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Calcium channels responsible for potassium‐induced transmitter release at rat cerebellar synapses.
Author(s) -
Momiyama A,
Takahashi T
Publication year - 1994
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1994.sp020123
Subject(s) - neurotransmission , chemistry , potassium channel , potassium , calcium channel blocker , calcium channel , potassium channel blocker , inhibitory postsynaptic potential , calcium , biophysics , tetrodotoxin , channel blocker , cerebellum , neuroscience , biology , biochemistry , receptor , organic chemistry
The effects of calcium channel blockers on potassium‐induced transmitter release were studied in thin slices of cerebellum from neonatal rats using whole‐cell patch clamp methods. Miniature inhibitory postsynaptic currents (mIPSCs) mediated by gamma‐aminobutyric acid (GABA) were recorded from deep cerebellar nuclear neurones in the presence of tetrodotoxin. The frequency of mIPSCs was reproducibly increased by a brief application of high‐potassium solution. In the presence of the L‐type Ca2+ channel blocker nicardipine (10 microM), the potassium‐induced increase in mIPSC frequency was suppressed by 49%. Neither the mean amplitude nor the time course of mIPSCs was affected by the blocker. The N‐type Ca2+ channel blocker omega‐conotoxin GVIA (omega‐CgTX, 3 microM) had no effect on the frequency of potassium‐induced mIPSCs. The P‐type Ca2+ channel blocker omega‐Aga‐IVA (200 nM) suppressed the potassium‐induced increase in mIPSC frequency by 83% without affecting the mean amplitude or time course of mIPSCs. Comparing these data with previous studies of neurally evoked transmission, it is concluded that the Ca2+ channel subtypes responsible for potassium‐induced transmitter release may be different from those mediating fast synaptic transmission.