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PubMed1987

The effects of QX-314 on medullary respiratory neurones.

The synaptic and current-evoked responses of respiratory neurones located in the nucleus of the tractus solitarius, the para- and retroambigual regions and the nucleus ambiguus, were examined after voltage-dependent sodium currents were blocked by intracellular application of the quaternary lidocaine derivative QX-314. (1) QX-314 abolished orthodromically and antidromically evoked action potential discharge. Only antidromic action potentials recovered during negative DC current injection. (2) QX-314 did not alter the amplitude or duration of small and short excitatory and inhibitory postsynaptic potentials evoked by vagus or superior laryngeal nerve stimulation. Larger and longer waves of spontaneous membrane depolarizations, however, were slightly diminished. (3) The repetitive discharge evoked by depolarizing current pulses was blocked by QX-314. Positive current pulses produced less membrane depolarization than under control and often evoked only a single action potential at the beginning of the pulse, indicating that QX-314 interferes with the processes responsible for repetitive firing. (4) When fast spike discharges were completely blocked, positive current pulses occasionally evoked depolarizing 'spikes' and potentials which were followed by a hyperpolarization. We conclude that a noninactivating sodium inward current and calcium currents contribute to the electroresponsiveness of respiratory neurones.

Action Potentials↗

PubMed1990

Locally evoked potentials in slices of the rat nucleus accumbens: NMDA and non-NMDA receptor mediated components and modulation by GABA.

In a slice preparation of the rat nucleus accumbens (Acb), local electrical stimulation elicited a field potential composed of two negative peaks, followed by a positive wave. The early negative peak was identified as a non-synaptic compound action potential, the late negative peak as a monosynaptic population spike (PS) and the positive wave as a mixture of an excitatory and an inhibitory postsynaptic potential (PSP). Both the PS and the PSP exhibited a marked degree of paired-pulse facilitation. The quisqualate/kainate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 2 microM) and the broadly acting glutamate receptor antagonist kynurenic acid (300 microM) reversibly abolished or reduced both the PS and PSP. In contrast, nicotinic, muscarinic and N-methyl-D-aspartate (NMDA) receptor antagonists had no suppressive action. Washout of Mg2+ from the superfusion medium reversibly enhanced and prolonged the PSP and this effect was blocked by the NMDA receptor antagonist D(-)-2-amino-5-phosphonopentanoic acid (D-AP-5). The gamma-aminobutyric acid antagonist picrotoxin (60 microM) enhanced the PS and induced secondary spikes which were superimposed on a prolonged PSP. Most of this prolongation was abolished by D-AP-5. It is concluded that locally evoked synaptic responses in the Acb are mediated by glutamate or aspartate, and that NMDA receptor mediated activity evoked by low frequency stimulation is substantial in Mg2(+)-free medium or during reduced GABAA receptor activity, but not under normal conditions.

2-Amino-5-phosphonovalerate↗

PubMed1996

Photoinactivation of an identified motoneurone in the locust Locusta migratoria.

1. The common inhibitory motoneurone 1 (CI1) in the mesothoracic ganglion of the locust was photoinactivated using a helium-cadmium laser or a mercury lamp as light source. Treated animals showed no signs of abnormal locomotory behaviour over periods of up to 40 days. 2. Photoinactivation of part of the neurone in the ganglion, i.e. the soma and the primary neurite, is sufficient to cause irreversible degeneration of all the peripheral extensions of the neurone. Three weeks after photoinactivation, all GABA immunoreactivity had disappeared from the axon branches of the photoinactivated neurone and from their terminals on one of the target muscles investigated, the anterior coxa rotator M92, and inhibitory postsynaptic potentials could no longer be elicited through stimulation. This was taken as proof of functional denervation of the muscle with regard to its inhibitory input. By this time, the axon of CI1 in nerve N3C1, which supplies M92, had also disappeared. 3. Animals treated during the fourth or fifth instars showed a permanent loss of the photoinactivated mesothoracic CI1 neurone after moulting into adulthood. 4. Denervation of M92 in the middle legs of instars and adults by axotomy of N3 always led to rapid functional reinnervation of the muscle. The first sign of reinnervation (excitatory neuromuscular activity upon mechanical stimulation of the tarsi) was detected electrophysiologically as early as 8 days after severing the motor nerve. 5. The elimination of CI1 by photoinactivation for a period of up to 40 days did not influence parameters of the target muscle, such as size, number of fibres and phenotypes of fibres defined histochemically according to their myofibrillar ATPase isoforms, irrespective of whether the operation was performed in instars or adults. Similarly, the short period of denervation following axotomy before reinnervation took place did not affect the fibre type composition of the muscle.

Animals↗

PubMed1987

The effects of noradrenaline on neurones in the rat dorsal motor nucleus of the vagus, in vitro.

1. Intracellular recordings were made from vagal motoneurones identified by antidromic stimulation in the dorsal motor nucleus of the vagus (d.m.v.) in slice preparations of rat medulla oblongata. 2. Noradrenaline (NA) applied by perfusion (0.01 microM to 1 mM) depolarized 55%, hyperpolarized 32% and produced a biphasic response (hyperpolarization followed by depolarization) in 9% of the d.m.v. neurones tested. 3. The NA effects persisted after complete elimination of synaptic inputs during perfusion with Ca2+-free high-Mg2+ solution, and therefore probably resulted from a direct action on the postsynaptic membranes. 4. The NA depolarization was blocked by prazosin and the NA hyperpolarization by yohimbine, but neither was blocked by propranolol or timolol. Phenoxybenzamine blocked both responses. The results indicate that NA depolarization is mediated by alpha 1-adrenoceptors and hyperpolarization by alpha 2-adrenoceptors. 5. The neurones which were depolarized by NA were also hyperpolarized by NA when the alpha 1-adrenoceptors were blocked by prazosin (all of seven neurones tested). This result suggests that most vagal motoneurones in the d.m.v. have both alpha 1-and alpha 2-adrenoceptors. 6. The NA depolarization was accompanied by a decrease in membrane conductance and the hyperpolarization by an increase in membrane conductance, both of which were measured under manual-clamp conditions. 7. The reversal potentials for the NA responses were around -85 mV in normal Ringer solution, and shifted as predicted by the Nernst equation when the extracellular K+ concentration was changed. 8. The inhibitory postsynaptic potentials evoked by focal electrical stimulation on the slice surface of the commissural part of the nucleus of the tractus solitarius (n.t.s.), which contains an A2 catecholaminergic cell group, were abolished by yohimbine. 9. The results suggest that NA modulates vagal output by decreasing or increasing the K+ conductance of d.m.v. neurones through alpha 1- or alpha 2-adrenoceptors. In addition, the A2 noradrenergic cell group within the n.t.s. may send inhibitory inputs to the d.m.v.

Action Potentials↗

PubMed2000

Synaptically released 5-HT modulates the activity of tonically discharging neuronal populations in the rostral ventral medulla (RVM).

There is substantial evidence for an important modulating role of monoamines (catecholamines and serotonin, 5-HT) in the rostral ventral medulla (RVM), a region which plays an important role in cardiovascular and nociceptive functions. We investigated in slices the role of endogenous monoamines in the synaptic control of the activity of rat RVM neuronal populations using intracellular recordings in the lateral RVM plus lateral aspect of nucleus paragigantocellularis lateralis. A triple-labelling protocol allowed us to identify the location of impaled neurons and their eventual monoaminergic phenotype within the serotonergic and catecholaminergic populations of the RVM. Focal electrical stimulation revealed the existence of a functional monoaminergic input onto RVM neurons which was mediated by endogenous 5-HT acting at inhibitory 5-HT1A receptors but did not involve noradrenergic neurotransmission. The slow 5-HT-mediated inhibitory postsynaptic potential (IPSP) was only observed in the regularly discharging neurons, which were found to be neither catecholaminergic nor serotonergic. The synaptic release of 5-HT was, itself, under an inhibitory control involving GABAA (gamma-aminobutyric acid) receptors. Moreover, we characterized the effect of the 5-HT-releasing agent fenfluramine on this functional 5-HT-mediated synaptic transmission. Our results show that the effect of fenfluramine is biphasic consisting of an initial prolongation of the serotonergic IPSP followed by a decrease in amplitude. Our data provide a basis for the previously reported inhibitory effects of exogenously applied serotonin agonists/antagonists on the autonomic functions controlled by the RVM. This 5-HT pathway, which functionally links the serotonergic and catecholaminergic regions, might play an important role in cardiovascular and nociceptive functions.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed1984

Rat hippocampal neurons in culture: voltage-clamp analysis of inhibitory synaptic connections.

Inhibitory postsynaptic potentials (IPSPs) recorded at room temperature in cultured rat hippocampal neurons had the same reversal potential as Cl--dependent voltage responses to gamma-aminobutyric acid (GABA). The IPSPs had a relatively short latency and long duration and could be evoked for hours without change in their properties. They were consistently depressed by picrotoxin applied near cell bodies of the neurons under study. Postsynaptic cells exhibiting IPSPs were voltage clamped with two electrodes for the purpose of studying the properties of evoked inhibitory postsynaptic currents (IPSCs). The IPSCs shared the same reversal potential and sensitivity to [Cl-]i as was observed with membrane current responses to GABA. They were both depressed by picrotoxin, with little if any change in the kinetics of ion channel activity either estimated from fluctuation analysis of drug-depressed current responses to GABA or calculated from semilogarithmic plots of IPSC decay. The decay of the IPSC was well fitted by a single exponential with a time constant of about 20 ms, which corresponded closely to the estimated average duration of an ion channel activated by GABA. IPSC decay was sensitive to the potential at which the cell was held, increasing by up to 50% in some cells clamped at positive potentials relative to values obtained at the level of the resting potential. IPSCs were enhanced in amplitude by diazepam, which also prolonged their time constant of decay. Diazepam potentiated membrane current responses to GABA and fluctuation analysis of potentiated responses indicated that the drug effects could be accounted for by an increase both in estimated channel duration and channel frequency. IPSCs were also altered by pentobarbital, which markedly prolonged their time constant of decay with little if any change in their amplitude. Pentobarbital enhanced current responses to GABA, an effect that could be accounted for primarily in terms of a pronounced increase in estimated channel lifetime. None of the drugs used in the present study affected the elementary conductance estimated from fluctuation analysis of GABA-evoked current response. The results suggest that IPSPs and IPSCs evoked in these cultured hippocampal cells are mediated by GABA, about 1,700 Cl- ion channels are activated at the peak of the synaptic conductance, and clinically important drugs act postsynaptically on the kinetics of the channels so as to change the amplitude and/or time course of the synaptic conductance.

Animals↗

PubMed1987

Synaptic control of pyramidal cell activation in the hippocampal slice preparation in the rat.

Recordings were made from CA1 pyramidal neurons in a rat hippocampal slice preparation to compare the effectiveness of orthodromic stimuli when delivered at different distances from the cells under study. A stimulating electrode placed in stratum radiatum was less effective in driving nearby pyramidal cells (within 200 micron) than those farther away (greater than 800 micron). Thus for a given field excitatory postsynaptic potential both the intracellular excitatory postsynaptic potential and the evoked population spike were smaller when evoked from a local stimulating electrode than from one more distant. Laminar mapping experiments indicated that the spatial distribution of activated excitatory synapses over the pyramidal cell dendrites was similar for local and distant stimuli. The firing threshold, and the amplitude of hyperpolarizing inhibitory postsynaptic potentials, were also similar for the two stimuli. Responses evoked by the local stimulating electrode were more sensitive to morphine, penicillin and pentobarbital than responses elicited by the distant stimulus, suggesting that some form of GABAergic inhibition limited the efficacy of the local stimulus. The data suggest that in the CA1 region a vertically oriented synaptic inhibitory system exists that powerfully regulates the ability of an orthodromic stimulus to activate pyramidal cells. These results also illustrate the practical importance of controlling the distance between stimulating and recording electrodes, when performing quantitative pharmacological studies of synaptic transmission in the hippocampus.

Animals↗

PubMed1975

[Maturation of interhippocampal responses. Report and localization of inhibitory and excitatory synapses in the horn of Ammon of the young rabbit].

Extracellular recording from hippocampal areas of new-born rabbits up to 3 months of age was carried out to examine the responses evoked by stimulation of the contralateral alveus of CA1. In CA1, the extracellular potential fields show a positive wave whose amplitude is maximal at the somata of the pyramidal cells at any age. This positive wave has the same latency as an inhibitory postsynaptic potential induced in the same conditions and presumably represents inhibition at this level. In stratum oriens and at the top of stratum pyramidale, this positive wave is accompanied by ripples (at a frequency of about 200 c/sec) that are produced by basket cells. These ripples exhibit a very small amplitude up to 10 days of age. This positivity decreases in the depth towards the apical dendrite, reverses at the beginning of stratum radiatum and becomes rapidly negative. A second positive wave with ripples could be recorded from the layer of deep pyramidal cell somata belonging to the underlying CA3-CA4, only after 7 days. It is concluded that, in both the new-born and the adult rabbit, inhibitory synaptic action from contralateral stimulation is present on or close to the pyramidal cell somata, whereas excitatory action is located in the apical dendrites near the main branching.

Age Factors↗

PubMed2003

Lack of vesicular zinc in mossy fibers does not affect synaptic excitability of CA3 pyramidal cells in zinc transporter 3 knockout mice.

Zinc is found throughout the CNS in synaptic vesicles of glutamatergic neurons and has been suggested to have a modulatory role in the brain because of its interaction with voltage- and ligand-gated ion channels. We took advantage of zinc transporter 3 knockout mice, which lack vesicular zinc, to study the possible physiological role of this heavy metal in hippocampal mossy fiber neurotransmission. We examined postsynaptic responses evoked by mossy fiber activation, recorded in CA3 pyramidal cells in hippocampal slices prepared from zinc transporter 3 knockout and wild-type mice. Field-potential response threshold and amplitude, input-output curves, and paired-pulse evoked responses were the same in slices from zinc transporter 3 knockout and wild-type mice. Furthermore, neither amplitude nor duration of pharmacologically isolated N-methyl-D-aspartate, non-N-methyl-D-aspartate, GABA(A), and GABA(B) receptor-mediated postsynaptic potentials differed between zinc transporter 3 knockout and wild-type mice. There was no difference in the magnitude of epileptiform discharges evoked by repetitive stimulation or kainic acid application. However, in slices from zinc transporter 3 knockout mice, there was greater attenuation of GABA(A)-mediated inhibitory postsynaptic potentials during tetanic stimulation compared with slices from wild-type animals. We conclude that lack of vesicular zinc in mossy fibers does not significantly affect the mossy fiber-associated synaptic excitability of CA3 pyramidal cells; however, zinc may modulate GABAergic synaptic transmission under conditions of intensive activation.

Animals↗

PubMed1995

Neurophysiological changes of spiny neurons in rat neostriatum after transient forebrain ischemia: an in vivo intracellular recording and staining study.

The spontaneous activities, evoked postsynaptic potentials and membrane properties of spiny neurons in rat neostriatum were compared before, during and after 5-8 min ischemia using intracellular recording and staining techniques in vivo. Severe forebrain ischemia was induced with the four-vessel occlusion method. Approximately 2.5 min after the onset of ischemia the baseline membrane potential quickly depolarized to -20 mV and remained at this level during ischemia. Repolarization began within 2 min after recirculation. The onset of ischemic depolarization was directly related to the severity of ischemia and its latency was inversely related to brain temperature. Spontaneous firing and membrane potential fluctuation of spiny neurons ceased immediately after ischemia and slowly recovered several hours after recirculation. No neuronal hyperactivity was observed up to 7 h after recirculation. Cortically evoked inhibitory postsynaptic potentials and late depolarizations disappeared earlier after ischemia and recovered later following recirculation than the initial excitatory postsynaptic potentials. Membrane input resistance of spiny neurons was significantly increased but the time constant remained the same following recirculation. The rheobase and spike threshold of spiny neurons were significantly increased and the repetitive firing evoked by depolarizing current pulse was suppressed shortly after recirculation. The results of the present study indicated that the spontaneous activity and evoked postsynaptic responses of spiny neurons are suppressed and the excitability of spiny neurons is decreased after transient ischemia. The polysynaptic responses are more sensitive to ischemia than the monosynaptic ones.

Animals↗

PubMed2005

Oscillatory synchronization requires precise and balanced feedback inhibition in a model of the insect antennal lobe.

In the insect olfactory system, odor-evoked transient synchronization of antennal lobe (AL) projection neurons (PNs) is phase-locked to the oscillations of the local field potential. Sensory information is contained in the spatiotemporal synchronization pattern formed by the identities of the phase-locked PNs. This article investigates the role of feedback inhibition from the local neurons (LNs) in this coding. First, experimental biological results are reproduced with a reduced computational spiking neural network model of the AL. Second, the low complexity of the model leads to a mathematical analysis from which a lower bound on the phase-locking probability is derived. Parameters involved in the bound indicate that PN phase locking depends not only on the number of LN-evoked inhibitory postsynaptic potentials (IPSPs) previously received, but also on their temporal jitter. If the inhibition received by a PN at the current oscillatory cycle is both perfectly balanced (i.e., equal to the mean inhibitory drive) and precise (without any jitter), then the PN will be phase-locked at the next oscillatory cycle with probability one.

Animals↗

PubMed1986

Intracellular recordings from rat nucleus accumbens neurons in vitro.

Intracellular recordings were obtained from rat nucleus accumbens (NAC) neurons in brain slice preparations. Local stimulations evoked depolarizing postsynaptic potential (DPSP). Injections of low intensity depolarizing currents decreased the amplitude of the DPSP and reversed a later portion of the DPSP into a hyperpolarizing potential. Superfusion of pentobarbital facilitated the reversal of this later portion of DPSP and bicuculline abolished this polarity reversal. These data suggested that the DPSP evoked by local stimulation consisted of a combination of an excitatory and an inhibitory postsynaptic potential, and that the latter was probably mediated by gamma-aminobutyric acid.

Animals↗

PubMed1978

Possible explanation for interictal-ictal transition: evolution of epileptiform activity in hippocampal slice by chloride depletion.

In thin hippocampal slices, paroxysmal epileptiform discharge was generated in high potassium medium. Removal of chloride from the high potassium medium caused explosive potentiation of the paroxysmal discharge and emergence of clonic relapsing discharges. Evolution of the paroxysm to regenerative seizure was attributed to the reduction of inhibitory postsynaptic potentials.

Action Potentials↗

PubMed1994

The 5-HT3 receptor agonist 2-methyl-5-HT reduces postsynaptic potentials in rat CA1 pyramidal neurons of the hippocampus in vitro.

The effects of the serotonin (5-HT)3 receptor agonist, 2-methyl-5-hydroxytryptamine (2-methyl-5-HT), were studied in CA1 pyramidal cells of the rat hippocampus in vitro using the whole cell gigaseal technique. 2-Methyl-5-HT (10 and 50 microM) did not change significantly the electrophysiologic properties of the cells but reversibly reduced excitatory and inhibitory postsynaptic potentials evoked by stimulation of the Schaffer collaterals. The onset and termination of this effect was in the order of minutes and no desensitization was observed. The selective 5-HT3 receptor antagonist, granisetron, when applied as a pretreatment completely prevented but did not reverse this action when given after administration of 2-methyl-5-HT while the non-specific 5-HT1,2 receptor antagonist, metergoline, was ineffective. These results suggest that the activation of 5-HT3 receptors reduces the efficacy of glutamatergic synaptic transmission in this area.

Animals↗

PubMed1992

Action of habenular efferents on ventral tegmental area neurons studied in vitro.

Action of habenular efferents on neurons of the ventral tegmental area (VTA) was studied with a slice preparation that preserved the habenula (Hb) and the VTA together with the interconnecting fiber bundle, the fasciculus retroflexus (FR). In the VTA, two types of neurons, presumably corresponding to the dopaminergic and nondopaminergic neurons, were discerned on the basis of the electrophysiological properties. Of 52 VTA neurons sampled, 42 [with the mean resting membrane potential of 56 +/- 7 mV (mean +/- SD)] responded with excitatory postsynaptic potentials (EPSPs) to FR stimulation. The EPSPs were monosynaptic in nature and rather weak in effect in the sense that they rarely triggered spikes. No significant differences in latency, duration, and time to peak were noted between the EPSPs generated in different types of neurons. FR stimulation evoked inhibitory postsynaptic potentials (IPSPs) in only six neurons, their resting membrane potential being 51 +/- 4 mV. The IPSPs frequently showed a fluctuation in latency. FR stimulation also produced antidromic responses in a few VTA neurons, but their long latencies precluded the possibility that the VTA-Hb projections contributed to the FR-evoked orthodromic responses in the VTA. EPSPs evoked by FR stimulation could be suppressed by kynurenic acid (1 mM). The findings indicate that the efferents of the Hb primarily have an excitatory effect on VTA neurons of any type and that the excitation may be mediated by amino acid receptors.

Animals↗

PubMed1983

Electrical properties of neurons recorded from the rat supraoptic nucleus in vitro.

The electrical properties of neurons in the supraoptic nucleus (so.n.) have been studied in the hypothalamic slice preparation by intracellular and extracellular recording techniques, with Lucifer Yellow CH dye injection to mark the recording site as being the so.n. Intracellular recordings from so.n. neurons revealed them to have an average membrane potential of -67 +/- 0.8 mV (mean +/- s.e.m.), membrane resistance of 145 +/- 9 M omega with linear current-voltage relations from 40 mV in the hyperpolarizing direction to the level of spike threshold in the depolarizing direction. Average cell time constant was 14 +/- 2.2 ms. So.n. action potentials ranged in amplitude from 55 to 95 mV, with a mean of 76 +/- 2 mV, and a spike width of 2.6 +/- 0.5 ms at 30% of maximal spike height. Both single spikes and trains of spikes were followed by a strong, long-lasting hyperpolarization with a decay fitted by a single exponential having a time constant of 8.6 +/- 1.8 ms. Action potentials could be blocked by 10(-6) M tetrodotoxin. Spontaneously active so.n. neurons were characterized by synaptic input in the form of excitatory and inhibitory postsynaptic potentials, the latter being apparently blocked when 4 M KCl electrodes were used. Both forms of synaptic activity were blocked by application of divalent cations such as Mg2+, Mn2+ or Co2+. 74% of so.n. neurons fired spontaneously at rates exceeding 0.1 spikes per second, with a mean for all cells of 2.9 +/- 0.2 s-1. Of these cells, 21% fired slowly and continuously at 0.1 - 1.0 s-1, 45% fired continuously at greater than 1 Hz, and the remaining 34% fired phasically in bursts of activity followed by silence or low frequency firing. Spontaneously firing phasic cells showed a mean burst length of 16.7 +/- 4.5 s and a silent period of 28.2 +/- 4.2 s. Intracellular recordings revealed the presence of slow variations in membrane potential which modified the neuron's proximity to spike threshold, and controlled phasic firing. Variations in synaptic input were not observed to influence firing in phasic cells.

Action Potentials↗

PubMed1993

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

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)

Animals↗

PubMed1997

Do GABAA and GABAB inhibitory postsynaptic responses originate from distinct interneurons in the hippocampus?

GABAergic inhibition of hippocampal pyramidal cells is mediated by two distinct subtypes of postsynaptic receptors, GABAA and GABAB. Electrical stimulation of inhibitory cells or fibres in the CA1 subfield of the hippocampus yields a biphasic inhibitory postsynaptic potential (IPSP) in pyramidal cells, consisting of an early GABAA- and a late GABAB-mediated component. CA1 interneurons are a heterogeneous population of cells, which differ on the basis of their morphology, physiological properties, target selectivity onto principal cells, and network connectivity. Inhibitory synaptic circuitry appears to be specialized, since feedback inhibition may invoke only postsynaptic GABAA receptors, whereas feedforward inhibition may invoke both postsynaptic GABAA and GABAB receptors. In this review, we examine the evidence for and against the notion that distinct interneurons may be responsible for GABAA- and GABAB-mediated inhibition. Overall, the evidence suggests that (i) certain interneurons may generate solely GABAA inhibition, but the available data do not distinguish whether other interneurons mediate (ii) solely GABAB inhibition or (iii) a combination of both GABAA and GABAB.

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