Rates of Release of GABA and Catecholamines in the Mediobasal Hypothalamus of Ovariectomized and Ovariectomized Estrogen-Treated Rats: Correlation with Blood Prolactin Levels

Abstract

Push-pull cannulae were implanted into the mediobasal hypothalamus of ovariectomized (ovx) rats. After recovery animals were treated with estradiolbenzoate (E₂B) or oil and they were perfused 3 days later. Only the E₂B-treated animals which exhibited prolactin surges in the afternoon without concomitant LH surges were used in this study. In ovx animals hypothalamic GABA release, measured in 5-min intervals, was pulsatile, with pulses occurring every 37 min. This pattern was profoundly affected by E₂B treatment: the pulse frequency was significantly reduced to 1 pulse every 117 min in steroid-treated rats. No differences in overall mean GABA release rates and pulse amplitudes were observed in ovx vs. E₂B-treated rats. Our earlier demonstration of the existence of a large number of estrogen-receptive, GABAergic neurons in the MBH of rats is suggestive that these neurons change their secretory pattern in response to estrogen treatment. Estrogen-induced prolactin surges were accompanied by increased hypothalamic NE release. Concomitant changes in DA or E release rates were not demonstrable since catecholamine concentrations were too low to be reliable. However, the daily overall release rates of these two catecholamines were lower in E₂B-treated rats compared to ovx animals. It is concluded that the positive feedback action of estradiol on prolactin release involves a stimulatory noradrenergic mechanism and may also involve estrogen-receptive, GABAergic neurons. The alterations of pulse frequency of these GABAergic neurons appear to define the particular signal transmitted to the endocrine target cells, whereas the total amount of GABA released over a longer period of time does not seem to be of importance for the estrogen-dependent function modulated by this GABAergic system. Whether this estrogen-dependent function is regulatory to prolactin and/or gonadotropin secretion remains to be determined.

Effects of 8-prenylnaringenin on the hypothalamo-pituitary-uterine axis in rats after 3-month treatment

“…After ovx or in postmenopausal women, the lack of estrogen causes changed release of these neurotransmitters (Jarry et al 1986(Jarry et al , 1990 and thereby overactivity of the pulse generator. The neurotransmitters involved in generating GnRH pulses spill over into neighboring neurons that regulate temperature and heart beat rate (Tataryn et al 1979, Gambone et al 1984, and this induces hot flushes and the associated tachycardiac attacks.…”

Ovarian Steroid Regulation of Glutamic Acid Decarboxylase Gene Expression in Individual Hypothalamic Nuclei

“…the zona incerta (ZI) (14)(15)(16)(17). The site of it's stimulatory effect is not really known, although some data indicate that it may be in the medial basdl hypothalamus (12,18,19). Within the hypothalaIlIus GABA stimulates prolactin release, but it is inhibitory at the level of the pituitary (12)(13)(14)20).…”

Regional Specificity of Gamma-Aminobutyric Acid Receptor Regulation by Estradiol

“…In addi tion. the concentration of GABA varies throughout the estrous cycle [2,21,32], and GABA release in the medial preoptic area and medial basal hypothalamus is influenced by endocrine state [14,25,41].Relatively little is known about the cellular mechanisms underlying the interaction of estradiol and GABA neuronal systems. In view of the findings that certain GAD-immunoreactive neurons contain estradiol-binding sites [20, 45], we investigated whether estradiol is a regulator of GAD activ ity in estradiol-sensitive brain areas.…”