Residual free calcium is not responsible for facilitation of neurotransmitter release.
An increase in internal free calcium ([Ca2+]i) in the presynaptic terminal is often assumed to directly produce facilitation of neurotransmitter release. Using a Ca(2+)-activated potassium conductance as a bioassay for free [Ca2+]i in the presynaptic terminal of the crayfish (Procambarus clarkii) opener neuromuscular junction, we now demonstrate that free [Ca2+]i has a decay time constant (tau) of 1-4 msec, whereas facilitation of neurotransmitter release has a decay tau of 7-43 msec. In addition, facilitation of neurotransmitter release can be markedly different at times when free [Ca2+]i values and presynaptic membrane voltages are equal. We conclude that free [Ca2+]i in the presynaptic terminal is not directly responsible for facilitation of neurotransmitter release. Our data suggest that facilitation results from bound Ca2+ or some long-lived consequence of bound Ca2+.
Blundon
J A
JA
Department of Zoology, University of Texas, Austin 78712.
Wright
S N
SN
Brodwick
M S
MS
Bittner
G D
GD
D000818:Animals; D003400:Astacoidea; D002118:Calcium / Q000502:physiology*; D015220:Calcium Channels / Q000502:physiology; D009469:Neuromuscular Junction / Q000502:physiology*; D018377:Neurotransmitter Agents / Q000378:metabolism*; D011188:Potassium / Q000502:physiology; D013570:Synaptic Membranes / Q000502:physiology*
D015220:Calcium Channels; D018377:Neurotransmitter Agents; D011188:Potassium; D002118:Calcium