Stimulation of β-adrenoceptors inhibits lordosis behavior in the female rat

Scott D. Mendelson, Boris B. Gorzalka
In: Pharmacology Biochemistry and Behavior · 1988 · vol. 29(4) , pp. 717–723 · doi:10.1016/0091-3057(88)90193-1 · PMID:2842808 · W1982957557
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Central beta-adrenoceptor activity inhibits lordosis behavior in female rats, as evidenced by metoprolol reversing beta-agonist effects and propranolol acting via membrane stabilization rather than beta-blockade.

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Abstract

Existing reports on the effects of beta-adrenergic antagonists on lordosis behavior appear contradictory, with (+/-) propranolol being reported to inhibit, and (+/-) pindolol to facilitate this behavior. In the present study, both the (-) and (+) optical isomers of propranolol were effective in inhibiting lordosis behavior in ovariectomized rats treated with estrogen and progesterone. This finding suggests that the lordosis-inhibiting effects of propranolol were not due to blockade of beta-adrenergic activity, but rather to the membrane stabilizing effect of the drug. An observed inhibition of lordosis following the peripheral administration of the local anesthetic lidocaine is consistent with this possibility. (+/-) Propranolol had no effect 30 min after peripheral administration in estrogen-treated, ovariectomized rats with low baseline levels of lordosis behavior. (+/-) and (-) pindolol, but not (+) pindolol also inhibited lordosis 30 min after administration. However, in addition to its antagonist effects, pindolol acts as a partial agonist in some tissues. Centrally active doses of the pure beta-antagonist (+/-) metoprolol produced no inhibitory effects. Indeed, metoprolol reversed the inhibitory effect of the beta-agonist (+/-) salbutamol. This suggests that the lordosis-inhibiting effects of pindolol were due to its partial agonist effects. Taken together, the present data indicate that activity at central beta-adrenoceptors inhibits rather than facilitates lordosis behavior.

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