ARACHIDONYL ETHANOLAMIDE (ANANDAMIDE) ACTIVATES THE PARVOCELLULAR PART OF HYPOTHALAMIC PARAVENTRICULAR NUCLEUS

Arachidonyl ethanolamide, anandamide (ANA) was administered to male ra ts via a single i.p. injection at a dose of 0.02mg/kg. In an parallel experiment ANA injection was preceded by the injection of SR 141716 (1 .0mg/kg), a selective and potent cannabinoid receptor antagonist. We o bserved using FOS protein immunocytochemistry that the parvocellular p art of hypothalamic paraventricular nucleus (PVN) was activated as soo n as 45 min. after ANA injection, i.e. the PVN showed an increased FOS immunoreactivity (FOSir). The peak level of FOSir was observed 90 min . after treatment. Meanwhile serum ACTH and corticosterone levels, as measured by radioimmunoassay, also significantly increased. 180 min. f ollowing drug injection both FOSir and serum hormone levels had return ed to normal. SR 141716 did not antagonize these effects of ANA. We po stulate that the locus of action of ANA the activation of the hypothal amo-pituitary-adrenal (HPA) axis is the parvocellular part of PVN. Thi s activation may occur via a possible central cannabinoid receptor for which SR 141716 is not an effective antagonist. The rapid central res ponse and activation of the HPA axis further support the view that ANA may be a central neurotransmitter or neuromodulator. (C) 1997 Academi c Press.