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Results for “Inhibitory Postsynaptic Potentials”

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PubMed1981

Effects of phenytoin on pyramidal neurons of the rat hippocampus.

The effects of phenytoin (35 micrograms/ml) on membrane properties and inhibitory postsynaptic potential (IPSPs) in CA1 and CA3 pyramidal neurons of the in vitro rat hippocampus were examined. No significant change was observed on input resistance or resting membrane potential. Action potential amplitude, overshoot, rate of rise and rate of decay were decreased. IPSP conductance increase and reversal potential, evoked in CA3 cells through mossy fiber stimulation and in CA1 cells through recurrent and Schaffer's collateral stimulation, were unaffected.

Animals↗

PubMed1982

Cholinergic disinhibition in hippocampal slices of the rat.

In hippocampal slices of the rat maintained in vitro the addition of carbachol to the perfusion medium caused a depolarization accompanied by a conductance decrease and a block of inhibitory postsynaptic potentials in CAl pyramidal cells. During tetrodotoxin poisoning a smaller depolarization with conductance decrease was observed. Atropine blocked the effects of carbachol.

Animals↗

PubMed1983

Immunocytochemical demonstration of GABAergic synapses on identified rubrospinal neurons.

GABAergic synapses on rubrospinal neurons were demonstrated with immunocytochemistry combined with intracellular injection of horseradish peroxidase. Sections containing red nucleus neurons were processed for glutamic acid decarboxylase (GAD) immunohistochemistry. GAD-immunoreactive synaptic endings formed synaptic contacts with somata and dendrites of red nucleus neurons and identified rubrospinal neurons. Our observation provides further evidence that GABA acts as an inhibitory transmitter mediating cortically evoked inhibitory postsynaptic potentials in red nucleus neurons.

Animals↗

PubMed1985

An intracellular analysis of the entopeduncular inputs on the centrum medianum-parafascicular nuclear complex in cats.

Intracellular recording from the CM-PF neurons was performed by stimulation of the EN, the caudate nucleus (Cd), the cerebellar nuclei (CN) and the motor cortex in the cat under Nembutal anesthesia. Twenty-seven neurons in the CM-PF nuclear complex and two neurons near the habenular nucleus received monosynaptic inhibitory postsynaptic potentials (IPSPs; latency of 1.0-4.0 ms, mean 2.3 ms) by EN stimulation. Cd stimulation evoked excitatory postsynaptic potentials (EPSPs) followed by long hyperpolarizations in most of the CM-PF neurons and produced antidromic activation in 7 neurons. Six neurons received EPSPs (latencies of 4-7 ms) by cortical stimulation. CN stimulation affected only two neurons in the present study. Intracellular HRP staining revealed that some CM-PF neurons have polygonal or spindle-shaped somata with fine, long and sparsely spinous dendrites.

Animals↗

PubMed1985

Some factors that influence the decrement in the response to GABA during its continuous iontophoretic application to hippocampal neurons.

The response decrement that occurs during continuous iontophoretic application of GABA to hippocampal neurons was characterized by intracellular methods in the rat hippocampal slice. Using several paradigms that compared the responses to GABA with those to poorly transported analogues, we then identified a large component of this decrement that appeared to be independent of GABA uptake and metabolism, and that is probably independent of intracellular chloride accumulation as well. This decrement, which both developed and recovered with half times that average between 3 and 5s, is too brief to directly account for long-term plasticity of the GABA synapse. However, its time course is appropriate to participation in the development of cellular responses to brief flurries of GABA-mediated inhibitory postsynaptic potentials that may occur normally, or that may occur abnormally during a seizure or artificial tetany.

Animals↗

PubMed1985

Pre- and postsynaptic effects of baclofen in the rat hippocampal slice.

CA1 pyramidal cells responded to baclofen with a hyperpolarization. This response was found in the apical and basal dendrites and, like the hyperpolarizing response of the dendrites to GABA, appeared to be Ca2+-dependent since it was blocked or reduced by intracellular injection of EGTA or extracellular application of cadmium. Baclofen also reduced the excitatory and inhibitory postsynaptic potentials produced by stimulation of the Schaffer collaterals. The pre- and postsynaptic effects on the synaptic waveform could be distinguished.

Animals↗

PubMed1986

Reticulo-olivary circuits: an intracellular HRP study in the rat.

Intracellular recordings were obtained from medullary reticular neurons subsequent to electrical stimulation of the ipsilateral or contralateral inferior cerebellar peduncle (ICP) and/or the midbrain. After recording physiological data, the neurons were intracellularly injected with horseradish peroxidase (HRP). Thirty-four HRP filled neurons were subjected to light microscopic analysis. They could be divided into two general groups: those which extend dendritic processes into the neuropil of the inferior olivary complex (n = 19); and those that have no anatomical relationship to the inferior olive (n = 15). These two populations of reticular neurons differ in their distribution, morphological characteristics and physiological responses. Neurons which extend dendritic processes into the inferior olive are located within 200 microns of the dorsal border of this nuclear complex, between the exiting fibers of the XIIth nerve and the raphe. The cell bodies are located in the nucleus reticularis gigantocellularis and are fusiform or multipolar in shape. Their dendrites extend for long distances in the mediolateral direction; are thin and relatively spine-free except at their distal tips where spines and varicose appendages are evident. Physiologically, midbrain stimulation elicits a fast rising hyperpolarization which is identified as an inhibitory postsynaptic potential. However, only rarely is a response observed subsequent to stimulation of either the ipsilateral or contralateral ICP. Dendrites from 4 neurons from the first group of reticular cells were analyzed at the ultrastructural level. Based on random and serial thin sections, the following features were noted: they contain numerous mitochondria when compared to olivary dendrites; they contribute to the postsynaptic elements within olivary synaptic clusters (glomeruli); and they exhibit focal clusters of synaptic vesicles although conventional synaptic complexes have not been observed. Reticular neurons of the second group, those that do not extend dendritic processes into the inferior olive, are located either lateral to the XIIth nerve or at distances greater than 200 microns from the dorsal border of the inferior olivary complex. Their cell bodies and dendrites are comparable morphologically to the reticular neurons whose dendrites do arborize in the inferior olive. However, rarely are the distal tips of their dendrites characterized by spines or varicose appendages. Physiologically, this population of reticular neurons respond to midbrain stimulation with a low amplitude, short latency depolarizing potential which is interrupted by a hyperpolarizing potential.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1986

Nipecotic acid, an uptake blocker, prevents fading of the gamma-aminobutyric acid effect.

In rats under urethane, iontophoretic applications of GABA (30-60 nA) in the str. pyramidale of CA1, showed a rapidly fading inhibitory effect. By contrast, GABA had a well-maintained inhibitory effect in str. radiatum. During iontophoresis of nipecotic acid (30-85 nA) identical applications of GABA in str. pyramidale caused a more prominent depression without fading, which suggests that removal of GABA, by uptake, can at least in part account for 'fading'. Nipecotic acid also prolonged the paired-pulse inhibition, presumably by prolonging the duration of inhibitory postsynaptic potentials.

Animals↗

PubMed1987

Slow IPSP and the noradrenaline-induced inhibition of the cat sympathetic preganglionic neuron in vitro.

Focal electrical stimulation of the slice of the cat thoracic cord evoked in sympathetic preganglionic neurons a slow inhibitory postsynaptic potential (IPSP) associated with decreased neuronal input resistance. The slow IPSP decreased in amplitude with membrane hyperpolarization and reversed at about -90 mV. It increased in amplitude in low potassium and decreased in high potassium. Noradrenaline (NA) at doses of 10-50 microM caused in some of these cells a hyperpolarization with properties similar to those of the slow IPSP. Both the slow IPSP and the NA-evoked hyperpolarization were abolished by yohimbine, but not by prazosin or propranolol. These data suggest that both responses are due to an increase in potassium conductance and that NA may be the mediator of the slow IPSP evoked by focal stimulation.

Action Potentials↗

PubMed1987

Is glycine an inhibitory transmitter in rat lateral horn cells?

Spontaneous inhibitory postsynaptic potentials (IPSPs) and evoked IPSPs were recorded from a portion of lateral horn cells situated in thin transverse thoracolumbar spinal cord slices removed from neonatal rats. The IPSPs were reduced by hyperpolarization and inverted at membrane potentials between -65 and -75 mV. Strychnine but not bicuculline reversibly eliminated the IPSPs. The hyperpolarizations elicited by exogenously applied glycine exhibited electrophysiological and pharmacological characteristics similar to that of IPSPs. The results are consistent with the suggestion that glycine mediates an IPSP in a population of lateral horn cells.

Animals↗

PubMed1987

Effect of inhibitory amino acid antagonists on IPSPs induced in lumbar motoneurons upon stimulation of the nucleus reticularis gigantocellularis during active sleep.

The present study was performed to generate data implicating glycine or gamma-aminobutyric acid as neurotransmitter candidates mediating the IPSPs which are recorded in lumbar motoneurons following electrical stimulation of the nucleus reticularis gigantocellularis (NRGc) during the atonia of active sleep. Accordingly, intracellular records were obtained from lumbar motoneurons in unanesthetized, normally respiring cats during naturally occurring states of active sleep, while inhibitory amino acid antagonists were microiontophoretically released next to the recorded cell. Electrical stimuli, applied to the NRGc during active sleep under drug-free conditions, evoked inhibitory postsynaptic potentials (IPSPs) in all of the lumbar motoneurons which were examined. These NRGc-induced IPSPs exhibited an average latency-to-onset of 26.6 +/- 1.3 ms, a latency-to-peak of 42.5 +/- 1.3 ms, an average amplitude of 3.9 +/- 0.4 mV and a duration of 34.4 +/- 2.1 ms. Strychnine, when applied microiontophoretically, abolished or markedly suppressed these NRGc-induced IPSPs. In contrast, the microiontophoretic application of picrotoxin or bicuculline methiodide failed to block these IPSPs. To the extent that strychnine may be considered to be a specific antagonist of glycine, the present results suggest that glycine (or a structurally related amino acid) participates in the generation of NRGc-induced IPSPs during the atonia of active sleep.

Animals↗

PubMed1987

Dissociation of the IPSP and response to GABA during spreading depression-like depolarizations in hippocampal slices.

We have compared the sensitivity of CA1 and CA3 hippocampal pyramidal cells, in mature and immature tissue, to spreading depression-like depolarization episodes. Using hippocampal slices from rabbit, we have found that mature and immature tissue, and CA1 and CA3 neurons, were differentially prone to depolarization episodes, depending on the method used to produce the depolarization. CA1 region was generally more sensitive than CA3. Spontaneous and stimulus-evoked depolarizations were seen more frequently in immature tissue than in mature slices, but anoxia-induced depolarizations were much more likely to occur in mature tissue. Synaptic transmission and responses to somatic gamma-aminobutyric acid (GABA) ejection were compared during anoxia-induced depolarizations in mature slices. The early component of the inhibitory postsynaptic potential (IPSP) normally had the same reversal potential as the GABA response. During anoxia-induced depolarization, both the drug response and the PSPs were lost. Synaptic transmission generally disappeared before the response to exogenous GABA application; the GABA response reappeared before synaptic function was restored. During the recovery of resting potential (RMP) following depolarization, the reversal potential of the early IPSP differed significantly from that of the GABA response; when the cell had recovered to RMP, the IPSP was depolarizing, whereas GABA application produced a 'normal' cell hyperpolarization. IPSPs and GABA-mediated responses attained their pre-depolarization form within a few minutes of RMP recovery. These observations suggest that, at least under special circumstances, the early component of the IPSP and GABA-mediated hyperpolarizations can be dissociated. Therefore, the early IPSP may be mediated by more complex mechanisms than a simple alteration in chloride conductance due to GABA-receptor interactions.

Aging↗

PubMed1988

Pharmacological studies in frog sympathetic ganglion: support for the cholinergic monosynaptic hypothesis for slow IPSP mediation.

The slow inhibitory postsynaptic potential (slow IPSP), the slow excitatory postsynaptic potential (slow EPSP), the late slow excitatory postsynaptic potential (late slow EPSP), and the fast excitatory postsynaptic potential/compound action potential (fast EPSP) were recorded from the 9th or 10th paravertebral sympathetic ganglia of bullfrogs (and some Rana pipiens frogs) by the sucrose-gap technique. The adrenergic antagonists phentolamine, dihydroergotamine and propranolol did not show any antagonistic effect on the slow IPSP when used at concentrations of up to 10, 100 and 10 microM, respectively. U-0521 (3',4'-dihydroxy-2-methylpropriophenone, 50 micrograms/ml), a specific inhibitor of catechol-O-methyltransferase, did not show any potentiating effect on the slow IPSP. The cholinesterase inhibitor neostigmine (0.5-1 microM) induced a large increase in the duration and amplitude of slow IPSP. When phentolamine and propranolol at concentrations greater than 10 microM were used the slow IPSP (and all other synaptic potentials) were non-specifically reduced in amplitude by these drugs. The results reported in this paper do not lend any support to the hypothesis that the slow IPSP in frog sympathetic ganglia is mediated by an adrenergic interneuron. The results are consistent with the proposal that the slow IPSP in this ganglion is mediated by a direct action of acetylcholine released from cholinergic preganglionic fibers.

Action Potentials↗

PubMed1988

Recurrent inhibition in the cat distal forelimb.

The pattern of recurrent pathways from motor axon collaterals to motoneurones has been investigated in the spinal cord of anaesthetized cats with intracellular techniques. Only recurrent inhibitory postsynaptic potentials (RIPSPs) were observed so far. They were very pronounced between the mechanical synergists acting at the elbow. The triceps muscles received substantial effects also from the extensor carpi ulnaris (ECU) and from palmar-located medialis (M) and ulnaris (Ul) muscles. The effects were much smaller in the motor nuclei acting on the wrist (ECU, EC radialis (ECR]. The motor nuclei to the muscles acting on the phalanges (extensor digitorum communis and lateralis, extensor indicis proprius, and abductor pollicis longus (EDC, EDL, EIP, APL] neither received nor emitted any recurrent effects, which may indicate a lack of the recurrent system in these distal motor nuclei. A comparison of the recurrent pattern with the distribution of monosynaptic excitation from large muscles spindle afferents (Ia) shows that there is a partial overlap of both systems only at the elbow joint.

Action Potentials↗

PubMed1988

GABAergic inhibition and epileptiform discharges in the turtle hippocampus in vitro.

The effects of excitatory amino acid (EAA) receptor antagonists were examined on intracellularly recorded epileptiform discharges in turtle hippocampal (ventromedial cortical) pyramidal neurons in vitro. Afferent synaptic activation of turtle hippocampal neurons evoked monophasic or biphasic GABAergic inhibitory postsynaptic potentials (IPSPs). In the presence of bicuculline (5 microM) or picrotoxin (100 microM) IPSPs were reduced, and long-lasting ictal-like discharges were transiently observed prior to the establishment of a regular rhythm of discharge of spontaneous paroxysmal depolarization shifts (PDSs). Bicuculline-induced PDSs were reversibly reduced in amplitude and duration, but not abolished by the EAA receptor antagonists kynurenic acid (1 mM), cis-2,3-piperidine dicarboxylic acid (cis-2,3-PDA) (1 mM), or DL-2-amino-5-phosphonovalerate (DL-AP-5) (100 microM), revealing a long-lasting hyperpolarizing afterpotential. These results indicate that the blockade of GABAergic inhibition leads to the genesis of epileptiform discharges, and EAA receptor antagonists (particularly those of the N-methyl-D-aspartate (NMDA) receptor subtype) block the maintained depolarization underlying PDSs, but do not prevent their spontaneous discharge in turtle hippocampus.

Afferent Pathways↗

PubMed1988

Verapamil blocks the afterhyperpolarization but not the spike frequency accommodation of rat CA1 pyramidal cells in vitro.

The effects of prolonged periods (up to 4 h) of perfusion with verapamil (100 microM) or D600 (100 microM) on synaptically and directly evoked responses of rat CA1 pyramidal cells were determined in vitro. The slow depolarization underlying burst generation and the slow afterhyperpolarization following directly evoked repetitive firing were blocked, but spike frequency accommodation was not. There was an increase in threshold for evoking synaptic responses and the amplitude of evoked inhibitory postsynaptic potentials (IPSPs) was decreased slightly. The results suggest that verapamil can partially block voltage dependent Ca influx into CA1 cells and that currents underlying accommodation and the slow afterhyperpolarization (AHP) may differ.

Action Potentials↗

PubMed1988

Sensory input to cerebellocerebral relay neurons in the cat thalamus.

Intracellular recording techniques were used to study the synaptic responses of feline ventrolateral neurons to dorsal column, spinothalamic and sensory cortex stimulation. More than 75% of the cells responded with short- and long-latency excitatory or inhibitory postsynaptic potentials to the one or/and other stimulation sites. These findings indicate that a considerable amount of somatosensory integration in the cerebellocerebral circuit occurs in the thalamic relay neurons.

Action Potentials↗

PubMed1988

A new class of small inhibitory interneurones in the lamprey spinal cord.

Paired intracellular recordings of interneurones and motoneurones have been performed in the lamprey spinal cord in vitro. One new type of small interneurone (10-15 microns in diameter) which produces monosynaptic inhibitory postsynaptic potentials (IPSPs) in motoneurones is described. The IPSP is strychnine-sensitive and thus presumably glycinergic. This type of interneurone undergoes rhythmical membrane potential oscillations during fictive locomotion and intracellular stimulation can have a profound effect on the burst generation occurring during fictive locomotion.

Animals↗