Effects of microinjection of neurotensin (NT) into the medial preoptic area on luteinizing hormone (LH) release were examined in unanesthetized ovariectomized rats with or without estrogen priming. Microinjection of NT (100 ng) into the medial preoptic area of ovariectomized estrogen-primed rats significantly facilitated the circadian afternoon rise of LH secretion as compared to the hormone values in control animals microinjected with physiological saline. The timing of the afternoon LH rise was not altered by the peptide. In ovariectomized estrogen-unprimed rats, on the other hand, NT did not affect the existing pulsatile LH secretion nor induced an afternoon rise of the hormone secretion. These results show that NT can stimulate the preoptic LH release mechanism which undergoes the circadian clock under the influence of estrogen.

The present study was undertaken to determine the role of the hypothalamic periventricular (PV) region in the regulation of the secretory pattern of growth hormone (GH) in adult male rats. The PV regions were destroyed stereotaxi-cally by means of a modified Halasz’s knife which was lowered through the midline and rotated several times at the level of the region. In sham-operated controls, the knife was lowered to the same region but no rotation was performed. Serial blood samplings were performed at 10-min intervals for 10 h (10.00–20.00 h), via an intracardiac cannula, at 2, 4 and 6 weeks postoperatively. In 7 sham-operated controls, GH was secreted with a surge period of about 3.5 h, with peak levels of 120–170 ng/ml whole blood and basal levels of about 10 ng/ml whole blood. In 11 PV-lesioned animals, the basal levels of GH were unaltered but the surge period decreased to about 3.0 h and peak levels increased to about twice as high as in sham-operated controls. Somatostatin concentrations in the median eminence of PV-lesioned rats were significantly decreased to about 32% of that of sham-operated rats. The results suggest that, via somatostatin neurons, the PV region plays an inhibitory role in the regulation of periodicity and peak levels of GH secretory bursts.

The purpose of this study was to examine the effect of monosodium glutamate on the visual performance in rats. The Wistar strain of neonatal rats were injected subcutaneously with a solution of the glutamate at doses of 1 or 2 or 4 mg/gm body weight on days 2, 4, 6, 8 and 10 postnatally. Control rats received an injection of physiological saline. At 1, 2 and 3 months of age, the rats were tested for visual performance (brightness discrimination, pattern discrimination and visual acuity). As a result, the 4 mg/gm glutamate treatment was observed to impair brightness discrimination performance at 1 month of age as compared to the control animals. This impairment was also observed in animals at 2 and 3 months as compared, in addition, to the values in other doses of glutamate treatment. Pattern discrimination performance in every group of animals was at the same level at 1 month of age. However, at 2 months of age, the performance in the 2- and 4 mg/gm glutamate-treated groups was lower than those in the control group. This comparison was more pronounced at 3 months of age. Visual acuity performance results were quite the same as the pattern discrimination performance at all ages of animals. In conclusion, glutamate treatment was shown to cause dose-dependent deficit in visual performance and this may reflect impairment of visual organs and brain function.

To study the secretory pattern of growth hormone (GH) in the adult male rat in a continuous sleep state, the GH concentration was measured in blood sampled at 10-min intervals through an intracardiac cannula for 9–10 h long-term anesthesia with thiopental sodium. The cortical EEG was monitored to maintain stable EEG sleep throughout the sampling period. In 41 animals subjectd to anesthesia, 32 showed an apparent fluctuation in GH levels. The analysis of the time series of the GH concentration in blood by the power spectrum and least-squares method revealed that 27 animals had periodicities within the mean ± 2SD range obtained for the unanesthetized, but similarly sampled, animals from 2.40 to 3.85 h. The mean (± SE) of the periodicities for 27 animals was 3.01 ± 0.06 h, similar to that obtained for the unanesthetized animals, approximately 3.0 h. The results indicate that, although the GH-controlling mechanism in the rat is facilitated under sleep, it has a 3.0-hour period ultradian rhythm mechanism that is indepedent from that for sleep.

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