PREOPTIC RATHER THAN MEDIOBASAL HYPOTHALAMIC AMINO-ACID NEUROTRANSMITTER RELEASE REGULATES GNRH SECRETION DURING THE ESTROGEN-INDUCED LH SURGE IN THE OVARIECTOMIZED RAT

Inhibitory and excitatory amino acid neurotransmitters have been sugge sted to participate in the feedback actions of estradiol (E(2)) on LH secretion. In the rat estrogen-receptive neurons have been demonstrate d in the preoptic/anterior hypothalamic area (POA) and mediobasal hypo thalamus/median eminence (MBH) and many of these neurons utilize gamma -aminobutyric acid (GABA) as neurotransmitter. The actions of excitato ry amino acids (EAA) differ in ovariectomized (ovx) and ovx E(2)-subst ituted rats indicating that EAAs also participate in the positive feed back action of E(2) on LH release. However, little information is avai lable as to whether in vivo these transmitters exert their effects in the POA, where most of the GnRH perikarya are located, or in the MBH, i.e. at the nerve terminals. Therefore we conducted push pull cannula perfusions to compare the release rates of GABA, aspartate (ASP) and g lutamate (GLU) in the MBH and POA. A subcutaneous implant of a silasti c tube containing E(2) resulted in LH surges in the afternoon of all t reated animals. Prior to and during this LH surge the MBH release rate s of neither GABA nor ASP nor GLU were significantly altered. In contr ast, a conspicuous drop in preoptic GABA release occurred prior to and during the time of estrogen-induced LH surges and this was accompanie d by enhanced preoptic secretion of ASP and GLU. In conclusion, we pre sent the first data about amino acid release in the MBH during the E(2 )-induced LH surge. Since only in the POA the LH surge is associated w ith changes in amino acid release, it appears that both inhibitory and excitatory amino acids act at the level of the GnRH cell bodies and/o r dendrites and not on GnRH nerve terminals to mediate the feedback me chanism of E(2) on LH release.