Growth Hormone Secretion after Hypothalamic Periventricular Lesions in the Rat

Abstract

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.

Effects of Cysteamine Pretreatment and Hypothalamic Periventricular Nucleus Lesion on the Cold‐Stimulated Thyrotropin Responses to Intracerebroventricular 5‐Hydroxytryptamine in Male Rats

“…Reduction by 19% to 28% only could be detected between lesioned and corresponding control groups. However, the present lesions were apparently less extensive than those in studies describing marked reductions in hypothalamic and/or median eminence SRIF content (27)(28)(29). Moreover, a 33% reduction in hypothalamus SRIF and elevation of basal TSH levels were produced by PeVN lesions of similar size (8).…”

Centrally Applied Somatostatin Inhibits the Estrogen-Induced Luteinizing Hormone Surge via Hypothalamic Gonadotropin-Releasing Hormone Cell Activation in Female Rats1

“…Physiological regulation of GH release involves, besides direct projections of periventricular SOM cells to the ME [34][35][36][37][38], projections of hypothalamic SOM cells to the GHRH cells in the ARC. Via these projections, SOM can decrease GHRH release from the ME, leading to a decrease in GH release from the pituitary [39][40][41][42][43][44].…”

Somatostatin in the rat periventricular nucleus: sex differences and effect of gonadal steroids

“…Release of GH from the pituitary is mainly regulated by the interplay between the stimulating effects of GH-releasing hormone (GHRH), synthesized in cells of the arcuate nucleus of the hypothalamus (ARC), and the inhibiting effects of somatostatin (SOM), synthesized in cells of the periventricular nucleus of the hypothalamus (PeVN) (Critchlow et al 1981 ; Gillies 1997 ; Katakami et al 1988 ; Praputpittaya et al 1987 ; Tannenbaum and Ling 1984 ; Tannenbaum et al 1990 ; Terry and Martin 1981 ; Urman et al 1985 ; Zeitler et al 1991 ). Also ghrelin is found to stimulate GH release and ghrelin-producing cells in the hypothalamus may stimulate GHRH cells in the ARC (Korbonits and Grossman 2004 ).…”