α-Fluoromethylhistidine influences somatostatin content, binding and inhibition of adenylyl cyclase activity in the rat frontoparietal cortex
Identifiers
Permanent link (URI): http://hdl.handle.net/10017/2319DOI: 10.1016/0167-0115(95)00080-U
ISSN: 0167-0115
Publisher
Elsevier
Date
1995Funders
This work was supported by a grant from
the Direcci6n General de Investigación Cientifica y Técnica of Spain.
Bibliographic citation
Regulatory Peptides, 1995, n. 59, p. 111-120
Keywords
α-Fluoromethylhistidine
Somatostatin receptor
Adenylyl cyclase
Rat
Frontoparietal cortex
Document type
info:eu-repo/semantics/article
Version
info:eu-repo/semantics/publishedVersion
Publisher's version
http://dx.doi.org/10.1016/0167-0115(95)00080-URights
© Elsevier Science, 1995
Access rights
info:eu-repo/semantics/openAccess
Abstract
Slow-wave sleep, wakefulness, locomotor activity and learning and memory are regulated in similar ways by somatostatin
(SS) and histamine. To clarify the possible role of endogenous histamine on the somatostatinergic system of the rat
frontoparietal cortex, we studied the effect of 50 /xg of a-fluoromethylhistidine (a-FMH), a specific inhibitor of histidine
decarboxylase, administered intracerebroventricularly (i.c.v.) at 1, 4 and 6 h, on somatostatin-like immunoreactivity (SSLI)
content and the SS receptor/effector system. The histamine content in the frontoparietal cortex decreased to about 67, 60
and 72% of control values at 1, 4 and 6 h after ot-FMH administration, respectively. At 6 h after a-FMH injection, there was
an increase in SSLI content and a decrease in the number of SS receptors, with no change in the apparent affinity. No
significant differences were seen for the basal and forskolin (FK)-stimulated adenylyl cyclase (AC) activities in the
frontoparietal cortex of a-FMH-treated rats when compared to the control group at all times studied. At 6 h after a-FMH
administration, however, the capacity of SS to inhibit basal and FK-stimulated AC activity in the frontoparietal cortex was
significantly lower than in the control group. The ability of the stable GTP analogue 5'-guanylylimidodiphosphate
(Gpp(NH)p) to inhibit FK-stimulated AC activity in frontoparietal cortex membranes was the same in the a-FMH-treated (6
h) and control animals. Therefore, the decreased SS-mediated inhibition of AC activity observed in the t~-FMI-I-treated rats
is not due to an alteration at the guanine nucleotide-binding inhibitory protein (G i) level but rather may be due to the
decrease in the number of SS receptors. Taken together, these data suggest that a-FMH influences the sensitivity to SS in
the rat frontoparietal cortex.
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