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• W2079738866 abstract "1. Simultaneous pre- and postsynaptic patch recordings were obtained from the varicosity synapses formed by Xenopus motoneurons on muscle cells in embryonic cultures, in order to elucidate the contribution of N- and L-type Ca(2+) channels to the varicosity Ca(2+) current (I(Ca)) and evoked transmitter release. 2. Although N-type channels are predominant in the varicosities and generally thought to be responsible for all evoked release, in most synapses a fraction of I(Ca) and release could be reversibly blocked by the L-type channel antagonist nifedipine, and enhanced by the agonist Bay K8644. Up to 50 % (mean, 21 %) of the I(Ca) evoked by a voltage clamp waveform mimicking a normal presynaptic action potential (APWF) is composed of L-type current. 3. Surprisingly, the nifedipine-sensitive (L) channels activated more rapidly (time-constant, 0.46 ms at +30 mV) than the nifedipine-insensitive (N) channels (time constant, 1.42 ms). Thus the L-type current would play a disproportionate role in the I(Ca) linked to a normal action potential. 4. The relationship between I(Ca) and release was the same for nifedipine-sensitive and -resistant components. The N- and L-components of I(Ca) are thus equally potent in evoking release. This may represent an immature stage before N-type channels become predominant. 5. Replacing Ca(2+) in the medium with Ba(2+) strongly enhanced the L-type component, suggesting that L-type channels may be inactivated at Ca(2+) levels close to those at rest. 6. We speculate that populations of L-type channels in different parts of the neuron may be recruited or inactivated by fluctuations of the cytosolic Ca(2+) concentration within the physiological range." @default.
• W2079738866 created "2016-06-24" @default.
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• W2079738866 date "2001-10-01" @default.
• W2079738866 modified "2023-10-16" @default.
• W2079738866 title "Contribution of L‐type Ca²⁺ channels to evoked transmitter release in cultured <i>Xenopus</i> nerve‐muscle synapses" @default.
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• W2079738866 doi "https://doi.org/10.1111/j.1469-7793.2001.00021.x" @default.
• W2079738866 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2278856" @default.
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