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J Neurophysiol 87: 1449-1472, 2002;
0022-3077/02 $5.00
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The Journal of Neurophysiology Vol. 87 No. 3 March 2002, pp. 1449-1472
Copyright ©2002 by the American Physiological Society

Calcium Transients in the Garter Snake Vomeronasal Organ

Angel R. Cinelli,1 Dalton Wang,2 Ping Chen,2 Weimin Liu,1 and Mimi Halpern1

 1Department of Anatomy and Cell Biology and  2Department of Biochemistry, State University of New York Downstate Medical Center, Brooklyn, New York 11203

Cinelli, Angel R., Dalton Wang, Ping Chen, Weimin Liu, and Mimi Halpern. Calcium Transients in the Garter Snake Vomeronasal Organ. J. Neurophysiol. 87: 1449-1472, 2002. The signaling cascade involved in chemosensory transduction in the VN organ is incompletely understood. In snakes, the response to nonvolatile prey chemicals is mediated by the vomeronasal (VN) system. Using optical techniques and fluorescent Ca2+ indicators, we found that prey-derived chemoattractants produce initially a transient cytosolic accumulation of [Ca2+]i in the dendritic regions of VN neurons via two pathways: Ca2+ release from IP3-sensitive intracellular stores and, to a lesser extent, Ca2+ influx through the plasma membrane. Both components seem to be dependent on IP3 production. Chemoattractants evoke a short-latency Ca2+ elevation even in the absence of extracellular Ca2+, suggesting that in snake VN neurons, Ca2+ release from intracellular stores is independent of a preceding Ca2+ influx, and both components are activated in parallel during early stages of chemosensory transduction. Once the response develops in apical dendritic segments, other mechanisms can also contribute to the amplification and modulation of these chemoattractant-mediated cytosolic Ca2+ transients. In regions close to the cell bodies of the VN neurons, the activation of voltage-sensitive Ca2+ channels and a Ca2+-induced Ca2+ release from intracellular ryanodine-sensitive stores secondarily boost initial cytosolic Ca2+ elevations increasing their magnitude and durations. Return of intracellular Ca2+ to prestimulation levels appears to involve a Ca2+ extrusion mediated by a Na+/Ca2+ exchanger mechanism that probably plays an important role in limiting the magnitude and duration of the stimulation-induced Ca2+ transients.




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