Journal article
Recordings from Single Neocortical Nerve Terminals Reveal a Nonselective Cation Channel Activated by Decreases in Extracellular Calcium
Neuron (Cambridge, Mass.), Vol.41(2), pp.243-256
2004
DOI: 10.1016/S0896-6273(03)00837-7
PMID: 14741105
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.
Details
- Title: Subtitle
- Recordings from Single Neocortical Nerve Terminals Reveal a Nonselective Cation Channel Activated by Decreases in Extracellular Calcium
- Creators
- Stephen M Smith - Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305 USAJeremy B Bergsman - Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305 USANobutoshi C Harata - Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305 USARichard H Scheller - Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305 USARichard W Tsien - Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305 USA
- Resource Type
- Journal article
- Publication Details
- Neuron (Cambridge, Mass.), Vol.41(2), pp.243-256
- Publisher
- Elsevier Inc
- DOI
- 10.1016/S0896-6273(03)00837-7
- PMID
- 14741105
- ISSN
- 0896-6273
- eISSN
- 1097-4199
- Language
- English
- Date published
- 2004
- Academic Unit
- Molecular Physiology and Biophysics
- Record Identifier
- 9984025320302771
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