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PubMed1997

Heterogeneity in use-dependent depression of inhibitory postsynaptic potentials in the rat neostriatum in vitro.

"Minimal stimulation" was applied to evoke responses in an "all-or-none" fashion in presumed medium spiny neurons of rat neostriatal slices in the presence of antagonists for glutamatergic excitation. For comparison, responses were evoked in the same cells by compound stimulation. Bicuculline (30 microM) blocked responses evoked by minimal stimulation, indicating that they were gamma-aminobutyric acid-A (GABAA)-receptor-mediated inhibitory postsynaptic potentials (IPSPS), whereas responses evoked by compound stimulation were only reduced in amplitude. Likewise, R(-)baclofen (1-20 microM) blocked IPSPS evoked by minimal stimulation in all but one cell. On the contrary, responses evoked by compound stimulation were always reduced in amplitude but never blocked. Paired-pulse depression (PPD) of averaged responses to minimal and compound stimulation was observed at a stimulus interval of 300 ms. The GABAB receptor antagonist CGP55845A (0.5 microM) had no effect on PPD evoked by compound stimulation but abolished PPD evoked by minimal stimulation. In a second set of experiments, the two stimulation paradigms were used to evoke responses in neostriatal slices continuously bathed in R(-)baclofen (10-20 microM). In R(-)baclofen a strong PPD was evoked by minimal and by compound stimulation. The amplitude of the response to compound stimulation increased on application of CGP55845A (0.5 microM). At the same time, PPD evoked by compound stimulation decreased. On the contrary, IPSP amplitude and PPD evoked by minimal stimulation remained unchanged. We conclude that two types of GABAergic terminals exist in the rat neostriatum, only one of which is regulated by GABAB receptors. However, the other class of terminals, not regulated by GABAB receptors, displays a much more pronounced PPD.

Animals↗
PubMed2002

Gamma-hydroxybutyrate reduces GABA(A)-mediated inhibitory postsynaptic potentials in the CA1 region of hippocampus.

Gamma-hydroxybutyric acid (GHB) is a psychoactive drug and a putative neurotransmitter, derived from gamma-aminobutyric acid (GABA). At micromolar concentrations GHB binds to specific high and low affinity binding sites present in discrete areas of the brain, while at millimolar concentrations GHB also binds to GABA(B) receptors. Previous studies indicated that GHB inhibits both NMDA and AMPA receptor mediated excitatory postsynaptic potentials in hippocampal CA1 pyramidal neurons. This action of GHB occurs in the presence of GABA(B) blockade and is antagonized by NCS-382, a specific GHB receptor antagonist, suggesting that it is mediated by GHB receptors. In the present study, we have investigated the effect of GHB on GABA(A) mediated inhibitory postsynaptic potentials (GABA(A)-IPSP) elicited in CA1 hippocampal pyramidal neurons by stimulation of Schaffer collateral-commissural fibers. We observed that GHB inhibited GABA(A)-IPSPs by about 40% at concentrations of 300-600 microM. GHB inhibition was blocked by NCS-382 (500 microM), which per se failed to modify GABA(A)-IPSPs. Moreover, GHB failed to modify cell membrane depolarization induced by the brief pressure application of GABA in the presence of tetrodotoxin (TTX), indicating that GHB does not inhibit postsynaptic GABA responses. However, GHB reduced the amplitude of GABA(A)-IPSPs elicited in pyramidal neurons by paired pulse stimulation and enhanced paired pulse facilitation with respect to control condition, suggesting that GHB reduces GABA release from nerve terminals. Finally, GHB failed to reduce the amplitude of GABA(A)-IPSPs in the presence of BaCl(2), suggesting that the effect of GHB is due to GHB receptor-mediated presynaptic inhibition of Ca(2)+ influx.

Animals↗
PubMed1993

Serotonin-containing neurons in lobsters: origins and characterization of inhibitory postsynaptic potentials.

1. The serotonin-containing neurons in the A1 ganglion of the lobster have been shown to act as "gain setters" in neuronal circuits that control the adoption of behaviorally relevant postures. These neurons are subject to tonic inhibition, which has been proposed as an important regulator of their activity. This study explores the pharmacological nature and anatomic location of the neurons responsible for inhibition of these A1 cells; the role played by inhibitory inputs in controlling the firing rates of these neurons is also examined. 2. Three classes of inhibitory postsynaptic potentials (IPSPs) are distinguished in the somata of A1 serotonin-containing neurons. The most common (type I) has amplitudes ranging from 0.4 to 1.5 mV; types II (2-5 mV) and III (< 0.4 mV) are less often seen. 3. Type I IPSPs are reversibly blocked by picrotoxin, a gamma-aminobutyric acid antagonist, but not by serotonin or octopamine antagonists known to act at other lobster synapses. 4. Elimination of type I IPSPs by reversible or irreversible blockage of conduction from the A3 ganglion results in a firing rate increase of approximately 50% in A1 serotonin-containing neurons; IPSP recovery results in a firing rate decrease of corresponding magnitude. Connective transections that do not affect IPSPs do not cause a firing rate increase. 5. Lesions studies suggest that type I IPSPs originate in neurons whose somata are located near the midline of the A3 ganglion; a cell impaled in this region showed action potentials that correlated with IPSPs in an A1 serotonin-containing neuron.

Aggression↗
PubMed1988

AF-DX 116: a selective antagonist of the slow inhibitory postsynaptic potential and methacholine-induced hyperpolarization in superior cervical ganglion of the rabbit.

AF-DX 116 [11-([2-[(diethylamino)methyl]-1-piperdinyl]acetyl)-5, 11-dihydro-6H-pyrido[2,3-b][1,4]benzodiaze pine-6-one], a muscarinic receptor antagonist that divides the M2-type muscarinic receptor into additional functional classes, modified muscarinic responses recorded from the superior cervical ganglion of the rabbit with sucrose or air gap techniques. Incubation of ganglia with AF-DX 116 suppressed the amplitude of the slow-inhibitory postsynaptic potential (s-IPSP) in a concentration-dependent and highly specific manner. At concentrations which reduced the amplitude of the s-IPSP by 80 to 90%, there was no significant reduction of the amplitudes of the muscarinic slow-excitatory postsynaptic potential or the nicotinic fast-excitatory postsynaptic potential. In addition, superfusion of ganglia with AF-DX 116 resulted in the concentration-dependent suppression of ganglionic hyperpolarization induced by methacholine without suppression of methacholine-induced depolarization. Ganglionic hyperpolarization that was produced by norepinephrine was unaffected by AF-DX 116. Increasing the level of acetylcholine available for interaction with muscarinic receptors by increasing the number of stimulus volleys that were applied to the preganglionic nerve resulted in a parallel shift, to the right, of the concentration-response curve for suppression of the s-IPSP by AF-DX 116. Similarly, incubation of ganglia with the specific antiacetylcholinesterase, BW 284 (1-5-bis[4-allyl dimethylammonium phenyl]pentan-3 one dibromide), increased the concentration of AF-DX 116 that was required to produce a comparable suppression of the s-IPSP. These results indicate that the s-IPSP in mammalian superior cervical ganglion involves an action of acetylcholine at the M2 type receptor that is preferentially blocked by AF-DX 116.

Animals↗
PubMed1979

Evidence for the existence of inhibitory postsynaptic potentials in dendrites and their functional significance in hippocampal pyramidal cells of adult rabbits.

(1) Hyperpolarizing potentials were studied in hippocampal pyramidal cells of normal, adult rabbits, anesthetized with Nembutal and, in addition, curarized. (2) Single shock stimulation of the fornix produced in these cells long-lasting hyperpolarizing potentials (400-2000 msec). As a rule, the early part of these potentials (about 200 msec from the onset) was influenced by the diffusion of Cl ions into the cell and current injections, whereas their late part was not. The early part exhibited impedance changes whereas the late part did not. From these results it was concluded that the former was the inhibitory postsynaptic potential (IPSP) occurring in the soma while the latter originated in the dendrites. Evidence was obtained suggesting that the latter was also a Cl-mediated IPSP. The hyperpolarization elicited in these cells by mesencephalic stimulation was similar in properties to the latter. (3) Disfacilitation in the dendrites and the functional significance of the dendritic IPSP were discussed.

Animals↗
PubMed1987

Repetitive inhibitory postsynaptic potentials evoked by 4-aminopyridine in hippocampal neurons in vitro.

The effects of topical application of microdrops containing 4-aminopyridine (4-AP) on properties of CA1 neurons were examined in the hippocampal slice preparation. 4-AP triggered repetitive large (4-10 mV) hyperpolarizing potentials (HPs) having a short rise time and slow (3-4 s) decay. There was a marked decrease in input resistance during the HPs. The HPs are likely to be caused by an increase in potassium conductance; their reversal potential was 15-20 mV negative to rest, the reversal potential shifted in the depolarizing direction when the slice was bathed in high potassium medium, and it was the same with KCl or potassium acetate recording electrodes. The HPs were not generated by release of neurotransmitter substances from terminals of extrinsic afferents since they were present in slices taken from deafferented hippocampus but they were blocked by tetrodotoxin (TTX) or Cd and Mn, indicating that they are synaptic potentials of local origin. HPs were still present when Ca-dependent K currents were blocked by acetylcholine and noradrenaline. Three of 56 cells recorded in the hippocampus could be classified as interneurons. They emitted high frequency trains of action potentials in response to 4-AP, at a rate corresponding to the HPs recorded in all other neurons. It is suggested that 4-AP excites a specific type of interneuron which in turn generates large K-mediated inhibitory postsynaptic potentials in the pyramidal neurons of CA1 region of the hippocampus.

1-Methyl-3-isobutylxanthine↗
PubMed2001

Diversity of neuron-specific K+-Cl- cotransporter expression and inhibitory postsynaptic potential depression in rat motoneurons.

Motoneurons receive a robust recurrent synaptic inhibition by gamma-aminobutyric acid and glycine, which activate Cl(-) channels. Thus, Cl(-) homeostasis determines the efficacy of synaptic inhibition in the motoneurons. In situ hybridization reveals that the neuronal K(+)-Cl(-) cotransporter isoform 2 (KCC2), a major mechanism in maintaining a low Cl(-) concentration in neurons, is abundantly expressed in the facial, hypoglossal (XII), and spinal motoneurons innervating striated muscle, whereas the dorsal vagal motoneurons (DMVs) controlling smooth muscle exhibited little expression of KCC2. This raises a general interest in the correlation between KCC2 expression and inhibitory postsynaptic potential (IPSP) performance in the native circuits. Intracellular and whole-cell patch recordings revealed that an activity-dependent depression of IPSPs and positive shift of IPSP reversal potentials were more prominent in the DMV than in the XII. Cl(-) influx through Cl(-) channels was extruded more potently in the XII than in the DMV, suggesting that differences in Cl(-) extrusion account for these dynamic differences of IPSP. Cl(-) extrusion was inhibited by either furosemide or an increase in extracellular potassium concentrations. Thus, the rigid maintenance of IPSP and rapid Cl(-) extrusion in the XII reflects an intense expression of KCC2. KCC2 expression may strongly influence the IPSP depression and functional properties of the motoneurons innervating striated muscles.

Animals↗
PubMed1985

Frequency-to-voltage conversion in the pyramidal tract neuron: an important role of the inhibitory postsynaptic potential.

Frequency-coded impulses are known to be converted into postsynaptic potentials (PSPs) at the synapse of a target neuron. This can be termed frequency-voltage (F-V) conversion. Studies on this problem in pyramidal tract neurons (PTNs) showed that not only the amplitude but also the duration of depolarizing PSPs was determined as a function of the input impulse frequency. Two opposite patterns of F-V conversion were observed following activation of two input systems to PTNs. Inhibitory postsynaptic potentials were found to play an important role in the regulation of the duration of PSPs by curtailing excitatory post-synaptic potentials.

Animals↗
PubMed1992

Reduction of GABAB inhibitory postsynaptic potentials by serotonin via pre- and postsynaptic mechanisms in CA3 pyramidal cells of rat hippocampus in vitro.

The action of serotonin (5-HT) on GABAergic synaptic transmission was investigated with intracellular recordings in CA3 pyramidal cells of rat hippocampal slices. Local application of 5-HT (500 microM) hyperpolarized CA3 pyramidal cells, decreased cellular input resistance, and reduced slow afterhyperpolarizations. Serotonin attenuated the late (GABAB) component of polysynaptic inhibitory postsynaptic potentials (IPSPs; 47% of control) without affecting the early (GABAA) component. During bath application of the excitatory amino acid antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) (20 microM) and 2-amino-5-phosphonovalerate (AP-5) (40 microM), 5-HT similarly decreased the amplitude of the late (GABAB) component (17% of control) of monosynaptic IPSPs but did not affect the early (GABAA) component. The mean reversal potentials of poly- and monosynaptic IPSPs were unaffected by 5-HT. The conductance increases associated with the late component of poly- and monosynaptic IPSPs were reduced by 5-HT. Hyperpolarizing responses evoked in CA3 pyramidal cells by somatic applications of gamma-aminobutyric acid (GABA) were unaffected by 5-HT. During bath application of bicuculline (20-50 microM), hyperpolarizing responses elicited by dendritic GABA application were reduced by 5-HT (71% of control). The effect of 5-HT on these direct GABAB hyperpolarizations (29% decrease in response) does not appear sufficient to fully account for the effect of 5-HT on late GABAB IPSPs (53-83% decrease in response). Therefore, 5-HT may reduce GABAB IPSPs in CA3 pyramidal cells 1) by a postsynaptic action on pyramidal cells and 2) by a selective presynaptic action on GABAergic interneurons mediating the GABAB IPSP. This presynaptic action of 5-HT does not appear to involve excitatory afferents onto inhibitory interneurons.

Animals↗
PubMed2001

Neostriatal and globus pallidus stimulation induced inhibitory postsynaptic potentials in entopeduncular neurons in rat brain slice preparations.

Recent anatomical studies revealed that the entopeduncular nucleus of the rat receives GABAergic inputs from both the neostriatum and the globus pallidus. The present study was undertaken to reveal the physiological features of these inputs using the intracellular recording method in rat brain slice preparations. Most of the entopeduncular nucleus neurons generated repetitive firing without spike accommodation with intracellular current stimulation and thus were classified as Type-I. A small number of neurons were classified as Type-II since they generated spikes with pronounced accommodation. Most of the Type-I, but none of Type-II, entopeduncular nucleus neurons exhibited monosynaptic GABAergic inhibitory postsynaptic potentials (IPSPs) after stimulation of the neostriatum and the globus pallidus. Neostriatal stimulation induced long latency IPSPs while pallidal stimulation induced long latency IPSPs compounded with short latency IPSPs. The IPSPs were mediated by GABA(A) receptors. The unitary IPSPs to striatal stimulation were small while those to pallidal stimulation were large in amplitude and able to reset ongoing rhythmic firing. The short latency IPSPs induced by pallidal stimulation reversed at a somatic membrane potential that was a few millivolts more depolarized than the long latency IPSPs, suggesting that the striatal inputs were evoked in more distal portions of the neurons than the pallidal inputs. Repetitive activation of these inputs resulted in a poor amplitude summation but a prolongation of the duration of the IPSPs. The results of the present study indicate that the pallidal projection to the entopeduncular nucleus is physiologically significant and that the neostriatum and the globus pallidus play important roles in controlling the activity of the entopeduncular nucleus, although in different ways.

Animals↗
PubMed1992

gamma-Hydroxybutyrate depresses monosynaptic excitatory and inhibitory postsynaptic potentials in rat hippocampal slices.

The action of gamma-hydroxybutyrate was studied on pre- and postsynaptic GABA(B) receptors in rat hippocampal neurones in vitro using intracellular recording. gamma-Hydroxybutyrate (1-10 mM) caused a 4-8 mV hyperpolarization of CA1 cells and a 20-80% decrease in monosynaptic excitatory and inhibitory postsynaptic potentials in a concentration-dependent manner. These actions were reversibly inhibited by a novel and selective GABA(B) antagonist, CGP 36742 (20-500 microM) suggesting that gamma-hydroxybutyrate can activate presynaptic as well as postsynaptic GABA(B) receptors.

Animals↗
PubMed1989

Late inhibitory postsynaptic potentials in rat prefrontal cortex may be mediated by GABAB receptors.

The GABAB antagonist phaclofen blocked the postsynaptic hyperpolarization induced by the GABAB agonist baclofen during intracellular recordings in rat cortical cells. This effect appears to be selective since responses to GABAA agonists (muscimol, THIP), GABA, 5-HT and L-glutamate were unaffected. Phaclofen also blocked synaptically evoked late inhibitory postsynaptic potentials (late IPSP). These results suggest that the late IPSPs in cortical neurons are mediated by GABA acting on GABAB receptors.

Animals↗
PubMed1995

Development of excitatory and inhibitory postsynaptic potentials in the rat neocortex.

The postnatal development of synaptic potentials in the rat neocortex is characterized by the sequential appearance of functional excitatory and inhibitory synapses. Morphological and electrophysiological studies provided evidence that at early stages of development, pyramidal cells are extensively coupled to each other, presumably via gap junctions. Thus, immature neurons are able to communicate through pathways that are not available or only weakly expressed in the mature neocortex. During the very early postnatal period, excitatory synaptic inputs prevail. Excitatory postsynaptic potentials (EPSPs) are characteristically long in duration and show high sensitivity to frequent stimulation. Although spontaneous inhibitory postsynaptic potentials (IPSPs) and mature responses to exogenously applied gamma-aminobutyric acid (GABA) have been described during the first postnatal week, evoked IPSPs do not develop before postnatal day 10 (P10). During the period of maximum synaptogenesis (P11 to P20), GABA-mediated synaptic inhibition develops and pyramidal cells respond to afferent activation with efficient EPSPs and IPSPs. These postsynaptic potentials gradually mature during the late postnatal period. The delayed development of synaptic inhibition in the neocortex simultaneously promotes synaptic plasticity while increasing seizure susceptibility. On the one hand, the functional lack of synaptic inhibition during early stages of development enables a period of enhanced neuronal activity and augmented synaptic plasticity necessary to form proper synaptic connections. On the other hand, the absence of inhibitory control over excitatory processes increases the vulnerability of the developing neocortex to seizure activity during postnatal ontogenesis.

Aging↗
PubMed1991

Endogenous opioids released from perforant path modulate norepinephrine actions and inhibitory postsynaptic potentials in guinea pig CA3 pyramidal cells.

The stimulus parameters needed for the release of endogenous opioid peptides were investigated using an in vitro radioligand displacement assay in living guinea pig hippocampal slices. Electrical stimulation of the enkephalin-containing fibers in the perforant path caused the release of endogenous opioid peptides and the subsequent displacement of [3H]-[D-Ala2,N-methyl-Phe4,glyol5]enkephalin binding. High frequency trains of stimuli (10 Hz for 1 sec every 10 sec) were more effective than lower frequency stimulation (1 Hz continuous) at evoking opioid peptide release. Having identified an effective stimulation paradigm able to release endogenous opioids, the electrophysiological effects of endogenous opioids on CA3 pyramidal cells were measured in the guinea pig hippocampal slice preparation. Unlike exogenously applied opioids, stimulated release of endogenous opioid peptides from the perforant path did not significantly reduce inhibitory postsynaptic potential (IPSP) amplitudes recorded in CA3 pyramidal cells. However, perforant path stimulation in the presence of naloxone did cause a dramatic increase in IPSP amplitudes. CA3 pyramidal cells were not directly affected by perforant path stimulation. The naloxone-sensitive increase in IPSPs was delayed 3 min in onset and lasted for several minutes. In addition, the increase in the IPSPs was specifically blocked either by the beta adrenergic antagonist propranolol or by pretreating the animals with reserpine. These findings indicate that endogenous opioids regulate the effects of norepinephrine in the CA3 region of the guinea pig hippocampus. In addition, endogenously released norepinephrine appeared to act on GABAergic interneurons to increase the amplitude of the IPSP recorded in CA3 pyramidal cells.

Animals↗
PubMed1988

Biphasic responses of thalamic neurons to GABA in isolated rat brain slices--II.

In isolated thalamic slices, responses of relay neurons to electrophoretically applied GABA were recorded intracellularly and compared with inhibitory postsynaptic potentials evoked by electrical stimulation of the reticularis nucleus of the thalamus. Both reduced the excitability of thalamic neurons and were biphasic in the majority of neurons studied, consisting of an early, negative-going and a later, positive-going component, when recorded close to reversal potential (mean reversal potentials -66.6 and -57.7 mV). Bicuculline and picrotoxin applied electrophoretically reduced conductance increases evoked by GABA in all neurons. The later, positive-going component was more sensitive to these antagonists (applied with submaximal doses) than the early component. Current-voltage relations for responses to GABA, like those for inhibitory postsynaptic potentials, were non-linear in the majority of neurons. In particular, there was a region of reduced slope resistance close to the reversal potential. Holding the membrane at a conditioning potential was found to change the subsequent response and its reversal potential. Positive holding potentials shifted reversal potentials in the positive direction only when GABA was applied during the conditioning period. Negative holding potentials were effective whether GABA was applied during the conditioning period or not. Recovery from these effects followed a similar time course at all membrane potentials tested. Injection of Cl- produced a positive shift in the reversal potential for both components of the response to GABA and of the evoked inhibitory postsynaptic potential. Inhibitory postsynaptic potentials evoked in thalamic relay neurons by stimulation of the nucleus reticularis resembled responses to GABA in their biphasic nature, reversal potentials and sensitivity to antagonists and to changes in intracellular chloride.

Animals↗