PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Inhibitory Postsynaptic Potentials”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 127 records · Page 7Linked to original sources
PubMed1980

Slow inhibitory postsynaptic potentials and hyperpolarization evoked by noradrenaline in the neurones of mammalian sympathetic ganglion.

Slow IPSPs evoked in the neurones of rabbit isolated superior cervical ganglion by repetitive orthodromic stimulation, and a response evoked in the neurones of this ganglion by perfusion of noradrenaline, were studied using intracellular microelectrodes. Slow IPSPs were observed in 36% of neurones studied, and when investigated after treatment with D-tubocurarine and neostigmine, had a mean amplitude of 4.4 +/- 0.2 mV (mean +/- S.E.) and duration of 5 sec to 1.5 min. Two types of slow IPSPs occurring in different neurones were found. The slow IPSP of the first type was followed by a decrease in cell input resistance, was increased by depolarization and decreased by hyperpolarization of the membrane, with the reversal potential, if estimated by extrapolation method, equal to -77.8 +/- 3.3 mV. The slow IPSP of the second type was not followed by any change in cell input resistance, was increased by hyperpolarization and decreased by depolarization. The slow IPSP of the second type was reversibly blocked by phentolamine (1.4 X 10(-4) M). Noradrenaline (1 X 10(-4) M) evoked hyperpolarization or hyperpolarization followed by depolarization in 55% of the neurones studied. Hyperpolarization evoked by noradrenaline had a mean amplitude to 5.0 +/- 0.2 mV, was not followed by any change in cell input resistance, was reversibly blocked by phentolamine (1.4 X 10(-4) M), and was decreased by both depolarization and hyperpolarization of the cell membrane. It has been concluded that there are two groups of neurones in superior cervical ganglia, different with respect to the ionic mechanisms underlying the slow IPSP. In the first group of neurones the slow IPSP is probably due to an increase in potassium permeability of the membrane. The ionic mechanisms underlying the slow IPSP in the second group of neurones of noradrenaline-induced hyperpolarization remain unclear.

Animals↗
PubMed1992

Vasoactive intestinal polypeptide modulates neuronal excitability in hippocampal slices of the rat.

Vasoactive intestinal polypeptide added at submicromolar concentrations to the perfusion fluid of rat hippocampal slices and slice cultures enhanced the excitability of CA1 and CA3 pyramidal cells in several ways. Specifically, cells were depolarized and the Ca(2+)- and cyclic AMP-dependent potassium conductance was blocked as demonstrated by reduction of the long-lasting afterhyperpolarization and the accommodation of firing. This was also found in tetrodotoxin-containing medium. In low Ca(2+)-high Mg2+ medium (in synaptic isolation) the firing rate was increased. Synaptic transmission was potentiated: extracellularly registered excitatory postsynaptic potentials and population spikes in response to stratum radiatum stimulation and intracellularly recorded excitatory postsynaptic potential-inhibitory postsynaptic potential sequences were enhanced. These results are in keeping with the known stimulation of adenylate cyclase by vasoactive intestinal polypeptide.

Animals↗
PubMed1996

Glycine-mediated inhibitory postsynaptic potentials in the medial pontine reticular formation of the rat in vitro.

Glycinergic neurotransmission was examined in rat medial pontine reticular formation neurons in vitro. Intracellular recordings using glass microelectrodes were made in acutely prepared brainstem slices 400 microns thick. Spontaneous and electrically evoked synaptic activity was blocked by the glycine antagonist strychnine (1-5 microM) but not by the GABA antagonists bicuculline methiodide (40 microM) or picrotoxin (40 microM). Strychnine-sensitive spontaneous and evoked postsynaptic potentials persisted in the presence of the glutamate antagonist (kynurenate, 1 mM). Whole-cell voltage-clamp recordings were carried out in organotypic cultures of rat brainstem. The reversal potential of synaptic currents and responses to exogenously applied glycine were similar and were sensitive to manipulations of the chloride equilibrium potential. Synaptic activity but not responses to exogenous glycine were blocked by tetrodotoxin (0.3 microM). These results indicate the presence of robust, chloride ion-mediated glycinergic inhibition of medial pontine reticular formation neurons, and suggest that glycinergic neurons play an important role in controlling pontine premotor circuitry.

Animals↗
PubMed1994

Diverse sources of hippocampal unitary inhibitory postsynaptic potentials and the number of synaptic release sites.

Dual intracellular recordings from microscopically identified neurons in the hippocampus reveal that the synaptic terminals of three morphologically distinct types of interneuron act through GABAA receptors. Each type of interneuron forms up to 12 synaptic contacts with a postsynaptic principal neuron, but each interneuron innervates a different domain of the surface of the postsynaptic neuron. Different kinetics of the postsynaptic effects, together with the strategic placement of synapses, indicate that these GABAergic interneurons serve distinct functions in the cortical network.

Animals↗
PubMed1988

Cl- - and K+-dependent inhibitory postsynaptic potentials evoked by interneurones of the rat lateral geniculate nucleus.

1. Hyperpolarizing potentials evoked by electrical stimulation of the optic tract were studied in projection cells of the rat dorsal lateral geniculate nucleus (LGN) in vitro. In the same cells the effects of gamma-amino butyric acid (GABA), baclofen and acetylcholine (ACh) were also investigated. 2. In the majority of cells a short- (SHP) (34 ms) and a long-lasting (LHP) (240 ms) hyperpolarizing potential could be recorded in the presence and in the absence of a preceding EPSP. They were blocked by tetrodotoxin (1 microM) and were more sensitive than the monosynaptic EPSP to a low-Ca2+-high-Mg2+ solution. 3. The SHP was associated with a marked decrease (75%) in input resistance, was blocked by bicuculline (1-100 microM) and its reversal potential (-67 mV) was dependent on the extracellular Cl- concentration. 4. The LHP was associated with a smaller decrease (45%) in input resistance and its reversal potential (-76 mV) was dependent on the extracellular K+ concentration. It was increased by bicuculline (100% at 50 microM) and nipecotic acid (30% at 10 microM), blocked by Ba2+ (1 mM), and unaffected by eserine (1-10 microM), neostigmine (1-10 microM) or by recording with EGTA-filled electrodes. In the presence of bicuculline, a single LHP was able to evoke, as a rebound response, a low-threshold Ca2+ spike that was, however, not followed by another LHP (or any other long-lasting hyperpolarization). 5. Ionophoretic applications of GABA evoked in the same cell a Cl- -dependent hyperpolarization (reversal potential: -65 mV) and/or depolarization, both of which were associated with a marked decrease (91%) in input resistance and abolished by bicuculline. GABA was also able to evoke a bicuculline-insensitive, K+-dependent hyperpolarization that had a reversal potential of -75 mV and was associated with a smaller decrease (43%) in input resistance. 6. Baclofen, applied by ionophoresis, pressure ejection or in the perfusion medium (1-100 microM), produced a hyperpolarization that had a reversal potential of -79 mV and was associated with a decrease (45%) in input resistance. 7. In the majority of cells (thirty-seven out of forty) ACh evoked a slow depolarization and only in three cells a hyperpolarization which had a reversal potential of -80 mV.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗
PubMed1986

[Effect of intracellular injections of chloride ion on the inhibitory postsynaptic potential and post-burst hyperpolarization of sensomotor cortex neurons in the cat].

Inversion of the early component of IPSPs in pyramidal neurons of the sensorimotor cortex by intracellular injection of chloride ions was demonstrated in cats immobilized by myorelaxants in acute experiments under moderate composed anesthesia (40 mg/kg nembutal and 20 mg/kg chloralose intraperitoneally). The late component of IPSPs as well as the post-burst hyperpolarization in pyramidal neurons were not inverted. It is concluded that during the early component of IPSPs of both pyramidal and nonpyramidal neurons the membrane permeability is increased for chloride ions, while both the late component of IPSPs and the post-burst hyperpolarization in pyramidal neurons are less dependent on the chloride permeability.

Action Potentials↗