Voltage-dependence of miniature inhibitory postsynaptic current frequency and amplitude in tectal neurons of Xenopus. (1/131)

Experiments were performed to study the voltage-dependence of miniature inhibitory postsynaptic current (mIPSC) frequency and amplitude using patch-clamp technique with whole cell recording in optic tectal slices of Xenopus. The following results have been observed. (1) When the membrane potentials of a neuron were depolarized or hyperpolarized stepwise from a resting potential via recording pipette to inject a DC current, the frequency and/or amplitude of mIPSCs increased or decreased respectively. The frequency of mIPSCs increased gradually with depolarizing membrane potential and it attained to the maximum as the membrane potential was held at +10 mV. (2) The amplitude increased slightly as the neuron was depolarized. When the depolarization of membrane potential reached -30 or -40 mV, the amplitudes of mIPSCs were maximal. Further depolarization resulted in a decrease of amplitude. Meanwhile, the large mIPSCs appeared when the membrane potential depolarized to a range between -20 mV and +10 mV. (3) With Ca(2+)-free bath solution, the frequency and amplitude of mIPSCs also increased stepwise progressively on depolarization of membrane potential, but the increase was less marked as corresponding value in normal saline perfusion. (4) When the [K(+)](o) in bath solution increased, the frequency of mIPSCs decreased markedly and the amplitude of mIPSCs decreased slightly. If the external K(+) concentration increased further to higher than 20 mmol/L, the neuron produced a marked slow inward or outward membrane current. The possible mechanism underlying the voltage-dependence of mIPSC frequency and amplitude is discussed briefly.  (+info)

Physiology and morphology of callosal projection neurons in mouse. (2/131)

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Modulation of murine gastric antrum smooth muscle STOC activity and excitability by phospholamban. (3/131)

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Ethanol decreases Purkinje neuron excitability by increasing GABA release in rat cerebellar slices. (4/131)

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Chronic benzodiazepine administration potentiates high voltage-activated calcium currents in hippocampal CA1 neurons. (5/131)

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Loss of transforming growth factor-beta 2 leads to impairment of central synapse function. (6/131)

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Presynaptic and postsynaptic NMDA receptors mediate distinct effects of brain-derived neurotrophic factor on synaptic transmission. (7/131)

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Unc-51 controls active zone density and protein composition by downregulating ERK signaling. (8/131)

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