Date of Award:
5-1-2003
Document Type:
Dissertation
Degree Name:
Doctor of Philosophy (PhD)
Department:
Biology
Committee Chair(s)
Brett A. Adams
Committee
Brett A. Adams
Committee
Daryll B. DeWald
Committee
Scott A. Ensign
Committee
Timothy A. Gilbertson
Committee
Jon Y. Takemoto
Abstract
Ca2+ entry through voltage-gated Ca2+ channels contributes to the regulation of neuronal membrane excitability, neurosecretion, and gene expression. The nervous system regulates these physiological processes through G protein-coupled receptors (GPCRs), which strongly modulate Ca2+ channel activity. This dissertation provides significant new information concerning modulation of neuronal L-, N,- and R-type Ca2+ channels by muscarinic acetylcholine receptors. The major findings of this work are: 1) CaV2.3 channels are differentially modulated by Gαq-coupled muscarinic receptors; 2) reconstituted slow muscarinic inhibition of CaV1.2c can be triggered by either M1, M3, or M5 muscarinic receptors; 3) the amino-terminus of Regulator of G protein signaling 2 (RGS2) targets RGS2 to the slow muscarinic cascade; 4) Activator of G protein signaling-1 (AGS-1) promotes tonic voltage-dependent inhibition of CaV2.2. My findings suggest that RGS proteins and AGS-1 may exert both acute and long-lasting effects on neuronal function by regulating Ca2+ influx through neuronal Ca2+ channels.
Recommended Citation
Bannister, Roger A., "Muscarinic Modulation of Neuronal Voltage-Gated Calcium Channels" (2003). Biology. 690.
https://digitalcommons.usu.edu/etd_biology/690
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