radiatum ◽  
Synaptic Inhibition ◽  
Firing Threshold ◽  
Single Action ◽  
Synchronous Firing ◽  
Ca3 Region

1. Mechanisms underlying the propagation of synchronous epileptiform activity in disinhibited hippocampal slices were examined in experimental and computer simulation studies. 2. Experiments were performed with longitudinal slices of the CA3 region. Synchronous firing was initiated by stimulating stratum radiatum fibers in the presence of picrotoxin. It propagated smoothly and without decrement at velocities close to 0.15 m/s over distances up to 10 mm. 3. In elevated extracellular calcium, neuronal firing threshold was increased and synchronous burst firing did not spread. Monophasic excitatory postsynaptic potentials (EPSPs) were recorded in cells at limited distances from a stimulus in the presence of 10 mM Ca and picrotoxin. Axonal conduction velocity, estimated from EPSP latencies, was several times faster than the spread of synchronous firing. 4. EPSPs recorded in 5-7 mM Ca and picrotoxin could consist of two components. The properties of the first component were similar to those of synaptic events recorded in 10 mM Ca. The second component was of longer latency and unlike the first component was suppressed in responses to paired stimuli at interval 50-300 ms. Recordings from cells at different distances from a stimulus suggested that the second component spread further and more slowly than the first component. 5. In computer simulations the CA3 region was represented by a spatially distributed network of 9,000 excitatory neurons and 900 inhibitory cells. Individual cells and synapses had properties based on experimental data. The effects of varying synaptic strength and connectivity on the spread of activity in the model was examined. 6. When synaptic inhibition was functional in simulations, firing was restricted to a single action potential in model cells close to the stimulus, as in experiments. Synchronous burst firing spread throughout the neuronal array when fast synaptic inhibition was absent. The velocity of propagation was slower than conduction in simulated axons when synaptic contacts made by excitatory cells were spatially limited. Propagation velocity increased with increases in the spatial extent of excitatory connectivity. 7. Increasing the threshold of neurons in a region of the model network reduced the speed at which synchronous firing spread. In experiments focal application of gamma-aminobutyric acid (GABA) elevated neuronal firing threshold and slowed the propagation of synchrony in a local region. 8. As the strength of synaptic inhibition was gradually reduced, neuronal activity spread further and faster through the simulated neuronal network.(ABSTRACT TRUNCATED AT 400 WORDS)

Abstract TP281: Increased Susceptibility to Excitotoxic Injury in Rat Hippocampal Slices Exposed to Intermittent Hypoxia

Stroke ◽  
2016 ◽  
Vol 47 (suppl_1) ◽  
Author(s):  
Rekha Jagadapillai ◽  
Nicholas Mellen ◽  
Leroy R Sachleben ◽  
Evelyne Gozal
Keyword(s):  
Intermittent Hypoxia ◽  
Glutamate Release ◽  
Hippocampal Slices ◽  
Optical Recording ◽  
Network Activity ◽  
Viable Cells ◽  
High K ◽  
Obstructive Sleep ◽  
Increased Risk ◽  
Glutamate Homeostasis

Introduction: The effect of sustained hypoxia (SH) on brain metabolism has been well studied. However less is known about intermittent hypoxia (IH), a hallmark of obstructive sleep apnea (OSA), associated with increased risk for stroke, outcome severity and functional consequences. Hypothesis: Impaired glutamate homeostasis after IH may underlie increased brain vulnerability to stroke-induced excitotoxicity. Methods: P4 organotypic rat hippocampal slices cultured for 7 days, were exposed for 7 additional days to IH (alternating 2 min 5% O2 - 15 min 21% O2), SH (5% O2) or normoxia (RA; 21% O2), followed by 3 glutamate challenges (first and last 200 μM, 15 min, emulating a physiological stimulus; second, 10 mM, 10 min, emulating stroke-induced excitotoxicity). Viability was assessed by propidium iodide (PI) uptake at baseline then after each glutamate challenge to assess whether hypoxia impairs the response to physiological or excitotoxic glutamate release. Glial GFAP, neuronal MAP2, EAAT1 and EAAT2 glutamate transporters expression was assessed by immunohistochemistry. Spontaneous and evoked Ca2+ transient activity was assessed in Fluo-8LTM AM loaded slices, by optical recording of Ca2+ spikes proximal to a bipolar stimulating electrode, before and after each of 3 single 2 ms stimuli (0.6 mA). Ca2+ transients after high K+ were used to determine the total number of viable cells. Results: Viability, GFAP, MAP2, EAAT1 and EAAT2 expression and basal Ca2+ spikes activity significantly decreased in IH. The number of neurons with spikes evoked within 500 ms of stimuli was not significantly different, but RA evoked responses were more tightly clustered. Residual network activity, assessed by number of neurons with spikes 500 ms post stimulus, was significantly different RA>SH>IH. Overall number of spiking cells after high K+, representing total viable cells, confirmed the viability data obtained with PI staining. Conclusions: IH is more detrimental to cell survival and glutamate homeostasis than SH, suggesting that in addition to vascular changes, impaired glutamate homeostasis may increase OSA patients’ susceptibility to ischemic events.

Burst characteristics of dentate gyrus granule cells: evidence for endogenous and nonsynaptic properties

1996 ◽  
Vol 75 (1) ◽  
pp. 124-132 ◽  
Author(s):  
E. Pan ◽  
J. L. Stringer
Keyword(s):  
Dentate Gyrus ◽  
Action Potentials ◽  
Granule Cells ◽  
Epileptiform Activity ◽  
Hippocampal Slices ◽  
Current Injection ◽  
Single Action ◽  
Epileptiform Discharges

1. Hippocampal slices bathed in 8 mM potassium and 0-added calcium exhibited spontaneous epileptiform activity in the dentate gyrus. Extracellular recording revealed recurrent prolonged bursts of population spikes and an associated negative DC shift. These episodes were very similar to the in vivo phenomenon termed maximal dentate activation (MDA). Therefore this in vitro activity will be referred to as MDA-like activity or events. 2. During the MDA-like activity, the individual granule cells exhibited a sustained depolarization that matched the duration of the negative extracellular DC shift. At the beginning of the MDA-like activity, there was a burst of action potentials. After the burst, most granule cells either continued to fire action potentials regularly or in bursts. Some cells exhibited this initial burst of activity and then a dramatic reduction in firing rate. This reduction in rate was followed by a gradual increase in the amplitude and frequency of the epileptiform activity recorded during the remainder of the MDA-like event. 3. Before and between MDA-like events, spontaneous cellular activity consisted of single action potentials and bursts of action potentials on a depolarizing envelope. In addition, depolarizing potentials, up to 13 mV, were recorded. There were no extracellular field potentials associated with these intracellularly recorded potentials. 4. In the 8 mM potassium, 0-added calcium test solution, the membrane potential threshold for burst production was significantly lower than in normal potassium and calcium medium. 5. The effect of depolarizing and hyperpolarizing current injections on the amplitude and frequency of the epileptiform activity was tested. Current injection had no effect on the frequency of the epileptiform activity recorded during the MDA-like events. However, the frequency of the cellular bursts between MDA-like events was very sensitive to current injection. Depolarizing current increased the frequency, and hyperpolarizing current decreased the frequency of the spontaneous activity. 6. This study has shown that in 8 mM potassium and 0-added calcium the granule cells of the dentate gyrus are capable of generating spontaneous bursts that appear to be mediated by endogenous mechanisms. In addition, synchronized epileptiform discharges were recorded from the granule cells at regular intervals that appear were recorded from the granule cells at regular intervals that appear to be mediated by exogenous nonsynaptic mechanisms.

Opponent effects of potassium on GABAA-mediated postsynaptic inhibition in the rat hippocampus

1993 ◽  
Vol 69 (3) ◽  
pp. 764-771 ◽  
Author(s):  
M. S. Jensen ◽  
E. Cherubini ◽  
Y. Yaari
Keyword(s):  
Time Course ◽  
Gabab Receptor ◽  
Hippocampal Slices ◽  
Gaba Release ◽  
Extracellular Potassium ◽  
Inhibitory Interneurons ◽  
Gamma Aminobutyric Acid ◽  
Outward Rectification ◽  
High K ◽  
Input Conductance

1. The effects of raising the concentration of extracellular potassium ([K+]o) on gamma aminobutyric acid (GABA)-mediated inhibitory postsynaptic potentials (IPSPs) were investigated in adult rat hippocampal slices using intracellular recording techniques. IPSPs were evoked in CA1 pyramidal neurons by direct activation of inhibitory interneurons in slices treated with glutamatergic antagonists to block excitatory synaptic transmission. The fast (Cl(-)-dependent, GABAA receptor-mediated) IPSPs (fIPSPs) were isolated from the slow (K(+)-dependent; GABAB receptor-mediated) IPSPs (sIPSPs) by intracellular injection of QX-314, which also suppressed fast (Na(+)-dependent) action potentials. 2. In normal (3.5 mM) and in high (7.5 mM) [K+]o, the peak fIPSP amplitude changed nonlinearly with membrane potential (VM) in a way consistent with outward rectification of the underlying conductance. The input conductance of the fIPSP (GfIPSP) measured around resting VM (about -67 mV) increased 1.7-fold on changing from normal to high-K+ saline, whereas resting VM depolarized 6.8 mV. Repolarizing VM reversed the increase in GfIPSP, suggesting that it was due to outward rectification. The resting input conductance of the neurons increased 1.4-fold in high K+. 3. The time course of fIPSPs was prolonged by high K+. The half time of fIPSP decay increased 1.4-fold, and in half of the neurons the decay became conspicuously multipeaked, suggesting that neurally evoked GABA release from inhibitory interneurons was prolonged. 4. In normal K+, the reversal potentials of fIPSPs (EfIPSP; -76.5 mV) was 9.7 mV more negative than resting VM. Polarizing VM 10–20 mV for 15 min with current injection did not change EfIPSP appreciably.(ABSTRACT TRUNCATED AT 250 WORDS)

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