α-Fluoromethylhistidine influences somatostatin content, binding and inhibition of adenylyl cyclase activity in the rat frontoparietal cortex
Identificadores
Enlace permanente (URI): http://hdl.handle.net/10017/2319DOI: 10.1016/0167-0115(95)00080-U
ISSN: 0167-0115
Editor
Elsevier
Fecha de publicación
1995Patrocinadores
This work was supported by a grant from
the Direcci6n General de Investigación Cientifica y Técnica of Spain.
Cita bibliográfica
Regulatory Peptides, 1995, n. 59, p. 111-120
Palabras clave
α-Fluoromethylhistidine
Somatostatin receptor
Adenylyl cyclase
Rat
Frontoparietal cortex
Tipo de documento
info:eu-repo/semantics/article
Versión
info:eu-repo/semantics/publishedVersion
Versión del editor
http://dx.doi.org/10.1016/0167-0115(95)00080-UDerechos
© Elsevier Science, 1995
Derechos de acceso
info:eu-repo/semantics/openAccess
Resumen
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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