Recordings from Single Neocortical Nerve Terminals Reveal a Nonselective Cation Channel Activated by Decreases in Extracellular Calcium

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-depende...

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Bibliographic Details
Published in:Neuron (Cambridge, Mass.) Mass.), 2004-01, Vol.41 (2), p.243-256
Main Authors: Smith, Stephen M, Bergsman, Jeremy B, Harata, Nobutoshi C, Scheller, Richard H, Tsien, Richard W
Format: Article
Language:English
Subjects:
Calcium
Calcium - metabolism
Calcium - physiology
Calcium Signaling - physiology
Cations, Divalent - pharmacology
Experiments
Extracellular Space - physiology
Fluorometry
Humans
Ion Channel Gating - physiology
Ion Channels - physiology
Medical research
Membrane Potentials - physiology
Microscopy, Electron
Neocortex - cytology
Neocortex - physiology
Neurotransmitter Agents - metabolism
Parkinson's disease
Patch-Clamp Techniques
Presynaptic Terminals - physiology
Receptors, Calcium-Sensing - physiology
Synaptosomes - metabolism
Synaptosomes - physiology
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Summary: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.
ISSN:0896-6273
1097-4199
DOI:10.1016/S0896-6273(03)00837-7