Recordings from single neocortical nerve terminals reveal a nonselective cation channel activated by decreases in extracellular calcium |
| |
Authors: | Smith Stephen M Bergsman Jeremy B Harata Nobutoshi C Scheller Richard H Tsien Richard W |
| |
Affiliation: | Department of Molecular and Cellular Physiology, Stanford University School of Medicine, CA 94305, USA. |
| |
Abstract: | Synaptic activity causes reductions in cleft [Ca(2+)] that may impact subsequent synaptic efficacy. Using modified patch-clamp techniques to record from single neocortical nerve terminals, we report that physiologically relevant reductions of extracellular [Ca(2+)] ([Ca(2+)](o)) activate voltage-dependent outward currents. These outward currents are carried by a novel nonselective cation (NSC) channel that is indirectly inhibited by various extracellular agents (rank order potency, Gd(3+) > spermidine > Ca(2+) > Mg(2+), typical for [Ca(2+)](o) receptors). The identification of a Ca(2+) sensor-NSC channel pathway establishes the existence of a mechanism by which presynaptic terminals can detect and respond to reductions in cleft [Ca(2+)]. Activation of NSC channels by falls in [Ca(2+)](o) would be expected during periods of high activity in the neocortex and may modulate the excitability of the presynaptic terminal. |
| |
Keywords: | |
本文献已被 ScienceDirect PubMed 等数据库收录! |