TY - JOUR
T1 - Involvement of brain histamine in basal and stress-induced release of prolactin in the rat
AU - Netti, C.
AU - Guidobono, F.
AU - Sibilia, V.
AU - Villa, I.
AU - Cazzamalli, E.
AU - Pecile, A.
PY - 1987/4
Y1 - 1987/4
N2 - We investigated whether inhibition of brain histamine (HA) synthesis by α-fluoromethylhistidine (α-FMH) can influence basal or stimulated prolactin (PRL) release in male rats. α-FMH was administered either into the carotid (i.a., 20 and 100 mg/kg) or intracerebroventriculary (i.c.v., 200 μg/rat) into freely moving rats with indwelling catheters. Plasma PRL levels were measured 90, 120, 180 min later. Both i.a. and i.c.v. administration of α-FMH significantly inhibited basal PRL secretion at 120 and 180 min. When PRL secretion was stimulated by exposing rats to restraint stress, α-FMH administered 3 h before the stress (20 and 100 mg/kg, i.a.; 200 μg/rat, i.c.v.) was able to prevent the PRL surges at 10 and 20 min after stress. These results suggest that endogenous brain HA has a facilitatory role in the control of PRL secretion in rats.
AB - We investigated whether inhibition of brain histamine (HA) synthesis by α-fluoromethylhistidine (α-FMH) can influence basal or stimulated prolactin (PRL) release in male rats. α-FMH was administered either into the carotid (i.a., 20 and 100 mg/kg) or intracerebroventriculary (i.c.v., 200 μg/rat) into freely moving rats with indwelling catheters. Plasma PRL levels were measured 90, 120, 180 min later. Both i.a. and i.c.v. administration of α-FMH significantly inhibited basal PRL secretion at 120 and 180 min. When PRL secretion was stimulated by exposing rats to restraint stress, α-FMH administered 3 h before the stress (20 and 100 mg/kg, i.a.; 200 μg/rat, i.c.v.) was able to prevent the PRL surges at 10 and 20 min after stress. These results suggest that endogenous brain HA has a facilitatory role in the control of PRL secretion in rats.
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U2 - 10.1007/BF02074679
DO - 10.1007/BF02074679
M3 - Article
C2 - 3604804
AN - SCOPUS:0023216016
VL - 20
SP - 236
EP - 238
JO - Inflammation Research
JF - Inflammation Research
SN - 1023-3830
IS - 3-4
ER -