TY - JOUR
T1 - Effects of brain histamine depletion on stimulated prolactin release in rats
AU - Netti, C.
AU - Guidobono, F.
AU - Sibilia, V.
AU - Cazzamalli, E.
AU - Villa, I.
AU - Pecile, A.
PY - 1989/4
Y1 - 1989/4
N2 - We examined the effects of an irreversible inhibitor of brain histamine (HA) synthesis, α-fluoromethyl-histidine (α-FMH), on prolactin (PRL) release induced by an opiate agonist (morphine, M) or by a serotonergic agonist (MK212). α-FMH was administered intracerebroventricularly (i.c.v., 200 μg/rat) into freely moving rats with indwelling catheters in the carotid. M (6 mg/kg, intracarotid, i.a.) was administered simultaneously with or 3 h after α-FMH. MK212 (2.5 mg/kg, i.a.) was administered 3 h after α-FMH. Blood samples for assay for PRL were drawn at 0, 10, 20, 40 min after M or MK212 administration. α-FMH (3 h before) significantly reduced the PRL-releasing effect of M and MK212 but did not modify PRL release by M when administered simultaneously. The present results showing that the facilitatory actions of the opiate and serotonergic systems on PRL are impaired when brain HA synthesis is reduced, suggest that there is an HA-dependent step in opiate and serotonergic control of PRL.
AB - We examined the effects of an irreversible inhibitor of brain histamine (HA) synthesis, α-fluoromethyl-histidine (α-FMH), on prolactin (PRL) release induced by an opiate agonist (morphine, M) or by a serotonergic agonist (MK212). α-FMH was administered intracerebroventricularly (i.c.v., 200 μg/rat) into freely moving rats with indwelling catheters in the carotid. M (6 mg/kg, intracarotid, i.a.) was administered simultaneously with or 3 h after α-FMH. MK212 (2.5 mg/kg, i.a.) was administered 3 h after α-FMH. Blood samples for assay for PRL were drawn at 0, 10, 20, 40 min after M or MK212 administration. α-FMH (3 h before) significantly reduced the PRL-releasing effect of M and MK212 but did not modify PRL release by M when administered simultaneously. The present results showing that the facilitatory actions of the opiate and serotonergic systems on PRL are impaired when brain HA synthesis is reduced, suggest that there is an HA-dependent step in opiate and serotonergic control of PRL.
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U2 - 10.1007/BF02222215
DO - 10.1007/BF02222215
M3 - Article
C2 - 2750583
AN - SCOPUS:0024597083
VL - 27
SP - 117
EP - 119
JO - Inflammation Research
JF - Inflammation Research
SN - 1023-3830
IS - 1-2
ER -