Volume 17, Number 16,
Issue of August 15, 1997
pp. 6302-6313
Copyright ©1997 Society for Neuroscience
Developmental Changes in Calcium Current Pharmacology and
Somatostatin Inhibition in Chick Parasympathetic Neurons
Received March 13, 1997; revised May 27, 1997; accepted May 30, 1997.
Michael G. White,
Mark A. Crumling, and
Stephen D. Meriney
Department of Neuroscience, University of Pittsburgh, Pittsburgh,
Pennsylvania 15260
Voltage-dependent calcium (Ca2+) currents were
characterized and modulatory effects of somatostatin were measured in
acutely dissociated chick ciliary ganglion neurons at embryonic stages 34, 37, and 40. This developmental time period coincides with the
period of synapse formation between ciliary ganglion neurons and
peripheral eye muscles. At all three developmental stages Ca2+ current could be blocked almost completely by
combined application of
-CgTX GVIA and nitrendipine. At young
embryonic ages there was significant overlap in sensitivity, with
~75% of the current sensitive to either blocker applied
independently. By stage 40, there was very little or no overlap in
sensitivity, with ~75% of the current blocked by
-CgTX GVIA
(N-type) and 30% blocked by nitrendipine (L-type). These data are
consistent with earlier findings that the pharmacology of acetylcholine
release from ciliary ganglion nerve terminals changes during
development from sensitivity to both dihydropyridines and
-CgTX GVIA
to selective sensitivity to
-CgTX GVIA ().
Somatostatin reduced Ca2+ current by 50-60% at all
three developmental stages. At early developmental stages somatostatin
receptors coupled predominantly to the current that was sensitive to
both
-CgTX GVIA and nitrendipine. By stage 40, somatostatin
primarily inhibited classically defined N-type current (selectively
sensitive to
-CgTX GVIA). Thus, somatostatin receptor coupling to
Ca2+ channels persisted throughout development as
Ca2+ current pharmacology changed.
Key words:
calcium channel;
somatostatin modulation;
development;
chick ciliary ganglion;
FPL 64176;
-CgTX GVIA;
dihydropyridines