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PMID: 8815883 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Modulation of high voltage-activated calcium channels by somatostatin in acutely isolated rat amygdaloid neurons.

The Journal of neuroscience : the official journal of the Society for Neuroscience ·Vol. 16 ·No. 19 ·1996-10-01 ·Pages 6000-11

Viana F, Hille B

Abstract

We investigated actions of somatostatin (Som) on voltagegated 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 microM) reduced the peak current by approximately 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 omega-conotoxin-GVIA (omega-CgTx) or omega-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 gamma 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 beta S also diminished the inhibition. A short preincubation with 50 microM 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.

MeSH Terms
Amygdala/cytology,metabolism Animals Calcium Channel Blockers/pharmacology Calcium Channels/drug effects,physiology Cell Separation Cyclic AMP/physiology Electrophysiology GTP-Binding Proteins/physiology Neurons/metabolism Rats Rats, Sprague-Dawley Receptors, Somatostatin/physiology Somatostatin/pharmacology
Chemicals
Calcium Channel Blockers Calcium Channels Receptors, Somatostatin Somatostatin Cyclic AMP GTP-Binding Proteins
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Viana F
Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle 98195-7290, USA.
Hille B
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Article Info
Journal
The Journal of neuroscience : the official journal of the Society for Neuroscience
Abbr.
J Neurosci
ISSN
0270-6474
Published
1996-10-01
Pages
6000-11
Language
English
Region
United States
NLM ID
8102140
PMCID
PMC6579191
Subset
IM
Grants
NINDS NIH HHS · R01 NS008174 · United States
NINDS NIH HHS · R37 NS008174 · United States
NINDS NIH HHS · NS-08174 · United States
External Links
PubMed source PMC Full Text View journal details
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