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PubMedDate not supplied

[Evaluation of synaptic potential dynamics from evoked impulse activity of neurons].

To evaluate intracellular potentials in the region of spike initiation of function lambda (t) is suggested which describes the dependence on time of the density of conditional probability of generation by the neuron of the first impulse in response to the stimulus. Qualitative correspondence of the dynamics of membrane potentials and function lambda (t) is demonstrated on the analog model. The application of the function lambda (t) to the classification of the neurons of auditory system is shown to be promising. The difference between the function lambda (t) and normalized poststimulus histogram allows to evaluate the refracteriness of the neuron.

Acoustic Stimulation↗
PubMed1992

Excitatory amino acid-mediated responses and synaptic potentials in medial pontine reticular formation neurons of the rat in vitro.

Neurons of the medial pontine reticular formation (mPRF) are involved in the execution of numerous behaviors including initiation of locomotion, eye movements, startle responses, and rapid eye movement sleep phenomena. Approximately half of the afferent projections to mPRF neurons come from within the reticular formation (Shammah-Lagnado et al., 1987). In spite of the importance of reticulo-reticular connections, virtually nothing is known about transmitters mediating these synapses. In order to identify a candidate excitatory neurotransmitter, the actions of excitatory amino acids (EAAs) on the membrane properties of mPRF neurons recorded in rat brainstem slices in vitro were studied. Standard intracellular recording methods, including single-electrode voltage clamp, were used to examine the postsynaptic actions of EAAs. We also tested whether EAA antagonists block EPSPs evoked by stimulation of the contralateral reticular formation in the slices. mPRF neurons responded to both non-NMDA and NMDA agonists. NMDA-induced conductances were voltage dependent and depressed by physiological concentrations of magnesium. Stimulation of the contralateral reticular formation elicited EPSPs that were depressed by the general EAA antagonist kynurenate. Evoked EPSPs were partially depressed by 6,7-dinitroquinoxaline-2,3-dione. The evoked EPSP was further reduced by the NMDA antagonist (+/-)-2-amino-5-phosphonopentanoic acid in some cases. These results suggest that excitatory reticulo-reticular neurotransmission is mediated by an EAA. Both non-NMDA and NMDA receptors contribute to EAA neurotransmission in the mPRF formation and play an integral role in reticular formation function.

Amino Acids↗
PubMed1991

Baclofen and adenosine inhibit synaptic potentials mediated by gamma-aminobutyric acid and glutamate release in rat nucleus accumbens.

Intracellular recordings were made from rat nucleus accumbens neurons in a tissue slice in vitro; postsynaptic potentials (p.s.p.) were evoked by focal electrical stimulation of the slice surface. P.s.p. were partially blocked by bicuculline (30 microM), partially blocked by a combination of 6-cyano-2,3-dihydroxy-7-nitroquinoxaline (CNQX, 10 microM) and DL-2-amino-5-phosphonovaleric acid (APV, 30 microM) and completely blocked when all three antagonists were applied together. Both the gamma-aminobutyric acid (GABA)-mediated p.s.p. (in CNQX and APV) and the glutamate-mediated p.s.p. (in bicuculline) were inhibited by baclofen (10-300 microM), adenosine (10-300 microM) and N6-(2-phenylisopropyl)adenosine (0.1-3 microM). Theophylline competitively antagonized the action of adenosine with an apparent dissociation equilibrium constant of about 15 microM. Baclofen, adenosine and N6-(2-phenylisopropyl)adenosine caused small (less than 10 mV) hyperpolarizations; voltage clamp experiments indicated that this resulted from an outward potassium current. It is concluded that activation of GABAB receptors and adenosine A1 receptors inhibits the release of glutamate and GABA at synapses in the nucleus accumbens.

2-Amino-5-phosphonovalerate↗
PubMed1991

Excitatory synaptic potentials in kainic acid-denervated rat CA1 pyramidal neurons.

Intracellular recordings were performed in the CA1 region of the rat hippocampus following an ipsilateral intraventricular injection of kainic acid. Seven days postlesion, graded bursts of up to four action potentials could be evoked by stimulation of the stratum radiatum. The evoked EPSPs underlying these bursts showed a prolonged 10-90% rise time and half-width compared to control EPSPs, an absence of a significant inhibitory phase, and an increase in magnitude and duration at depolarized resting levels. The evoked EPSPs also exhibited a significant decrease in amplitude and time course in response to D-APV (D-2-amino-5-phosphonovaleric acid; 1-20 microM), though this effect was variable from cell to cell. The prolonged time course, voltage sensitivity, and response to a selective NMDA antagonist confirmed that the major component of the EPSP in neurons from lesioned slices was mediated by NMDA receptors. The partial denervation of the CA1 area induced by the kainic acid led to both an enhanced NMDA-mediated excitatory phase and a decrease in postsynaptic inhibition, resulting in the pronounced hyperexcitability noted in the lesioned slices.

2-Amino-5-phosphonovalerate↗
PubMed1990

[The generation of nonadrenergic inhibiting synaptic potentials in the smooth muscles of the gastrointestinal tract by substituting cesium ions for potassium ions].

Nonadrenergic inhibitory junction potentials (IJPs) evoked by intramural stimulation were investigated in smooth muscle of guinea pig stomach, caecum and colon by means of sucrose-gap method. IJPs disappeared in the smooth muscle preexposed to K-free Krebs solution for 4-9 h and restored by addition 6mM Cs+. The amplitude of IJPs was half as much as one in normal conditions but the latency and duration were significantly prolonged. In most cases apamin blocks IJPs in these muscles. The results presented suggest that IJPs generation is due to Cs+ ions permeated through Ca(2+)-activated apamin-sensitive potassium channels of small conductance in these conditions. As the responses to ATP were affected in parallel with IJPs, these results are consistent with the purinergic hypothesis.

Animals↗
PubMed1988

NMDA- and non-NMDA-receptor components of excitatory synaptic potentials recorded from cells in layer V of rat visual cortex.

The pharmacological properties of excitatory synapses on pyramidal cells in layer V of rat visual cortex were investigated by recording EPSPs intracellularly in tissue slices. The EPSPs were evoked by electrically stimulating cells in layer II/III or axons in white matter. All of the layer V neurons were pyramidal in nature as determined by injections of Lucifer yellow or by electrophysiological criteria. Application of the broadly acting antagonists kynurenic acid and gamma-D-glutamylglycine reversibly antagonized the EPSPs from both presynaptic sources in a dose-dependent manner: 1 and 5 mM kynurenic acid produced 63 and 79% reductions, respectively, of control responses. The specific NMDA antagonist APV (50 microM) caused a small reduction in peak amplitude and a more significant reduction in the duration of the falling phase of EPSPs. When slices were bathed in Mg2+-free medium, the amplitude of the EPSP increased substantially. Under these conditions APV reduced the size of the EPSP to that observed with APV in the presence of 1 mM Mg2+. The voltage sensitivities of the APV-sensitive and APV-insensitive components of the layer II/III-evoked EPSPs were examined. The APV-insensitive component was not voltage dependent and had an extrapolated reversal potential of -10 mV. In contrast, the APV-sensitive component showed an NMDA-like voltage dependency; it was greatest at the most positive potentials tested (-45 mV) and nearly absent at membrane potentials below rest. At potentials near threshold, the APV-sensitive component contributed approximately half of the total response. Although the time to peak and decay were longer for the APV-sensitive component, the latency was the same as that of the APV-insensitive component. These results provide evidence that the layer II/III to V pathway, which comprises a major interlaminar circuit in cortex, is mediated directly through NMDA as well as non-NMDA receptors located on the layer V cells. This finding has implications for the role of this circuit in cortical visual plasticity.

2-Amino-5-phosphonovalerate↗