PubMed Health⌕ Search

Biomedical subjects

Y Grossman

Publications and source records attributed to Y Grossman.

At least 19 recordsLinked to original sources
PubMed1999

Reduced synaptic facilitation between pyramidal neurons in the piriform cortex after odor learning.

Learning-related cellular modifications were studied in the rat piriform cortex after operand conditioning. Rats were trained to discriminate positive cues in pairs of odors. In one experimental paradigm, rats were trained to memorize 35-50 pairs of odors ("extensive training"). In another paradigm, training was continued only until rats acquired the rule of the task, usually after learning the first two pairs of odors ("short training"). "Pseudotrained" and "naive" rats served as controls. We have previously shown that "rule learning" of this task was accompanied by reduced spike afterhyperpolarization in pyramidal neurons in brain slices of the piriform cortex. In the present study, synaptic inputs to the same cells were examined. Pairs of electrical stimuli applied to the intrinsic fibers that interconnect layer II pyramidal neurons revealed significant reduction in paired-pulse facilitation (PPF) in this pathway even after short training. PPF in shortly trained rats was reduced to the same extent as in extensively trained rats. PPF reduction did not result from modification of membrane properties in the postsynaptic cells, change in postsynaptic inhibition, or impairment of the facilitation mechanism. Extracellular field potential recordings showed enhanced synaptic transmission in these synapses. The reduction in PPF became apparent only 3 d after task acquisition and returned to control value 5 d later. PPF evoked by stimulating the afferent fibers to the same neurons was increased 1 d after training for 2 d. We suggest that the transient enhancement in connectivity in the intrinsic pathway is related to the enhanced learning capability and not to memory for specific odors, which lasts for weeks.

Afferent Pathways↗
PubMed1999

Spontaneous Na+ and Ca2+ spike firing of cerebellar Purkinje neurons at high pressure.

The effects of high pressure (up to 10.1 MPa) on the spontaneous firing of Purkinje neurons in guinea-pig cerebellar slices were studied using the macropatch clamp technique. Pressure did not significantly alter the single somatic Na+ spike parameters or the frequency of regular Na+ spike firing. When Na+ currents were blocked by 0.5-1 microM tetrodotoxin (TTX), a pressure of 10.1 MPa slightly reduced the dendritic Ca2+ spike amplitude to 90.2+/-3.1% of its control value, and slowed its kinetics. The effects of pressure on the single Ca2+ spike were even less prominent when K+ currents were blocked by 5 mM 4-aminopyridine (4-AP). Pressure prolonged the active period of Ca2+ spike firing to 152.2+/-10.4% of the control value. Within the active period pressure increased the inter-spike interval to 164.9+/-8.7% and suppressed the typical firing of doublets. The latter changes were reversed by a high extracellular potassium concentration ([K+]o) and 1 microM 4-AP, whereas in the presence of 5 mM 4-AP the pattern was insensitive to pressure. A high [Ca2+]o reduced the firing frequency and suppressed doublet firing in a manner reminiscent of the pressure effect, but these changes could not be reversed by 4-AP. A low [Ca2+]o slightly increased the firing of doublets. These results show that the single somatic Na+ spike is insensitive and the dendritic Ca2+ spike is only mildly sensitive to pressure. However, alterations in Ca2+ spike firing pattern suggest that modulation of dendritic K+ currents induce depression of dendritic excitability at pressure.

4-Aminopyridine↗
PubMed1998

Potassium currents modulation of calcium spike firing in dendrites of cerebellar Purkinje cells.

The pattern of sustained Ca2+ spike firing was investigated, using macropatch clamp and intracellular recordings, in guinea pig cerebellar Purkinje cells. Under our standard experimental conditions (30 degrees C, 5 mM [K+]o, 2 mM [Ca2+]o, 1 microM tetrodotoxin), each firing period started with uniform firing and gradually turned into a doublet pattern with a large spike afterhyperpolarization (AHP) between the doublets. Macropatch clamp recordings from localized dendritic regions revealed that each doublet is composed of two similar inward current deflections. This result indicated, for both peaks, an active process in the recording site and contradicted the possibility that they reflect firing in two completely separated dendritic regions. When [K+]o was increased the transition to a doublet pattern occurred earlier and the doublets became more pronounced. A similar but more prominent effect occurred following application of 1-10 microM 4-aminopyridine, which also reduced the threshold, increased the spike amplitude, and shortened the initial delay of evoked Ca2+ spike firing. In contrast, membrane depolarization, increased [Ca2+]o, and application of quinidine (but not apamine) markedly suppressed the generation of doublet pattern. During uniform initial firing, a short hyperpolarizing pulse that mimicked a large AHP induced a subsequent doublet. A short depolarizing pulse following a single spike induced an artificial doublet followed by a large AHP. These results indicate that the pattern of Ca2+ spike firing in the dendrites of Purkinje cells is dynamically modulated by a highly aminopyridine-sensitive K+ current, and probably also by a Ca2+-activated potassium current.

4-Aminopyridine↗
PubMed1998

The effect of a high partial pressure of carbon dioxide environment on metabolism and immune functions of human peritoneal cells-relevance to carbon dioxide pneumoperitoneum.

OBJECTIVE: Our purpose was to evaluate in vitro the effect of a high partial pressure of carbon dioxide environment used in laparoscopy on metabolic and immune response of various human peritoneal cells. STUDY DESIGN: Polymorphonuclear leukocytes were obtained from 5 healthy volunteers, peritoneal macrophages were obtained from the effluent of 8 patients undergoing continuous ambulatory peritoneal dialysis, and human peritoneal mesothelial cell cultures were prepared from omentum derived from 5 patients undergoing elective surgery. The cells were exposed to a laparoscopy-like environment (1 atmosphere carbon dioxide and 0.2 atmosphere oxygen), to a control gas mixture (1 atmosphere helium and 0.2 atmosphere oxygen), or air for 3 hours. After exposure to gas mixtures, cell functions were tested at various recovery periods. RESULTS: Three hours of exposure to a high partial pressure of carbon dioxide had no effect on viability of peritoneal macrophages and human peritoneal mesothelial cells, tested by trypan blue dye uptake and lactate dehydrogenase release. A high partial pressure of carbon dioxide decreased the mitochondrial dehydrogenases activity of peritoneal macrophages and human peritoneal macrophage cells by 60%, assayed by 3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide reduction. High partial pressure of carbon dioxide blocked the superoxide release from activated polymorphonuclear leukocytes and the secretion of interleukin 1beta from stimulated peritoneal macrophages, and human peritoneal macrophage cells were decreased by 15% and 30% and the secretion of tumor necrosis factor-alpha from peritoneal macrophages was suppressed by 85%. Mitochondrial activity, polymorphonuclear leukocyte function, and interleukin 1beta and tumor necrosis factor-alpha secretion returned to normal after a recovery period of 12 to 24 hours, 4.5 hours, and 24 hours, respectively. In the control experiments exposure of cells to helium had no suppressive effect. CONCLUSIONS: Exposure of cells to a high partial pressure of carbon dioxide environment suppresses the inflammatory and metabolic responses of peritoneal cells. We suggest that this suppressive effect may contribute to the low postsurgery adhesion formation and the reduction in postoperative pain observed in laparoscopy. Nevertheless, the suppression of the immune response should also be taken into account for operations involving a high risk of bacterial dissemination.

Ascitic Fluid↗
PubMed1998

Reduced after-hyperpolarization in rat piriform cortex pyramidal neurons is associated with increased learning capability during operant conditioning.

Learning-related cellular modifications were studied in the rat piriform cortex. Water-deprived rats were divided to three groups: 'trained' rats were trained in a four-arm maze to discriminate positive cues in pairs of odours, 'control' rats were 'pseudo-trained' by random water rewarding, and 'naive' rats were water-deprived only. In one experimental paradigm, the trained group was exposed to extensive training with rats learning to discriminate between 35 and 50 pairs of odours. Piriform cortex pyramidal neurons from 'trained', 'control' and 'naive' rats did not differ in their passive membrane properties and single spike characteristics. However, the after-hyperpolarizations (AHPs) that follow six-spike trains were reduced after 'extensive training' by 43% and 36% compared with 'control' and 'naive', respectively. This effect was not observed in the piriform cortex of another group of rats, in which hyperexcitability was induced by chemical kindling. In another experimental paradigm rats were trained only until they demonstrated 'rule learning', usually after discriminating between one and two pairs of odours ('mild training'). In this experiment, a smaller, yet significant, reduction (20%) in AHPs was observed. AHP reduction was apparent in most of the sampled neurons. AHP remained reduced up to 3 days after the last training session. 5 days or more after the last training session, AHP amplitude recovered to pre-training value and did not differ between 'trained' rats and the others. Accordingly, training suspension for 5 days or more resulted in slower learning of novel odours. We suggest that increased neuronal excitability, manifested as reduced AHP, is related to the ability of the cortical network to enter a 'learning mode' which creates favourable conditions for enhanced learning capability.

Animals↗
PubMed1996

GABA metabolism controls inhibition efficacy in the mammalian CNS.

The effects of changes in gamma-aminobutyric acid (GABA) metabolism or inhibitory processes was studied in the perforant path-dentate gyrus synapses in rat cortico-hippocampal slices, and in the monosynaptic-reflex circuit in isolated newborn, rat spinal cord. GABA metabolism was modulated by pharmacological block of either the anabolic enzyme glutamate decarboxylase (GAD) or the catabolic enzyme GABA transaminase (GABA-T). The results support the notion that GABA concentration determines the efficacy of inhibition in these regions of the central nervous system (CNS).

3-Mercaptopropionic Acid↗
PubMed1996

Pressure exposure unmasks differences in release properties between high and low yield excitatory synapses of a single crustacean axon.

The cellular mechanisms underlying the effect of high pressure on synaptic transmission at two types of synapses were studied in the opener muscle of the lobster walking leg. Excitatory postsynaptic currents (EPSCs) were recorded using a loose macropatch clamp technique at normal pressure and 3.5, 6.9 MPa helium pressure. Responses of the single excitatory axon could be grouped into two types: low yield (L) synapse exhibiting a small mean EPSC with a considerable number of failures, and high yield (H) synapse having a larger mean EPSC with very few failures. The change in several synaptic transmission parameters indicated that high pressure similarly reduced presynaptic evoked release in both L and H synapses. However, some differences in the kinetics and probability of release could be detected. A major difference was the spontaneous miniature EPSCs (mEPSCs) activity. Many of the mEPSC, observed only in L synapses, were 'giant' (size of 2-5 q). High pressure selectively increased the frequency of the giant mEPSCs in the L synapse but had little effect on their amplitude histogram. High pressure depressed evoked synaptic transmission in both synapses by modulating the presynaptic quantal release parameters, but concomitantly enhanced spontaneous quantal release in L synapses by an unknown mechanism.

Animals↗
PubMed1996

Block of glutamate decarboxylase decreases GABAergic inhibition at the crayfish synapses: possible role of presynaptic metabotropic mechanisms.

1. The cytosolic concentration of a neurotransmitter is believed to be an important factor determining its release. The effects of 3-mercaptopropionic acid (MP) and aminooxyacetic acid (AOAA), glutamate decarboxylase (GAD) blockers, on GABAergic postsynaptic and presynaptic inhibitory neurotransmission were examined in the crayfish (Procambarus clarkii) opener neuromuscular synapses. 2. Intracellular recordings of evoked excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials (IPSPs) as well as loose macropatch clamp measurements of excitatory postsynaptic currents (EPSCs) and inhibitory postsynaptic currents (IPSCs) were used to evaluate the effects of the drugs, which were applied exclusively to the nerve bundle. 3. Under normal conditions, a stimulus train to the inhibitor preceding the excitor stimulation elicited a large reduction in EPSP amplitude in a time interval-dependent manner. This inhibition is effected by postsynaptic as well as presynaptic processes. 4. Treatment with MP or AOAA decreased the IPSP amplitude and its altered conductance but had no effect on the IPSP reversal potential or the resting potential of the cell. They did, however, slightly increase the Rin of the fiber. 5. Quantal analysis of single IPSCs revealed that GAD blockers increased the number of failures and thus reduced quantal content (m), diminished the probability of release (p), but did not affect the quantum current (q) or the statistical parameter (n), believed to be the number of available active zones. 6. Quantal analysis of EPSCs, released after interaction with the inhibitor, revealed a reduction in m without any effect on q. GAD blockers greatly reduced the efficacy of this inhibition without affecting the EPSC q. 7. GAD blockers increased the output of the excitor release sites by the following mechanisms: 1) increased EPSC, 2) increased EPSC facilitation, or 3) enhancement of spontaneous activity (miniature EPSCs). 8. Short time incubation with picrotoxin and CGP-35348 eliminated IPSCs and evoked inhibition. However, longer exposure (90 min) increased the excitor responses, similarly to the effects of GAD blockers. 9. Baclofen, a gamma-aminobutyric acid-B (GABAB) agonist, antagonized AOAA effects on evoked inhibition. 10. These results demonstrate that GAD blockers decrease postsynaptic and presynaptic inhibition by reducing both tonic and evoked release, most likely by diminishing p. 11. The reduction in GABA synthesis and release revealed a complex mechanism for GABAergic metabotropic regulation of inhibition efficacy and the release from the excitor glutamatergic terminals.

3-Mercaptopropionic Acid↗
PubMed1995

Analysis of evoked and spontaneous quantal release at high pressure in crustacean excitatory synapses.

The cellular mechanisms underlying the effect of high pressure on synaptic transmission were studied in the opener muscle of the lobster walking leg. Excitatory postsynaptic currents (EPSCs) were recorded using a loose macropatch-clamp technique at normal pressure and 3.5, 6.9 MPa helium pressure. Responses of the single excitatory axon could be grouped into two types: low-yield (L) synapses exhibiting small EPSCs with a considerable number of failures, and high-yield (H) synapses having larger EPSCs with very few failures. High pressure reduced the average EPSC amplitude in all synapses and shifted their amplitude histograms to the left by decreasing the quantal content (m) without changing their quantum current (q). A binomial distribution fit of EPSC amplitudes revealed that high pressure greatly decreased n, the number of available active zones, but the effect on p, the probability of release for each zone, was not consistent. Many of the spontaneous miniature EPSCs (mEPSCs), observed only in L-type synapses, were "giant" (size = 2-5 q). High pressure increased the frequency of the giant mEPSCs but had little effect on their amplitude histogram. High pressure depressed evoked synaptic transmission by modulating the presynaptic quantal release parameters, but concomitantly enhanced spontaneous quantal release by an unknown mechanism.

Air Pressure↗
PubMed1995

Extracellular ATP induces hyperpolarization and motility stimulation of ciliary cells.

Cellular membrane potential and ciliary motility were examined in tissues cultures prepared from frog palate and esophagus epithelia. Addition of micromolar concentrations of extracellular ATP caused membrane hyperpolarization and enhanced the beat frequency. These two effects of ATP were 1) dose dependent, reaching a maximum at 10 microM ATP; 2) dependent on the presence of extracellular Ca2+ or Mg2+; 3) insensitive to inhibitors of voltage-gated calcium channels; 4) abolished after depleting the intracellular Ca2+ stores with thapsigargin; 5) attenuated by quinidine (1 mM), Cs+ (5-20 mM), and replacement of extracellular Na+ by K+; 6) insensitive to charybdotoxin (5-20 nM), TEA (1-20 microM), and apamin (0.1-1 microM); 7) independent of initial membrane potential; and 8) unaffected by amiloride. In addition, extracellular ATP induced an appreciable rise in intracellular Ca2+. Addition of thapsigargin caused an initial enhancement of the ciliary beat frequency and membrane hyperpolarization. These results strongly suggest the involvement of calcium-dependent potassium channels in the response to ATP. The results show that moderate hyperpolarization is closely associated with a sustained enhancement of ciliary beating by extracellular ATP.

Adenosine Triphosphate↗
PubMed1995

Laminar pattern of synaptic inhibition during convulsive activity induced by 4-aminopyridine in neocortical slices.

1. Epileptiform activity was induced in rat neocortical brain slices by application of a low concentration (10 microM) of 4-aminopyridine (4-AP). In intracellular recordings from regular spiking neurons, the activity was characterized by prolonged, all-or-none depolarizing events, with variable delay to a threshold stimulus. 2. At this concentration, 4-AP had no measurable effect on passive electrical properties or on action-potential characteristics. 3. Paroxysmal responses in neurons of deeper layers differed markedly from those of superficial cells. In deep neurons, responses resembled those generated by neocortical neurons exposed to GABAergic blockers. A low-intensity stimulus to the white matter evoked an excitatory postsynaptic potential (EPSP) that was followed with variable latency by a paroxysmal depolarizing shift that reversed at suprathreshold membrane potentials and upon which superimposed repetitive firing was always evident. By contrast, in superficial (layer II-III) neurons, the same stimulus evoked an EPSP that was followed by a prolonged response whose late component reversed at subthreshold membrane potentials (between -50 and -80 mV). These cells rarely fired more than a single spike throughout the response. 4. Repetitive stimulation at relatively low frequencies (0.3-1 Hz) caused a gradual change in the synchronized responses that was most marked in superficial neurons. The reversal potential of the response shifted toward suprathreshold membrane potentials, and subsequently, superimposed repetitive firing became evident. These changes were not associated with measurable changes in input resistance or membrane potential.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Aminopyridine↗
PubMed1994

Quantal analysis of presynaptic inhibition, low [Ca2+]0, and high pressure interactions at crustacean excitatory synapses.

The cellular mechanisms underlying the effects of high pressure, GABAergic presynaptic inhibition, and low [Ca2+]0 on glutamatergic excitatory synaptic transmission were studied in the opener muscle of the lobster walking leg. Excitatory postsynaptic currents (EPSCs) were recorded with or without prior stimulation of the inhibitor using a loose macropatch clamp technique at atmospheric pressure and at 6.9 MPA helium pressure. High pressure reduced the mean EPSC amplitude and variance, decreased the quantal content (m), but did not affect the quantum current (q). Pressure shifted the median of the amplitude histogram to the left by 1-2 q. Under normal pressure conditions, presynaptic inhibition and low [Ca2+]0 induced similar effects. However, quantal analysis using a binomial frequency distribution model revealed that high pressure and low [Ca2+]0 diminished n (available active zones) and slightly increased p (probability of release), but presynaptic inhibition reduced p and slightly increased n. At high pressure, presynaptic inhibition was reduced, at which time the major contributor to the inhibitory process appeared to be reduction in n and not p. The similarity of the alterations in quantal parameters of release at high pressure, low [Ca2+]0, and in some conditions of presynaptic inhibition is consistent with the hypothesis that pressure reduces Ca2+ inflow into the presynaptic nerve terminals to affect the Ca(2+)-dependent quantal release parameters n and p.

Animals↗
PubMed1994

Block of GABA-transaminase modifies GABAergic transmission at the crayfish synapses.

1. The cytosolic concentration of a neurotransmitter is believed to be an important factor determining its release. The effects of ethanolamine-O-sulfate (EOS), a gamma-aminobutyric acid (GABA)-transaminase blocker, on GABAergic postsynaptic and presynaptic inhibitory neurotransmission were examined in the crayfish opener neuromuscular synapses. 2. Intracellular recordings of evoked excitatory (EPSPs) and inhibitory postsynaptic potentials (IPSPs) as well as loose macropatch clamp measurements of excitatory (EPSCs) and inhibitory postsynaptic currents (IPSCs) were used to evaluate the effects of the drug, which was applied exclusively to the nerve bundle. 3. Under normal conditions, a stimulus train to the inhibitor before the excitor stimulation elicited two phases of inhibition: 1) a large reduction in EPSP amplitude associated with a decrease in its time constant of decay (tau D) at time intervals of 0-15 ms and 2) a moderate decrease in EPSP amplitude with a small change in EPSP tau D at intervals of 15-90 ms. EOS treatment selectively increased the inhibition of phase 2. 4. The muscle membrane electrical parameters and the existing postsynaptic tonic release of GABA were not affected by the drug. 5. EOS did not alter the IPSP's parameters such as amplitude, reversal potential, and conductance. 6. Quantal analysis of single IPSCs revealed no significant changes in the statistical parameters such as quantum size (q), quantal content (m), number of active zones (n), or probability of release (p). 7. Quantal analysis of EPSCs, released after interaction with the inhibitor, did exhibit a large reduction in m without any effect on q. 8. These results demonstrate that EOS has a specific and differential effect on neural transmission in two synapses of the same axon: it increases presynaptic inhibition without significant effect on the postsynaptic inhibitory mechanism.

4-Aminobutyrate Transaminase↗
PubMed1994

Long-term changes in neocortical activity after chemical kindling with systemic pentylenetetrazole: an in vitro study.

1. Rats were chemically kindled by systemic administration of pentylenetetrazole (PTZ) every 48 h. An initially subthreshold dose that did not elicit a motor response when first applied caused severe epileptiform seizures when the animal was kindled. Once kindled, animals continued to respond to the initially subthreshold dose with a full-blown seizure for > 2 mo, even when regular administration ceased for > or = 1 mo. 2. In neocortical slices taken from kindled rats, low-intensity electrical stimulation evoked generation of prolonged (hundreds of milliseconds) paroxysmal extracellular field potentials and intracellular depolarizing potentials, indicating synchronized activity of large populations of neurons. This hyperexcitability usually appeared as an all-or-none event of variable latency. In a few cases it increased gradually with increasing stimulus intensity. The intensity of the paroxysmal response was greatly enhanced by application of gamma-aminobutyric acid-A (GABAa) receptor blockers to the bath. 3. Intracellular recordings revealed that PTZ-kindled cells differ from normal cells in their higher input resistance (42.4 + 13.6 vs. 26.4 + 9.2 M omega, mean +/- SE). Spikes generated by kindled cells differed significantly from those in normal cells in that they were of longer duration (1.65 + 0.3 vs. 1.40 + 0.15 ms) and had a slower maximal rate of fall (103 + 29.7 vs. 126 + 20.8 volts/s). 4. Injection of the lidocaine derivative QX-314 to the recorded neurons (100 mM) blocked the fast Na+ spikes. Under these conditions slow spikes, probably Ca2+ mediated, were evoked from the soma in neurons from kindled but not from normal cortex. 5. The role of N-methyl-D-aspartate (NMDA) receptors in generating paroxysmal events was evaluated by application of 20 microM 2-amino-5-phosphonovaleric acid, a specific blocker of this glutamate receptor type. Blockage of NMDA receptors cut short the paroxysmal field potentials but did not prevent their generation. Intracellularly recorded paroxysmal responses were also cut short but not abolished by intracellular hyperpolarization. 6. In slices from kindled animals intracellular responses in neurons of deeper layers differed markedly from those of superficial cells. In deep neurons, responses resembled those generated by neocortical neurons exposed to GABAergic blockers. A low-intensity stimulus to the white matter evoked an excitatory postsynaptic potential (EPSP) followed with variable latency by a paroxysmal depolarizing shift that reversed at suprathreshold membrane potentials and on which superimposed repetitive firing was always evident.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Evaluation of a hyperbaric system to be used in conjunction with a fluorometer.

A high-pressure chamber that can be used inside the sample chamber of a spectrofluorometer is described and some performance characteristics are presented. The chamber body, constructed of 316 stainless steel, is temperature regulated using resistive heating elements and a microprocessor-based proportional integral derivative controller. The chamber holds a standard 1-cm2 cuvette that indexes with an electromagnetic stirrer. Injection of different solutions into the closed and pressurized (6.8 MPa) vessel is accomplished by computer-controlled, low-volume solenoids attached to separate microliter injection ports. Repetitive injections of fluids down to a volume of 7 microliters are possible in the pressurized chamber. Temperature stability of the chamber is +/- 0.2 degrees C at atmospheric or elevated pressure. However, during the initial phase (first 3 min) of pressurization, at a compression rate of 0.62 MPa/min, a 0.23 degrees C/min increase in temperature occurs. The chamber windows depress the relative intensity of the emitted light by approximately 20% for visible light and 40% for near UV; however, total sensitivity of the system is sufficient to accomplish most determinations while maintaining a good signal-to-noise ratio. This system can be used to evaluate the response of several molecular and cellular events during compression and at depth with the use of various fluorometric probes.

Atmosphere Exposure Chambers↗
PubMed1992

Effects of anticonvulsant drugs on axonal conduction in mammalian corpus callosum.

The frequency-dependent effect of various anticonvulsant drugs on the conduction in central axons was studied in the corpus callosum of rat and guinea pig brain slices from the parietal region. Extracellularly recorded compound action potentials (CAPs) were evoked by either single stimulus or high frequency stimulation (40-80 Hz). The CAP in rats consisted of an early component (fast axons, 1.2-1.8 m/s) and a late component (slow axons, 0.5-0.7 m/s), while in the guinea pig only the slow phase was observed. Diphenylhydantoin increased the latency of a single response by 10%, and had no effect on the CAP amplitude. In contrast, both phenobarbital and pentobarbital reduced the amplitude of singly evoked CAPs. Stimulation at high frequency alone decreased the CAP amplitude by 10-20%. Identical stimulation in the presence of the drugs further suppressed the CAP amplitude by an additional 31%, with varying degree of drug efficacy. The depressant effect was significant for the slow axons but the fast axons were virtually unaffected by any of the drugs. The results are consistent with the hypothesis that the antiepileptic drugs DPH, Phe and Pnt may block axonal conduction from an epileptic focus into neighbouring areas of the brain.

Action Potentials↗
PubMed1992

Synaptic transmission at high pressure: effects of [Ca2+]o.

1. The effects of pressure on synaptic currents were examined in crayfish abdominal muscles. 2. Helium pressure (10.1 MPa) considerably decreased extracellularly-recorded excitatory junctional potentials associated with increased short-term facilitation. 3. These effects could be mimicked by a reduction of [Ca2+]o, and partially compensated by an increase in [Ca2+]o. 4. Pressure also reduced the amplitude of the extracellular nerve terminal potentials (ENTP) by up to 25%, and significantly increased synaptic delay in a [Ca2+]o-dependent manner. 5. The interaction between compression and various [Ca2+]o were analysed in terms of an existing model of transmitter release. The results were consistent with the hypothesis that high pressure decreases the maximal Ca2+ influx into nerve terminals. 6. The decreased ENTP and increased synaptic delay suggest that additional processes may be involved in pressure effects on synaptic transmission.

Animals↗