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Volume 16, Number 19,
Issue of October 1, 1996
pp. 6000-6011
Copyright ©1996 Society for Neuroscience
Modulation of High Voltage-Activated Calcium Channels by
Somatostatin in Acutely Isolated Rat Amygdaloid Neurons
Received June 3, 1996; revised July 11, 1996; accepted July 16, 1996.
Félix Viana and
Bertil Hille
Department of Physiology and Biophysics, University of Washington
School of Medicine, Seattle, Washington 98195-7290
We investigated actions of somatostatin (Som) on voltage-gated
calcium channels in acutely isolated rat amygdaloid neurons.
Somatostatin caused a dose-dependent inhibition of the high
voltage-activated (HVA) Ca2+ current, with little or no
effect on the low voltage-activated (LVA) current. Nifedipine (2-10
µM) reduced the peak current by ~15% without reducing
inhibition of current by Som significantly, ruling out L-type channels
as the target of modulation. The modulation appears to involve N- and
P/Q-type calcium channels. After pretreatment with  -conotoxin-GVIA
(-CgTx) or -agatoxin-IVA, the inhibition was reduced but not
abolished, whereas the combined application of both toxins nearly
abolished the modulation. The Som analog BIM-23060 mimicked the effects
of Som, whereas BIM-23058 had no effect, implicating Som type-2
receptors (SSTR-2). The inhibition was voltage-dependent, being minimal
for small depolarizations, and was often accompanied by a slowing of
the activation time course. Strong depolarizing prepulses partially
relieved the inhibition and restored the time course of activation.
Intracellular dialysis with GTP S led to spontaneous inhibition and a
slowing of the current like that with Som and occluded the effects of
the peptide. Dialysis with GDP S also diminished the inhibition. A
short preincubation with 50 µM of the alkylating agent
N-ethylmaleimide (NEM) prevented the action of
somatostatin. These results suggest a role for NEM-sensitive G-proteins
in the Som inhibition. Application of 8-CPT-cAMP and IBMX did not mimic
or prevent the effects of Som.
Key words:
amygdala;
neuropeptide;
G-protein;
NEM;
somatostatin;
calcium channels;
limbic system
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