Treatment with the
dopamine beta-hydroxylase (DBH) inhibitor
U-14,624 (50, 100, or 150 mg/kg) blocked the induction of
lordosis behavior be
estradiol benzoate (EB) and
progesterone (P) in ovariectomized guinea pigs.
After treatment with
U-14,624 (100 mg/kg),
norepinephrine (NE) content of medial basal hypothalamus, preoptic area and cortex was reduced (by 55%) and
dopamine (DA) content of medial basal hypothalamus was increased (by 155%) during the period when females treated with EB and P normally display
lordosis. Treatment with the NE receptor stimulator
clonidine (1.0 mg/kg) restored
lordosis behavior in females treated with EB, P, and
U-14,624 (100 mg/kg), but the putative DA and
serotonin (5-HT) receptor blockers
pimozide (1.0 mg/kg) and
methysergide (20.0 mg/kg) were ineffective in this respect. Thus, inhibition of
lordosis after treatment with
U-14,624 appeared to be attributable primarily to a reduction in NE neurotransmission, rather than to increase in DA or
5-HT activity. Because
clonidine induced
lordosis in females treated with EB, P, and
U-14,624, it seemed unlikely that the facilitatory effects of
clonidine on
lordosis were mediated by activation of presynaptic
alpha-adrenergic receptors (i.e. inhibitory NE
autoreceptors) rather than by postsynaptic alpha-receptors. In addition, pretreatment with the postsynaptic alpha-
adrenergic antagonist phenoxybenzamine (20.0 mg/kg) blocked the facilitation of
lordosis by
clonidine (1.0 mg/kg) in females primed with EB alone and with EB plus P. Thus, the facilitatory effects of
clonidine on
lordosis appear to be mediated by activation of postsynaptic alpha-
adrenergic (i.e. NE) receptors. The results of this study provide further evidence that NE neurotransmission facilitates the expression of female sexual behavior in guinea pigs.