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

Stephen M. Smith; Jeremy B. Bergsman; Nobutoshi C. Harata; Richard H. Scheller; Richard W. Tsien

doi:10.1016/S0896-6273(03)00837-7

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

Stephen M. Smith, Jeremy B. Bergsman, Nobutoshi C. Harata, Richard H. Scheller, Richard W. Tsien

Pulmonary and Critical Care Medicine

Research output: Contribution to journal › Article › peer-review

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Abstract

Synaptic activity causes reductions in cleft [Ca²⁺] 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 [Ca²⁺] ([Ca²⁺] _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, Gd³⁺ > spermidine > Ca²⁺ > Mg²⁺, typical for [Ca²⁺]_o receptors). The identification of a Ca²⁺ sensor-NSC channel pathway establishes the existence of a mechanism by which presynaptic terminals can detect and respond to reductions in cleft [Ca²⁺]. 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.

Original language	English (US)
Pages (from-to)	243-256
Number of pages	14
Journal	Neuron
Volume	41
Issue number	2
DOIs	https://doi.org/10.1016/S0896-6273(03)00837-7
State	Published - Jan 22 2004

ASJC Scopus subject areas

General Neuroscience

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

abstract = "Synaptic activity causes reductions in cleft [Ca2+] 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 [Ca2+] ([Ca2+] 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, Gd3+ > spermidine > Ca2+ > Mg2+, typical for [Ca2+]o receptors). The identification of a Ca2+ sensor-NSC channel pathway establishes the existence of a mechanism by which presynaptic terminals can detect and respond to reductions in cleft [Ca2+]. 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.",

author = "Smith, {Stephen M.} and Bergsman, {Jeremy B.} and Harata, {Nobutoshi C.} and Scheller, {Richard H.} and Tsien, {Richard W.}",

note = "Funding Information: We thank Dr. Frank Horrigan for providing analysis macros and NPS Pharmaceuticals for the gift of NPS R-467. We also thank Drs. H. von Gersdorff, H. Taschenberger, and J. Waters for useful discussions and Drs. R. Aldrich and R. Lewis for helpful comments on an earlier version of the manuscript. This work was supported by grants from HHMI, NIH, and NINDS.",

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AU - Scheller, Richard H.

AU - Tsien, Richard W.

N1 - Funding Information: We thank Dr. Frank Horrigan for providing analysis macros and NPS Pharmaceuticals for the gift of NPS R-467. We also thank Drs. H. von Gersdorff, H. Taschenberger, and J. Waters for useful discussions and Drs. R. Aldrich and R. Lewis for helpful comments on an earlier version of the manuscript. This work was supported by grants from HHMI, NIH, and NINDS.

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N2 - Synaptic activity causes reductions in cleft [Ca2+] 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 [Ca2+] ([Ca2+] 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, Gd3+ > spermidine > Ca2+ > Mg2+, typical for [Ca2+]o receptors). The identification of a Ca2+ sensor-NSC channel pathway establishes the existence of a mechanism by which presynaptic terminals can detect and respond to reductions in cleft [Ca2+]. 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.

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

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