No abstract

The effects of increasing brain GABA levels by administration of aminooxyacetic acid (AOAA), a GABA-transaminase inhibitor, on tonic and induced LH release were evaluated in ovariectomized rats.Pulsatile LH release was clearly inhibited by AOAA. Mean plasma LH levels fell, the frequently of pulses decreased, and the intervals between pulses increased. An absence of LH pulses was seen in some animals. Administration of the GABA antagonist, bicuculline, prevented these modifications. In addition, it enhanced mean plasma LH levels. AOAA blunted the rise of plasma LH levels produced by either oestradiol or progesterone in oestradiol-primed ovariectomized rats. In contrast, the AOAA treatment apparently facilitated the inhibitory feedback of oestradiol on LH release. The acute release of LH produced by LRH injection was not altered by AOAA.The results support the view that brain GABA exerts an inhibitory action on LH release in the rat.

No abstract

The effects of 3rd ventricle injection of metiamide, an H₂-histamine receptor antagonist and pyrilamine, an H₁-histamine receptor antagonist, on the increase of plasma prolactin induced by two doses of histamine in normal male rats were studied. Metiamide did prevent the stimulating action of histamine whereas pyrilamine was not effective. Histamine-induced prolactin release was also blocked by low doses of the 2 antihistamines given in combination. Metiamide per se has no effect but high doses of pyrilamine increased plasma prolactin levels and augmented the hormone response to histamine. The results suggest mediation of H₂-receptors in the facilitatory action of histamine on prolactin release.

The possible role of histamine (HA) locally applied into the hippocampus on memory mechanisms of the rats was studied. The acquisition of a one-way active avoidance response to an ultrasonic 40 kHz sinus-wave tone anticipating an electric shock was used as experimental model. Learning sessions consisted in placing animals into a two compartment cage were they learnt to escape to the safe compartment after an ultrasonic tone anticipating an electric feet shock. After acquiring the conditioned avoidance response, animals were implanted with microinjection cannulae and injected with 1 microliter of saline, or increasing doses of histamine (9, 22.5, 45, and 90 nmol) into the hippocampus. In the experimental sessions, 4 trials before (PRE) and 4 trials afterward treatment (POST), the percentage of conditioned avoidance responses (% CAR) and the latency time to escape (LT) were measured. Results showed that HA increased significantly the LT and this effect was grossly dose-dependent. % CAR was also affected and the score was significantly inhibited by the imidazolamine administration. Results suggest that HA may be involved in memory retrieval processes in the hippocampus.