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PubMed1985

Functional plasticity in two afferent systems of the granule cells in the rat dentate area: frequency-related changes, long-term potentiation and heterosynaptic depression.

Monosynaptic evoked field potentials (MEFP) were recorded in the dentate gyrus of male Wistar rats upon stimulation of either the perforant path or the commissural system. While the perforant path potential exhibited in acute experiments a clear reversal point of the field excitatory postsynaptic potential (EPSP) and population spike when protruding the registration electrode from the hippocampal fissura to the hilus of the dentate gyrus, the simultaneously registered commissural potential elicited by stimulation of the contralateral hilus showed no reversal of the negative monophasic wave but merely an amplitude maximum 40 microns above the reversal point of the perforant path potential. Frequency-related changes of the MEFPs during short tetanic stimulation with 15 Hz both in acute and chronic experiments, revealed differences in the properties of the input systems in that the commissural potential exhibited a clear frequency potentiation whereas the perforant path potential showed frequency depression. Pronounced long-term potentiation of the perforant path potential induced by 4 trains of tetanizing stimuli and lasting up to 72 h was accompanied by a long-term heterosynaptic depression of the commissural potential for up to 7 days after tetanization. Both the different frequency-related changes of the inputs and the extremely long duration of the heterosynaptic depression are discussed with respect to their proposed functions in the mechanisms of functional plasticity.

Animals↗
PubMed1987

Caffeine inhibits post-tetanic potentiation but does not alter long-term potentiation in the rat hippocampal slice.

The effects of caffeine were investigated on the extracellular excitatory postsynaptic potentials (EPSPs) recorded in the stratum radiatum of CA1 of the rat hippocampal slice in response to stimulation of the Schaffer collaterals. Caffeine in concentrations from 500 microM to 10 mM caused an increase in the amplitude of the EPSP, which reached a peak after 5-10 min perfusion. This increase was antagonized by pretreatment with 20 microM trifluoperazine. Paired-pulse facilitation, augmentation and potentiation were strongly inhibited by caffeine. Augmentation was most sensitive to caffeine, being abolished by 500 microM caffeine. Long-term potentiation (LTP) induced by high-frequency stimulation was not significantly inhibited by caffeine either by 5-10 min or by 60 min perfusion with 10 mM caffeine. Moreover, the caffeine-induced increase in the low-frequency EPSP could be reversed by 30 min washout, demonstrating that it was not an LTP type increase.

Afferent Pathways↗
PubMed1996

Fucose and fucosyllactose enhance in-vitro hippocampal long-term potentiation.

Bath application of L-fucose and 2-fucosyllactose (2FI) increases the potentiation of the population spike amplitude (POP-spike) and the field excitatory postsynaptic potential (fEPSP) after tetanization of the Schaffer collaterals of the rat hippocampus. The ineffective isomers D-fucose and 3-fucosyllactose (3-FI) have no such effect. Since not only the maintenance of long-term potentiation LTP is influenced but also its induction is drastically improved, an effect of the sugars via the formation of glycoproteins but also via different actions on induction mechanisms is discussed.

Animals↗
PubMed1989

In vitro electrophysiological analysis of mature rat hippocampal transplants in oculo.

We have investigated the maturation of isolated rat hippocampus grafted into the anterior chamber of the eye. Electrophysiological responses from transplants were compared to those recorded from the in vitro hippocampal slice preparation. Intracellular recording demonstrated that the passive membrane characteristics of intraocular hippocampal neurons were similar to those of the CA1 pyramidal cells in the in vitro slice preparation. However, the slow after-hyperpolarization which normally follows depolarization-induced action potentials was reduced or completely absent in the intraocular transplants, and the excitatory postsynaptic potential (EPSP) evoked by local stimulation was prolonged. The duration of the EPSP was reduced by perfusion with D-aminophosphonovaleric acid (2.5-50 microM), an N-methyl-D-aspartate receptor antagonist. Normal levels of glutamate decarboxylase (a marker for gamma-aminobutyric acidergic neurons) were found in the transplants, and responses to adenosine, bicuculline, and norepinephrine were similar in the in oculo transplants and in vitro slices. The data suggest that although many properties of hippocampal neurons are intrinsically determined, other aspects of the physiology of mature hippocampus either fail to develop, or develop abnormally in the absence of external inputs in oculo.

2-Amino-5-phosphonovalerate↗
PubMed1992

Long-term potentiation induced by patterned stimulation of the commissural pathway to hippocampal CA1 region in freely moving rats.

In urethane-anesthetized rats, stimulation of the contralateral hippocampal CA1 region resulted in activation of the homotopic CA1 region. Current-source-density analysis revealed that both basal and apical dendrites were activated. However, alveolar and stratum oriens stimulation in CA1 gave about equal peak excitation of the basal and apical dendrites while CA1 stratum radiatum/moleculare and CA3c stimulation gave stronger apical than basal dendritic excitation. In chronically implanted and freely moving rats, tetanic patterned stimulation of the contralateral CA1, irrespective of depth, resulted in a robust long-term potentiation of the ipsilateral CA1 basal dendritic synapse. The population basal dendritic excitatory postsynaptic potential was initially potentiated to greater than 200% of the baseline and decayed with a 3 h time constant; it lasted at least two days. Patterned stimulation of the commissural inputs at 2 x threshold stimulus intensity seldom potentiated the apical dendritic synapse in CA1; rather, long-term depression was sometimes observed. After tetanic stimulations at 3 x threshold, a small potentiation of the apical dendritic excitation was seen in about half of the experiments. The average apical dendritic potentiation peaked at about 25% and persisted to at least one day. This study provides original evidence that the properties of long-term potentiation are different at the commissural basal dendritic and apical dendritic synapses in CA1 of the behaving rat. Basal dendritic potentiation is low-threshold, high-amplitude and decayed rapidly in the first 3 h. Apical dendritic potentiation is high-threshold, low-amplitude and not rapidly decaying. A long-lasting enhancement of synaptic transmission has been postulated as a physiological correlate of memory. This paper reports properties of this synaptic enhancement for two different types of synapses on the same cells in the behaving animal. The basal dendritic synapse on hippocampal pyramidal cells readily increased their efficacy, up to at least two days, after a brief, patterned stimulation. In the same preparation, it was difficult to obtain a long-lasting increase in the apical dendritic excitation, in contrast to studies on isolated hippocampal slices in vitro.

Animals↗
PubMed1992

Connections between utricular nerve and dorsal neck motoneurons of the decerebrate cat.

1. We studied connections between the utricular (UT) nerve and dorsal neck motoneurons in decerebrate cats. Electrodes were fixed in place on the UT nerve under visual observation; the other branches of the vestibular nerve were transected. 2. The N1 field potential evoked by UT nerve stimulation was recorded in the vestibular nuclei at the start of each experiment. The potential typically grew until it reached a plateau. Stimulus spread (if any) to the central ends of other nerve branches was revealed by an additional increase in N1 amplitude after the plateau was reached. 3. We recorded intracellularly from 55 motoneurons in C1-C3. Some were identified as having axons in the dorsal rami, which innervate dorsal neck muscles. Others projected in nerves that were not available for stimulation. 4. UT nerve stimulation evoked synaptic potentials in essentially all motoneurons studied. The predominant pattern consisted of disynaptic excitatory postsynaptic potentials in ipsilateral motoneurons and inhibitory postsynaptic potentials that were at least trisynaptic in contralateral motoneurons. 5. The results demonstrate the presence of short-latency connections between the utricular nerve and dorsal neck motoneurons. The functional role of this pathway remains to be investigated.

Animals↗
PubMed1997

Excitatory amino acid receptors at a feedback pathway in the electrosensory system: implications for the searchlight hypothesis.

The electrosensory lateral line lobe (ELL) of the South American gymnotiform fish Apteronotus leptorhynchus has a laminar structure: electroreceptor afferents terminate ventrally whereas feedback input distributes to a superficial molecular layer containing the dendrites of the ELL principle (pyramidal) cells. There are two feedback pathways: a direct feedback projection that enters the ELL via a myelinated tract (stratum fibrosum, StF) and terminates in the ventral molecular layer (VML) and an indirect projection that enters as parallel fibers and terminates in the dorsal molecular layer. It has been proposed that the direct feedback pathway serves as a "searchlight" mechanism. This study characterizes StF synaptic transmission to determine whether the physiology of the direct feedback projection is consistent with this hypothesis. We used field and intracellular recordings from the ELL to investigate synaptic transmission of the StF in an in vitro slice preparation. Stimulation of the StF produced field potentials with a maximal negativity confined to a narrow band of tissue dorsal to the StF. Current source density analysis revealed two current sinks: an early sink within the StF and a later sink that corresponded to the anatomically defined VML. Field potential recordings from VML demonstrated that stimulation of the StF evoked an excitatory postsynaptic potential (EPSP) that peaked at a latency of 4-7 ms with a slow decay ( approximately 50 ms) to baseline. Intracellular recordings from pyramidal cells revealed that StF-evoked EPSPs consisted of at least two components: a fast gap junction mediated EPSP (peak 1.2-1.8 ms) and a chemical synaptic potential (peak 4-7 ms) with a slow decay phase ( approximately 50 ms). The amplitudes of the peak and decay phases of the chemical EPSP were increased by depolarizing current injection. Pharmacological studies demonstrated that the chemical EPSP was mainly due to ionotropic glutamate receptors with bothN-methyl--aspartate (NMDA) and non-NMDA components. NMDA receptors contributed substantially to both the early and late phase of the EPSP, whereas non-NMDA receptors contributed mainly to the early phase. Stimulation of the StF at physiological rates (100-200 Hz, 100 ms) produced an augmenting depolarization of the membrane potential of pyramidal cells. Temporal summation and a voltage-dependent enhancement of later EPSPs in the stimulus train permitted the compound EPSP to reach spike threshold. The nonlinear behavior of StF synaptic potentials is appropriate for the putative role of the direct feedback pathway as part of a searchlight mechanism allowing these fish to increase the electrodetectability of scanned objects.

Animals↗
PubMed1994

Changes in paired-pulse facilitation suggest presynaptic involvement in long-term potentiation.

Long-term potentiation (LTP) is a use-dependent form of synaptic plasticity that is of great interest as a potential cellular substrate underlying memory. It is important to determine the pre- and/or postsynaptic locus of LTP expression in order to study its underlying mechanisms. Despite intensive investigation, however, its locus of expression remains uncertain. It has been hypothesized that if LTP expression includes a presynaptic locus then it may alter the expression of another presynaptically mediated form of potentiation like paired-pulse facilitation (PPF), which is an increase in a second population excitatory postsynaptic potential when it is elicited shortly after a first. Previous authors have found no change in PPF in association with LTP. We re-examined the hypothesis, however, to reconcile the negative PPF data with other data that have suggested presynaptic involvement in LTP. Extracellular recordings were made in area CA1 of the rat hippocampal slice preparation. Surprisingly, PPF both increased and decreased significantly in association with LTP. The changes in PPF occurred in a predictable way, however. They correlated inversely with initial PPF magnitude so that a larger initial PPF was associated with a decrease in PPF with LTP while a smaller initial PPF was associated with an increase. Because PPF increased or decreased in individual slices in association with LTP, the average PPF of all slices did not change, in agreement with previous studies. The changes in PPF were also specific to LTP; that is, they were input specific, were not due to changes in inhibition or nonspecific effects of high-frequency stimulation, were not due to active postsynaptic currents or their nonlinear summation, and PPF changed with the same time course as LTP. We conclude that the mechanism of early LTP expression includes at least the presynaptic locus. Two hypotheses regarding the presynaptic mechanism underlying LTP expression, which are consistent with finding both increases and decreases in PPF with LTP, are (1) that there is an increase in the number of release sites with LTP or (2) that there is an increase in both the number of release sites and the probability of neurotransmitter release. Increases in the probability of neurotransmitter release alone would not appear to account for our findings since such increases have been associated only with decreases in PPF. Our findings do not exclude additional postsynaptic involvement.(ABSTRACT TRUNCATED AT 400 WORDS)

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1993

Postsynaptic potentials and morphological features of tectal cells in homing pigeons.

In this study postsynaptic potentials responding to the electrical stimulation of the optic nerve and the nucleus isthmi pars parvocellularis (Ipc) were intracellularly recorded from 86 tectal cells in pigeons, 13 of which were marked with Lucifer yellow (LY). According to types of postsynaptic potentials and their succession, the postsynaptic responses could be classified into four types: excitatory postsynaptic potential (EPSP)-inhibitory postsynaptic potential (IPSP) sequence (EI type), E, I and IE types. Among them, E or EI responses were mainly produced to the optic nerve stimulation, while the electrical stimulation of the Ipc elicited I responses in more than half the recorded cells. LY-marked tectal cells included five ganglionic cells, four pyramidal cells, two bipolar cells and two stellate cells. The ganglionic cells were mainly located in tectal layers III and IV, whereas the others were in layer II. It appears from both intracellular recordings and fluorescent markings that there is some correlation between the morphological features and the postsynaptic response types of tectal cells.

Animals↗
PubMed1997

Ethanol as a general anesthetic: actions in spinal cord.

Ethanol, usually studied in relation to intoxication, is also capable of producing general anesthesia. The most common standard of anesthetic potency is the concentration which produces immobility in response to a noxious stimulus. This concentration will be referred to as the anesthetic concentration. Immobilization is a spinal effect. Ethanol effects were studied in spinal cord from 2-7-day-old rats at concentrations which included the anesthetic concentration in both adult rats (97 mM) and 6-7-day-old rats (235 mM). At neonatal but not adult anesthetic concentrations, ethanol depressed monosynaptic reflex amplitude (mediated by glutamate AMPA receptors + compound action potential). At both neonatal and adult anesthetic concentrations ethanol reversibly depressed the population excitatory postsynaptic potential (pEPSP) (glutamate AMPA and NMDA receptors), the slow ventral root potential (NMDA + metabotropic receptors), and the dorsal root potential (GABA(A) receptors, via glutamate-excited interneurons). Effects were greater on NMDA receptor-mediated components than on AMPA-receptor-mediated components of the pEPSP and greater on NMDA than on metabotropic receptor-mediated components of the slow ventral root potential. The profile of ethanol effects on spinal cord resembles that of inhalation general anesthetics. The results show that both AMPA and NMDA receptor-mediated transmission are sensitive to ethanol and that enhancement of GABAergic neurotransmission is overridden by depression of excitation to the interneurons. They provide no obvious explanation for ethanol's lower general anesthetic potency in the neonate.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1997

Shunting inhibition does not have a divisive effect on firing rates.

Shunting inhibition, a conductance increase with a reversal potential close to the resting potential of the cell, has been shown to have a divisive effect on subthreshold excitatory postsynaptic potential amplitudes. It has therefore been assumed to have the same divisive effect on firing rates. We show that shunting inhibition actually has a subtractive effect on the firing rate in most circumstances. Averaged over several interspike intervals, the spiking mechanism effectively clamps the somatic membrane potential to a value significantly above the resting potential, so that the current through the shunting conductance is approximately independent of the firing rate. This leads to a subtractive rather than a divisive effect. In addition, at distal synapses, shunting inhibition will also have an approximately subtractive effect if the excitatory conductance is not small compared to the inhibitory conductance. Therefore regulating a cell's passive membrane conductance-for instance, via massive feedback-is not an adequate mechanism for normalizing or scaling its output.

Animals↗
PubMed1984

Analysis of intracellularly recorded phasic bursting by mammalian neuroendocrine cells.

Phasic bursting by magnocellular neuroendocrine cells (MNCs) in the mammalian supraoptic and paraventricular nuclei (SON and PVN) consists of successive periods of action potentials and inactivity. It has previously been correlated with increased release of vasopressin from the neurohypophysis. In the present studies we investigated the neuronal mechanisms underlying this firing pattern. Using coronal slices of rat hypothalamus, we recorded intracellularly from neurons that are considered to be MNCs, based on several criteria. Eight of the 29 cells in this study displayed phasic burst patterns similar to those previously recorded extracellularly from MNCs in intact animals. Among the eight phasic cells, low levels of steady current injection could dramatically alter burst periodicity. Steady hyperpolarization revealed patterned synaptic input in only one case; in the remainder of the cells, nonsynaptic mechanisms appeared to account for periodic bursting. The phasic burst pattern usually appeared to be spike dependent, each burst arising from one or several depolarizing after-potentials (DAPs). Summed DAPs formed a plateau potential, which provided a depolarizing drive for further spiking. Spike frequency decreased late in the burst, and then the plateau potential terminated. During the quiescent period, burst excitability appeared to increase coincident with a small slow depolarization. Spikes and their summating DAPs could then initiate another burst. In several silent MNCs, a brief supra-threshold current pulse could initiate a prolonged afterdischarge, which had the properties of a phasic burst. Two MNCs that fired with a fast-continuous pattern were tested with brief hyperpolarizing current pulses; after each pulse, spike activity ceased and a plateau potential was revealed. Therefore, it appears that a maintained plateau potential (summed DAPs) can drive fast-continuous firing. In one case a periodic bombardment of excitatory postsynaptic potentials (EPSPs) generated a phasic firing pattern. The dependence of the burst characteristics on membrane potential, the apparent lack of patterned synaptic input in most cells, and the ability to evoke bursts with brief stimuli support the hypothesis that bursting in some MNCs involves an endogenous mechanism. Furthermore, phasic firing may be driven by tonic excitatory input. The data on phasic, silent, and fast-continuous cells suggest that many MNCs can generate DAPs and plateau potentials.

Action Potentials↗
PubMed1999

Serotonergic modulation of neurotransmission in the rat basolateral amygdala.

Whole cell patch-clamp recordings were obtained from projection neurons and interneurons of the rat basolateral amygdala (BLA) to understand local network interactions in morphologically identified neurons and their modulation by serotonin. Projection neurons and interneurons were characterized morphologically and electrophysiologically according to their intrinsic membrane properties and synaptic characteristics. Synaptic activity in projection neurons was dominated by spontaneous inhibitory postsynaptic currents (IPSCs) that were multiphasic, reached 181 +/- 38 pA in amplitude, lasted 296 +/- 27 mS, and were blocked by the GABAA receptor antagonist, bicuculline methiodide (30 microM). In interneurons, spontaneous synaptic activity was characterized by a burst-firing discharge patterns (200 +/- 40 Hz) that correlated with the occurrence of 6-cyano-7-nitroquinoxaline-2,3-dione-sensitive, high-amplitude (260 +/- 42 pA), long-duration (139 +/- 19 mS) inward excitatory postsynaptic currents (EPSCs). The interevent interval of 831 +/- 344 mS for compound inhibitory postsynaptic potentials (IPSPs), and 916 +/- 270 mS for EPSC bursts, suggested that spontaneous IPSP/Cs in projection neurons are driven by burst of action potentials in interneurons. Hence, BLA interneurons may regulate the excitability of projection neurons and thus determine the degree of synchrony within ensembles of BLA neurons. In interneurons 5-hydroxytryptamine oxalate (5-HT) evoked a direct, dose-dependent, membrane depolarization mediated by a 45 +/- 6.9 pA inward current, which had a reversal potential of -90 mV. The effect of 5-HT was mimicked by the 5-HT2 receptor agonist, alpha-methyl-5-hydroxytryptamine (alpha-methyl-5-HT), but not by the 5-HT1A receptor agonist, (+/-) 8-hydroxydipropylaminotetralin hydrobromide (8-OH-DPAT), or the 5-HT1B agonist, CGS 12066A. In projection neurons, 5-HT evoked an indirect membrane hyperpolarization ( approximately 2 mV) that was associated with a 75 +/- 42 pA outward current and had a reversal potential of -70 mV. The response was independent of 5-HT concentration, blocked by TTX, mimicked by alpha-methyl-5-HT but not by 8-OH-DPAT. In interneurons, 5-HT reduced the amplitude of the evoked EPSC and in the presence of TTX (0.6 microM) reduced the frequency of miniature EPSCs but not their quantal content. In projection neurons, 5-HT also caused a dose-dependent reduction in the amplitude of stimulus evoked EPSCs and IPSCs. These results suggest that acute serotonin release would directly activate GABAergic interneurons of the BLA, via an activation of 5-HT2 receptors, and increase the frequency of inhibitory synaptic events in projection neurons. Chronic serotonin release, or high levels of serotonin, would reduce the excitatory drive onto interneurons and may act as a feedback mechanism to prevent excess inhibition within the nucleus.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1997

Dorsal spinocerebellar tract neurons are not subjected to postsynaptic inhibition during carbachol-induced motor inhibition.

Dorsal spinocerebellar tract (DSCT) neurons in Clarke's column in the lumbar spinal cord of cats anesthetized with alpha-chloralose were recorded intracellularly. The membrane potential activity and electrophysiological properties of these neurons were examined before and during the state of active-sleep-like motor inhibition induced by the injection of carbachol into the nucleus pontis oralis. The synaptic activity of DSCT neurons during carbachol-induced motor inhibition did not change compared with that during control conditions. In particular, there was an absence of inhibitory postsynaptic potentials (IPSPs) in high-gain recordings from DSCT neurons and the resting membrane potential of DSCT neurons was not significantly hyperpolarized during carbachol-induced motor inhibition. The mean amplitude of both monosynaptic excitatory postsynaptic potentials and disynaptic IPSPs evoked in DSCT neurons following stimulation of group I muscle afferents after the injection of carbachol was similar to that evoked before the injection of carbachol. There were no significant changes in the mean input resistance and membrane time constant of DSCT neurons during carbachol-induced motor inhibition. We conclude that, in contrast to lumbar motoneurons, DSCT neurons in Clarke's column are not postsynaptically inhibited during carbachol-induced motor inhibition. Therefore the population of spinal cord Ib interneurons that inhibit both DSCT neurons and lumbar motoneurons is not likely to be the interneurons that are responsible for the postsynaptic inhibition of motoneurons that occurs during carbachol-induced motor inhibition. The present findings also indicate that transmission through the DSCT is not modulated by postsynaptic inhibition at the level of DSCT neurons during carbachol-induced motor inhibition.

Animals↗
PubMed1995

Reduction of GABA-mediated inhibitory postsynaptic potentials in hippocampal CA1 pyramidal neurons following oral flurazepam administration.

Oral administration of the benzodiazepine, flurazepam, for one week results in tolerance in vivo and in vitro and in a reduction in recurrent and feedforward inhibition in vitro in the CA1 pyramidal cell region of hippocampus. In the present study CA1 pyramidal cells were examined intracellularly in vitro in rat hippocampal slices (500 microns) from rats sacrificed two or seven days after cessation of oral flurazepam treatment. Following drug treatment, the membrane characteristics of CA1 pyramidal cells were not significantly different from control neurons. GABAA-mediated, early inhibitory postsynaptic potentials were significantly reduced in amplitude (60%) in pyramidal neurons from rats killed two days, but not in those killed seven days, after the end of drug administration. The decrease in early inhibitory postsynaptic potential amplitude was observed using just-subthreshold, threshold and supramaximal orthodromic stimulation as well as following antidromic activation. The magnitude of the decrease in the early inhibitory postsynaptic potential amplitude was similar in the presence of the GABAB antagonist, CGP 35348, and could not be attributed to differences in the strength of afferent stimulation between flurazepam-treated and control groups. The size of the GABAB-mediated, late inhibitory postsynaptic potentials was also significantly decreased (45%) in comparison to control cells. Reversal potentials for both the early (-72 mV) and late (-92 mV) hyperpolarizations were not significantly different between groups. Following high intensity orthodromic stimulation, in the presence of an intracellular sodium channel blocker (QX-314) which also blocks the GABAB-mediated late hyperpolarization, a bicuculline-sensitive late depolarizing potential was unmasked in neurons from FZP-treated rats, but never from control cells. Excitatory postsynaptic potential amplitude was significantly increased in flurazepam-treated neurons and the threshold for the synaptically-evoked action potential was significantly increased. Following depolarizing current injection, the duration and frequency of pyramidal cell discharges and the action potential threshold were not altered by oral flurazepam treatment. The amplitude of the fast afterhyperpolarization was also not changed. Overall, the findings indicate an impairment of transmission at GABAergic synapses onto hippocampal CA1 pyramidal cell neurons after chronic benzodiazepine treatment at a time when rats are tolerant to the anticonvulsant effects of the benzodiazepines in vivo.

Acetates↗
PubMed1984

Facilitation of transmission at the crayfish neuromuscular synapse by a convulsant phenol.

The effects of the convulsant drug 4-Cl phenol on synaptic transmission were studied in the opener muscle of the crayfish walking leg. 4-Cl phenol was found to increase the amplitude of the excitatory postsynaptic potential without affecting the resting potential or input resistance of the muscle fiber. The drug did not change the frequency of spontaneous miniature postsynaptic potentials in K+-depolarized fibers. The postsynaptic voltage response to bath-applied glutamate (the excitatory transmitter compound) was decreased while the Cl(-) -conductance increase related to the action of bath-applied gamma-aminobutyric acid (the inhibitory transmitter) was not affected. In the light of previous results obtained on crayfish axons it is concluded that convulsant phenols induce an increase in the evoked release of transmitter by increasing the duration of the presynaptic depolarization through a block of voltage-dependent potassium channels.

Action Potentials↗
PubMed1987

Properties of stereotyped series of postsynaptic potentials in hypoglossal motoneurons.

A stereotyped series of postsynaptic potentials produced in cat hypoglossal motoneurons by stimulation of the cerebral cortex, the inferior alveolar nerve or the lingual nerve was studied. These include an excitatory postsynaptic potentials (EPSP) and subsequently 3 different types of inhibitory postsynaptic potentials (IPSPs). The first is a short-lasting IPSP which was blocked by strychnine administration. The second is a gamma-aminobutyric acid (GABA) IPSP which was blocked by picrotoxin administration. This IPSP was sensitive to membrane polarization and dependent on a conductance increase. The third is a long-duration hyperpolarizing potential which was enhanced by the injection of picrotoxin and insensitive to membrane polarization. Moreover, we have demonstrated that the amplitude of cortically induced EPSPs decreased greatly with depolarization.

Animals↗
PubMed1996

Physiological properties of rat ventral pallidal neurons recorded intracellularly in vivo.

1. The physiology of ventral pallidal (VP) cells was investigated using in vivo intracellular recording and staining techniques in adult rats. Based on electrophysiological criteria, three different types of cells were found: type A cells, which fired phasic spikes that did not exhibit a substantial afterhyperpolarization (AHP), type B cells, which exhibited a slow ramplike depolarization that preceded the short-duration action potential; the spike was followed by a prominent AHP, and type C cells, which were the only cells that fired spikes in couplets or bursts, with the spikes in a burst exhibiting a progressive increase in duration and a decrease in amplitude. These cells also exhibited a rebound low threshold spikelike event. Furthermore, 18% of the VP cells recorded exhibited a slow subthreshold oscillation of the membrane potential (< 1 Hz). 2. The response of VP cells to stimulation of fibers arising from the prefrontal cortex, nucleus accumbens, and mediodorsal thalamic nucleus (MD) was examined. In contrast to our initial predictions, all cells responded to nucleus accumbens stimulation with excitation. Type A and B cells responded to nucleus accumbens stimulation with excitation and to MD stimulation with antidromic-like responses, orthodromic excitation, or evoked inhibitory postsynaptic potentials. Only type A cells responded to prefrontal cortical stimulation. Type C cells only responded to stimulation of the nucleus accumbens, which resulted in evoked excitatory postsynaptic potentials. 3. The cells in the VP therefore can be segregated into three physiologically defined groups according to action potential discharge patterns and their response to afferent fiber stimulation.

Action Potentials↗