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Results for “Excitatory Postsynaptic Potentials”

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At least 109 records · Page 6Linked to original sources
PubMed1988

A novel muscarinic receptor antagonist AF-DX 116 differentially blocks slow inhibitory and slow excitatory postsynaptic potentials in the rabbit sympathetic ganglia.

Muscarinic, slow postsynaptic potentials (s-epsp and s-ipsp) in the rabbit superior cervical ganglia were shown to be differentially depressed by a novel cardioselective M2-type antagonist AF-DX 116: it antagonized the s-ipsp with IC50 value of 1.5 X 10(-7) M, which is 16-fold more potent in depressing the s-ipsp than the s-epsp. A hyperpolarizing component in the biphasic potential changes induced by a muscarinic agonist, methacholine, was selectively eliminated by this antagonist. AF-DX 116 was thus shown to be an useful tool for discriminating the M2-type muscarinic responses from those of M1-type in the nervous system.

Action Potentials↗
PubMed1993

Simultaneous intracellular recordings from enteric neurons reveal that myenteric AH neurons transmit via slow excitatory postsynaptic potentials.

Simultaneous intracellular electrical recordings were made from pairs of neurons separated circumferentially by 100-200 microns of the myenteric plexus of the guinea-pig ileum in vitro. The recording electrodes were filled with the dye neurobiotin which was injected into impaled nerve cells, and later revealed histochemically. Intracellular current pulses were used to evoke action potentials via the recording electrode in one type of myenteric neuron, in most cases an AH neuron, while a second electrode was used to record from a simultaneously impaled S neuron or AH neuron. AH neurons are thought to be primary sensory neurons, whereas S neurons are interneurons and motor neurons. Ninety pairs of neurons were adequately tested for interaction. From these, 17 S neurons and three AH neurons that responded to AH neuron stimulation were detected. In each case, the response was a slow depolarization that was seen only in response to a train of stimuli at 10 Hz. The slow depolarizations were enhanced by passing depolarizing current and diminished by hyperpolarization. Responses were also diminished by lowering external Ca.2+ and elevating Mg2+. In all cases in which intracellular recording indicated communication between neurons, morphological evidence of connection was seen. In no case was there communication without connection, but in four instances, morphological connections appeared to exist, although no physiological evidence of communication was obtained.

Action Potentials↗
PubMed1970

Excitatory postsynaptic potential and monosynaptic reflex discharge of spinal motoneurons during anoxic insult.

Almost universally held is the concept that in transmission from one neuron to another the so-called postsynaptic potential is the essential step leading to discharge of the secondary neurons. According to the present experiments this is not so in the monosynaptic reflex system of the cat spinal cord. Its role in facilitation of response and certain other essential data are mentioned.

Animals↗
PubMed1977

[Excitatory postsynaptic potentials in the lumbar motor neurons of frogs induced by stimulation of muscle and cutaneous nerves].

The postsynaptic effects evoked in lumbar motoneurons by stimulation of different muscle and cutaneous nerves of hindlimbs were studied by means of intracellular recording in the frog isolated spinal cord. The data obtained confirm presence of monosynaptic connections between primary afferents and spinal motoneurons. Monosynaptic EPSPs were shown to be due to low threshold muscle afferent volleys in homonymous nerves and did not generate spike discharges. The mean amplitude of monosynaptic EPSPs was 1.1 +/- 0.12 mV, time-to-peak 1.76 +/- 0.16 msec, time constant of decay from 6.0 to 15.0 msec. EPSPs with no synaptic delay were recorded in some motoneurons which suggest existence of an electrical mechanism of transmission.

Animals↗
PubMed1990

[The effect of glycine and gamma-aminobutyric acid on the excitatory postsynaptic potentials of the spinal motor neurons in the lamprey in the presence of antagonists].

Effect of bath application of the inhibitory amino acids (glycine and GABA) on motoneurons of EPSPs was studied in the normal physiological solutions and after preliminary administration of antagonists: strychnine (10(-6) mol/l), bicuculline (10(-4) mol/l) or picrotoxin (10(-4) mol/l). All these antagonists diminished the depression of monosynaptic EPSPs which were elicited by both amino acids (glycine and GABA). Data obtained in this study and previously reported ones permit concluding that motoneuron membranes in the spinal cord of lamprey possess the unit receptor channel complex sensitive to both amino acids.

Animals↗
PubMed1988

Synaptic transmission mediated by single club endings on the goldfish Mauthner cell. II. Plasticity of excitatory postsynaptic potentials.

Simultaneous pre- and postsynaptic intracellular recordings were used to analyze the properties of chemically mediated synaptic transmission between single club endings of eighth nerve afferents and the goldfish Mauthner (M-) cell lateral dendrite. The EPSPs exhibited pronounced facilitation when the presynaptic fiber fired high-frequency bursts of 2 or 3 impulses at intervals of 2-4 msec. The amplitudes of the EPSPs evoked by the second and third presynaptic impulses of a burst were, on average, 99 and 108% larger than that evoked by the first impulse. A cross-correlation analysis showed that the amplitudes of the control and facilitated EPSPs fluctuated independently, indicating that the facilitation was mediated by a presynaptic mechanism. This conclusion was supported by a comparison of the coefficient of variation for the control and facilitated EPSPs, on the basis of a binomial release model. In addition, the value of binomial n, the number of presynaptic release units, was not changed during facilitation. The origin of EPSP fluctuations was analyzed by examining the correlation between the amplitudes of EPSPs and those of the electrotonic coupling potentials associated with them. The absence of correlation between the 2 variables suggested that the fluctuations of EPSPs were not due to a variable presynaptic impulse invasion. The EPSP fluctuations were further analyzed by assuming that the facilitation was associated with an increase in the probability (p) of transmitter release and that the release process followed simple binomial statistics. The binomial variables thus calculated were n = 6-11, p = 0.29-0.44, and q = 31-61 microV, values comparable to the estimates for other CNS synapses. More importantly, these parameters provided satisfactory fits to the amplitude histograms of the control and facilitated EPSPs. The number of release units, n, was smaller than, but in a range similar to, the number of active zones identified in the freeze-fracture study of the club endings (Kohno and Noguchi, 1986). This correlation is consistent with the notion that active zones are the structural correlates of quantal release units. In the preceding paper, it was shown that impulses in a majority of club endings electrotonically coupled to the M-cell do not produce a detectable chemically mediated EPSP, although the contacts have the morphological correlates of chemical synapses. In an attempt to activate these "silent" connections, 2 approaches were used. First, the burst-firing paradigm, which could effectively facilitate EPSPs already present, failed to reveal any EPSPs at the silent junctions.(ABSTRACT TRUNCATED AT 400 WORDS)

Algorithms↗