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J. Biol. Chem., Vol. 277, Issue 18, 16172-16178, May 3, 2002
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From the Department of Pharmacology and Physiology, University of
Medicine and Dentistry of New Jersey, Newark, New Jersey 07103
Transient receptor
potential (TRP) channels form a large family of plasma
membrane cation channels. Mammalian members of the "short" TRP
family (TRP channel (TRPC) 1-7 are Ca2+-permeant,
non-selective cation channels that are widely expressed in various cell
types, including neurons. TRPC activity is linked through unknown
mechanisms to G-protein-coupled receptors or receptor tyrosine kinases
that activate phospholipase C. To investigate the properties and
function of TRPC4 in neuronally derived cells, we transiently
expressed mouse TRPC4 and histamine H1 receptor in mouse
adrenal chromaffin cells and PC12 cells. Histamine, but not
thapsigargin, stimulated Mn2+ influx in transfected cells.
In the whole-cell patch clamp mode, histamine triggered a transient
current in TRPC4-expressing cells. No current was evoked by perfusion
with inositol 1,4,5-trisphosphate. When exocytosis was monitored with
the capacitance detection technique, the magnitude of the membrane
capacitance increase (
TRPC4 Can Be Activated by G-protein-coupled Receptors and
Provides Sufficient Ca2+ to Trigger Exocytosis in
Neuroendocrine Cells*
Cm) on application of
histamine in H1 receptor/TRPC4-expressing chromaffin cells
was comparable with that triggered by a train of depolarizing pulses.
Our results indicate that TRPC4 channels behave as receptor, but not
store-operated, channels in neuronally derived cells. TRPC4 channels
can provide sufficient Ca2+ influx to trigger a robust
secretory response in voltage-clamped neurosecretory cells. Similar
mechanisms may modulate exocytosis in other neuronal systems.
*
This work was supported by National Institutes of Health
Grant NS40167 (to M. C. N.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Dept. of Pharmacology
and Physiology, UMDNJ-New Jersey Medical School, 185 S. Orange
Ave., Newark, NJ 07103. Tel.: 973-972-4391; Fax: 973-972-4554; E-mail: mnowycky@compuserve.com.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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