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Contribution of L-type Ca²⁺ channels to evoked transmitter release in cultured Xenopus nerve-muscle synapses

Olav Sand *, Bo-Ming Chen and Alan D. Grinnell

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 Ca²⁺ channels to the varicosity Ca²⁺ 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 Ca²⁺ in the medium with Ba²⁺ strongly enhanced the L-type component, suggesting that L-type channels may be inactivated at Ca²⁺ 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 Ca²⁺ concentration within the physiological range.

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