RRC ID 45899
Author Zahratka JA, Williams PD, Summers PJ, Komuniecki RW, Bamber BA.
Title Serotonin differentially modulates Ca2+ transients and depolarization in a C. elegans nociceptor.
Journal J Neurophysiol
Abstract Monoamines and neuropeptides modulate neuronal excitability and synaptic strengths, shaping circuit activity to optimize behavioral output. In C. elegans, a pair of bipolar polymodal nociceptors, the ASHs, sense 1-octanol to initiate escape responses. In the present study, 1-octanol stimulated large increases in ASH Ca(2+), mediated by L-type voltage-gated Ca(2+) channels (VGCCs) in the cell soma and L-plus P/Q-type VGCCs in the axon, which were further amplified by Ca(2+) released from intracellular stores. Importantly, 1-octanol-dependent aversive responses were not inhibited by reducing ASH L-VGCC activity genetically or pharmacologically. Serotonin, an enhancer of 1-octanol avoidance, potentiated 1-octanol-dependent ASH depolarization measured electrophysiologically, but surprisingly, decreased the ASH somal Ca(2+) transients. These results suggest that ASH somal Ca(2+) transient amplitudes may not always be predictive of neuronal depolarization and synaptic output. Therefore, although increases in steady-state Ca(2+) can reliably indicate when neurons become active, quantitative relationships between Ca(2+) transient amplitudes and neuronal activity may not be as straightforward as previously anticipated.
Volume 113(4)
Pages 1041-50
Published 2015-2-15
DOI 10.1152/jn.00665.2014
PII jn.00665.2014
PMID 25411461
PMC PMC4329441
MeSH 1-Octanol / pharmacology Action Potentials* Animals Axons / metabolism Axons / physiology Caenorhabditis elegans / metabolism* Caenorhabditis elegans / physiology Calcium Channels / metabolism Calcium Signaling* Nociceptors / drug effects Nociceptors / metabolism* Nociceptors / physiology Serotonin / pharmacology*
IF 2.234
Times Cited 18
C.elegans tm2654