A. Chiba et al., DIFFERENTIAL INHIBITION OF NMDA-INDUCED AND NALOXONE-INDUCED LH-RELEASE BY NMDA RECEPTOR ANTAGONIST AND CRH IN OVARIECTOMIZED ESTROGEN-PRIMED RATS, Neuroendocrinology, 65(2), 1997, pp. 141-146
A possible functional relationship between endogenous opioid peptides
(EOPs), corticotropin-releasing hormone (CRH) and excitatory amino aci
ds (EAAs) in the control of LH secretion was investigated in ovariecto
mized estrogen-primed rats. An intraventricular (icy) injection of an
EAA agonist, N-methyl-D-aspartate (NMDA), or an EOP antagonist, naloxo
ne, produced an abrupt increase in the serum LH level. While icy pretr
eatment of the animals with 2-amino-5-phosphonovaleric acid, a specifi
c NMDA receptor antagonist, did not affect by itself basal LH levels,
it significantly suppressed the NMDA-induced and also the naloxone-ind
uced LH release. An icy injection of CRH also interfered with the nalo
xone-induced LH release. However, the NMDA-induced LH release was not
affected by an icy injection of CRH or of beta-endorphin. These result
s suggest that the sites of EOP and CRH inhibition may be located upst
ream of the site of NMDA stimulation on the GnRH neuronal pathway, and
that CRH can inhibit LH secretion without mediation by EOP neurons.