title: The effect of anandamide on prolactin secretion is modulated by estrogen.
abstract: Recent research has revealed that endogenous cannabinoid receptors (CB1 and CB2) react with the active ingredient of marijuana, Delta(9)-tetrahydrocannabinol. Two endogenous ligands activate these receptors. The principal one, anandamide (AEA), activates CB1. AEA and CB1 are localized to various neurons within the brain. Because Delta(9)-tetrahydrocannabinol inhibited prolactin (Prl) secretion following its intraventricular injection into male rats, we hypothesized that AEA would have a similar effect. Estrogen modifies many hormonal responses and is known to increase Prl secretion. Therefore, we hypothesized that responses to intraventricular AEA would change depending on the gonadal steroid environment. Consequently, we evaluated the effects of lateral cerebral ventricular microinjection of AEA (20 ng) into male, ovariectomized (OVX), and estrogen-primed (OVX-E) rats. AEA decreased plasma Prl in male rats, had little effect in OVX females, and increased Prl in OVX-E rats. The results were at least partially mediated by changes in dopaminergic turnover, altering the inhibitory dopaminergic control of Prl release by the anterior pituitary gland. Thus, dopamine turnover was increased in the male rats and decreased significantly in OVX and in OVX-E rats. The changes in Prl may be caused not only by altered dopamine input to the anterior pituitary gland but also by effects of AEA on other transmitters known to alter Prl release. Importantly, in OVX-E rats, the elevated Prl release and the response to AEA were blocked by the AEA antagonist, indicating that AEA is a synaptic transmitter released from neurons that decrease inhibitory control of Prl release.
authors.affiliation: Centro de Estudios Farmacológicos y Botánicos, Consejo Nacional de Investigaciones Cientificas y Técnicas, Serrano 669, 1414 Buenos Aires, Argentina.
authors.forename: Camila
authors.initials: C
authors.lastname: Scorticati
authors.forename: Claudia
authors.initials: C
authors.lastname: Mohn
authors.forename: Andrea
authors.initials: A
authors.lastname: De Laurentiis
authors.forename: Paula
authors.initials: P
authors.lastname: Vissio
authors.forename: Javier
authors.initials: J
authors.lastname: Fernández Solari
authors.forename: Adriana
authors.initials: A
authors.lastname: Seilicovich
authors.forename: Samuel M
authors.initials: SM
authors.lastname: McCann
authors.forename: Valeria
authors.initials: V
authors.lastname: Rettori
mesh_terms: D015102:3,4-Dihydroxyphenylacetic Acid / Q000378:metabolism; D000818:Animals; D001095:Arachidonic Acids / Q000494:pharmacology*; D004298:Dopamine / Q000378:metabolism; D063388:Endocannabinoids; D004967:Estrogens / Q000502:physiology*; D005260:Female; D007031:Hypothalamus / Q000166:cytology / Q000378:metabolism; D008297:Male; D009474:Neurons / Q000378:metabolism; D010052:Ovariectomy; D053284:Polyunsaturated Alkamides; D011388:Prolactin / Q000097:blood / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D043885:Receptor, Cannabinoid, CB2; D043882:Receptors, Cannabinoid; D011955:Receptors, Drug / Q000378:metabolism
chemical_list: D001095:Arachidonic Acids; C469526:Cnr2 protein, rat; D063388:Endocannabinoids; D004967:Estrogens; D053284:Polyunsaturated Alkamides; D043885:Receptor, Cannabinoid, CB2; D043882:Receptors, Cannabinoid; D011955:Receptors, Drug; D015102:3,4-Dihydroxyphenylacetic Acid; D011388:Prolactin; C078814:anandamide; D004298:Dopamine