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Calcium Transients in the Garter Snake Vomeronasal Organ
1 Department of Anatomy and Cell Biology and 2 Department 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. Neuroph...
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Published in: | Journal of neurophysiology 2002-03, Vol.87 (3), p.1449-1472 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
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Online Access: | Get full text |
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Summary: | 1 Department of Anatomy and Cell Biology and
2 Department 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 Ca 2+ indicators, we
found that prey-derived chemoattractants produce initially a transient
cytosolic accumulation of
[Ca 2+ ] i in the dendritic
regions of VN neurons via two pathways: Ca 2+
release from IP 3 -sensitive intracellular stores
and, to a lesser extent, Ca 2+ influx through the
plasma membrane. Both components seem to be dependent on
IP 3 production. Chemoattractants evoke a
short-latency Ca 2+ elevation even in the absence
of extracellular Ca 2+ , suggesting that in snake
VN neurons, Ca 2+ release from intracellular
stores is independent of a preceding Ca 2+ 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 Ca 2+ transients. In regions close to
the cell bodies of the VN neurons, the activation of voltage-sensitive
Ca 2+ channels and a
Ca 2+ -induced Ca 2+ release
from intracellular ryanodine-sensitive stores secondarily boost initial
cytosolic Ca 2+ elevations increasing their
magnitude and durations. Return of intracellular
Ca 2+ to prestimulation levels appears to involve
a Ca 2+ extrusion mediated by a
Na + /Ca 2+ exchanger
mechanism that probably plays an important role in limiting the
magnitude and duration of the stimulation-induced Ca 2+ transients. |
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ISSN: | 0022-3077 1522-1598 |
DOI: | 10.1152/jn.00651.2001 |