ABSTRACT
1. The present study was designed to examine the role of central epinephrine pathways in the control of stress-induced prolactin secretion in male adulto Wistar rats. 2. Intracerebroventricular adminsitration of two epinephrine synthesis inhibitors, SKF64139 (5 and 10 µg/rat) and LY 134046 (10 and 20 µg/rat), 6 h before the onset of immobilization stress blocked prolactin secretion in a dose-dependent manner. Prolactin values before stress were about 4.0 ng/ml and increased to almost 50 ng/ml in the control group. SKF 64139 injection in the higher dose (10 µg/rat) induced a complete blockade of the stress-induced prolactin release, whereas partial blockade was observed after the higher dose (20 µg/rat) of LY 134046. 3.Salbutamol pretreatment (10 µg/rat) completely restored stress-induced prolactin secretion in animals receiving a central injection of both epinephrine synthesis inhibitors under the same conditions as described above. 4. It is suggested that epinephrine pathways in the brain play an important role in the control of prolactin release occuring during immobilization stress
Subject(s)
Animals , Male , Rats , Benzazepines/pharmacology , Isoquinolines/pharmacology , Monoamine Oxidase Inhibitors/pharmacology , Prolactin/metabolism , Albuterol/pharmacology , Benzazepines/administration & dosage , Injections, Intraventricular , Isoquinolines/administration & dosage , Monoamine Oxidase Inhibitors/administration & dosage , Prolactin/blood , Rats, Inbred Strains , Stress, Physiological/physiopathologyABSTRACT
The present study was designed to examine the relationship between beta-adrenoceptors and the enhanced, sustained prolactin secretion induced by immobilization stress in rats. Chronic administration of desipramine (15 mg kg**-1 day**-1, intraperitoneally) for 7 days, a procedure that desensitizes central beta-adrenoceptors, partially inhibits stress-induced prolactin release. Intracerebroventricular adminsitration of the beta-2 adrenoceptor agonist salbutamol (1 microng/rat) to rats pretreated with desipramine for 7 days, 15 min before immobilization, significantly relieved the inhibition by desipramine 5 and 10 min after the initiation of stress but the effect was not demonstrable after 20 and 40 min. We conclude that beta-2 adrenoceptors play a role in the control prolactin release in response to stress