Alpha and beta noradrenergic mediation of NMDA glutamatergic effects on lordosis behaviour and plasmatic LH concentrations in the primed female rat

Abstract

In previous studies we have found that blockade of NMDA (N-Methyl-D-Aspartic-Acid)-type glutamatergic receptor with intracerebroventricular (ICV) selective drugs induces an inhibition of lordosis in ovariectomized (OVX) estrogen primed rats receiving progesterone or luteinizing hormone releasing hormone (LHRH). By the opposite way, stimulation with NMDA in OVX estrogen primed rats induced a significant increase of lordosis. In the present study the action of an alpha1-noradrenergic antagonist, HEAT (BE 2254/2-beta-4-Hydroxyphenyl-Ethyl-Aminomethyl-1-Tetralone), and Metoprolol, a beta-noradrenergic antagonist, were studied injecting them ICV previously to NMDA administration in treated OVX estrogen primed rats. In experiment 1, the enhancing effect on lordosis induced by NMDA at high dose (1 microg) was abolished by HEAT administration (P < 0.001 for 3 and 6 microg), and the LH plasma levels were decreased only with the higher dose (P < 0.05), suggesting that behavioral effects are quite more sensitive to the alpha-blockade than hormonal effects. In experiment 2, enhancing effects on lordosis behavior were not observed with neither the NMDA at low dose (0.5 microg) nor the metoprolol alone (5.71 microg), but a synergism was observed when both were simultaneously administered (P < 0.001). The LH plasma levels were increased by Metoprolol alone (P < 0.05), and powered by the combination with NMDA at low dose (P < 0.01 vs. SAL and NMDA alone); no differences were observed with Metoprolol. LH increase was observed with Metoprolol even without behavioural modifications. These findings strongly suggest that facilitatory and inhibitory effects of NMDA in this model are mediated by alpha- and beta-adrenergic transmission in both, behavioral and hormonal effects.

Identification of neural cells activated by mating stimulus in the periaqueductal gray in female rats

“…The results of the study show that (1) a mating stimulus activates neurons in the lateral PAG, (2) 50% of lateral PAG neurons activated by the mating stimulus project to the RF, (3) 56% of these neurons are glutamatergic, and (4) there are glutamatergic neurons projecting to the RF. The PAG and MRF are essential sites for lordosis behavior in female rats (Pfaff, 1980 ) and there is a clear relationship between glutamate and induction of lordosis (Gargiulo et al, 1992 ; Gargiulo and Donoso, 1995 ; Landa et al, 2009 ). Our findings provide further evidence that glutamatergic neurons in the lateral PAG project to the MRF and are involved in lordosis in female rats.…”

“…Contradictory effects of glutamate on lordosis have been found. Icv injection of NMDA accelerated lordosis in low estrogen-primed OVX rats that rarely showed lordosis (Gargiulo and Donoso, 1995 ; Landa et al, 2009 ); whereas local injection of NMDA into the VMH inhibited lordosis in estrogen- and progesterone-treated OVX rats that showed frequent lordosis behavior (Georgescu and Pfaus, 2006 ). In similar rats, subcutaneous injection of MK-801, a NMDA antagonist, inhibited lordosis (Fleischmann et al, 1991 ), but injection into the ventral tegmental area increased lordosis (Petralia et al, 2007 ).…”

Anxiolytic-like effects of Atenolol injected into the nucleus accumbens septi in rats after restrain stress in the elevated plus maze test

“…As an alternative strategy, antagonism of secondary neurons activated by glutamate could be attempted. We have previously shown that noradrenergic blockade antagonizes some effects of glutamatergic stimulation on behavioural and endocrine parameters (Landa et al, 2006;Landa et al, 2009). It allows thinking that noradrenergic antagonism may mimic the anxiolytic effect of glutamate antagonists.…”