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Evidence suggests that somatostatin (SRIF) inhibits nonstress GH and TSH secretion and suppresses GH secretion in response to stress. The aims of this study were to determine whether placement of lesions in the hypothalamic periventricular (PV) nucleus, the location of SRIF neurons which seem to be responsible for most median eminence SRIF, causes elevation of nonstress plasma GH and TSH levels and blocks stress-induced suppression of these hormones. Electrolytic lesions were placed in female rats, and blood was obtained for assessing nonstress and stress plasma levels of GH and TSH at several intervals after surgery until autopsy, 56 weeks after surgery, when median eminences were collected. PV lesions produced only transient elevation of nonstress plasma GH levels and failed to block the suppression of GH secretion by stress. In contrast, PV lesions caused long term elevation of nonstress plasma TSH levels and blockade of stress-induced suppression of TSH secretion. The content and concentration of SRIF in the median eminence were reduced 90% in the PV-lesioned group. These data demonstrate that PV lesions, which result in marked depletion of median eminence SRIF, can cause long term elevations of plasma TSH levels and disruption of the TSH response to stress without producing alterations in GH secretion. Thus, the hypothalamic PV nucleus, its SRIF neurons and most median eminence SRIF are not essential for maintaining normal GH secretion, but seem to be involved in the regulation of TSH release. It appears that different brain structures are involved in inhibiting GH and TSH secretion.

These experiments were designed to determine whether it is possible using in vitro perifusion to identify a sex difference in anterior pituitary (AP) release of growth hormone (GH) and, if so, to determine whether this difference is correlated with a sex difference in hypothalamic release or content of somatostatin (SRIF). Age-matched rats of both sexes were decapitated at approximately 09.00 h, and blood was collected for determination of non-stress plasma concentrations of GH. Each pituitary was rapidly removed and prepared for perifusion of the AP, and each preoptic-medial basal hypothalamus (PO-MBH) was removed and placed in a separate perifusion chamber. The effluent fractions from perifused APs were assayed for GH and prolactin (Prl), and those from PO-MBH blocks were assayed for SRIF. Non-stress plasma GH concentrations were similar in males and females. During perifusion, baseline GH release was higher (P less than 0.001) from male than from female APs. Release of GH from the APs of both sexes was similarly inhibited (P less than 0.001) by a 1-h administration of SRIF (10(-7) M), and high K+ (50 mM) caused larger (P less than 0.05) GH responses from male than from female APs. In contrast, baseline Prl release was higher (P less than 0.01) from female than from male glands, and Prl release was not affected by SRIF. Male and female PO-MBH tissues showed similar baseline release of SRIF and similar responses to high K+. After perifusion, GH content and concentration were higher in APs from males than from females, but SRIF content in the perifused male and female PO-MBH tissues was similar.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypothalamic periventricular (PV) nucleus lesions reduce median eminence (ME) SRIF content by approximately equal to 80% without affecting non-stress plasma growth hormone (GH) levels or the GH response to stress. Our aim was to study the effects of PV lesions on SRIF released during perifusion of preoptic-anterior hypothalamic (PO-AH) tissue. Female rats received anterior or posterior PV lesions; sham-lesioned and intact rats served as controls. Non-stress and stress plasma GH levels were similar in all groups at 2, 4 and 16 weeks after surgery. At 18 weeks after surgery, the perifused PO-AHs of the PV- and sham-lesioned rats released similar amounts of SRIF, and these were higher (P less than 0.001) than amounts released from PO-AHs of intact rats. The PO-AHs from all groups showed similar increases in SRIF release after 56 mM K+. Two rats were chosen randomly from each group to assess ME SRIF content; PV lesions caused almost 80% depletion of SRIF, sham lesions did not. These results confirm that most SRIF neurons in the PV nucleus and 80% of ME SRIF content are not essential for the control of GH levels under non-stress conditions or for the GH response to stress and indicate that PV or sham lesions in the rostral forebrain enhance in vitro SRIF release, perhaps from neurons outside the PV nucleus.

Two experiments were performed to study the role of somatostatin (SRIF) neurons of the preoptic-anterior hypothalamic area (PO-AHA) in regulating growth hormone (GH) and thyrotropin (TSH) secretion in rats. Small lesions were placed in the periventricular (PV) zone and blood was collected at 24 h and 15 days after surgery. Blood samples were obtained at 3 min and at 15 min after ether exposure for assessing non-stress levels, respectively, of plasma GH and TSH. Non-stress blood samples were also collected at decapitation at 4 weeks. The brains from the first experiment were dissected and processed for measuring SRIF content in several regions. At 24 h and 15 days, non-stress GH and TSH levels were significantly elevated in rats with PV lesions. Stress-induced decrements in GH levels persisted in all groups. Although non-stress plasma GH and TSH levels returned to normal in lesioned rats at 4 weeks, SRIF content was decreased 83% in the median eminence and 33% in the hypothalamus. These results show that discrete lesions in the PV zone of the PO-AHA cause transient elevations in non-stress secretion of GH and TSH and that normal levels of such secretion can be reinstated despite reductions of SRIF in the median eminence and hypothalamus.

The purpose of this study was to determine the effects of destroying somatostatin (SRIF) neurons of the periventricular (PV) nucleus of the hypothalamus on the pulsatile pattern of growth hormone (GH) secretion in female rats. At 6-10 days after placement of PV lesions, blood samples collected every 15 min for 3-4 h showed an elevation in baseline GH levels and an increase in the amplitude of GH secretory peaks; the frequency of pulses was not affected. These changes were associated with an increase in mean integrated plasma GH levels. The alterations appeared transient because nonstress plasma GH levels were normal in two blood samples collected between 6 and 17 weeks after lesion placement and at autopsy at 17 weeks. Stress-induced suppression of GH secretion was also unaffected by the PV lesions. These lesions severely compromised the SRIF system that projects to the median eminence because the median eminence content of SRIF was approximately 85% depleted in the lesioned group. These results confirm that the hypothalamic PV nucleus is essential for maintaining most of the SRIF in the median eminence and demonstrate that damage to the PV nucleus causes transient alterations in the pulsatile pattern of GH secretion. However, the PV nucleus does not appear to play a major role in driving pulsatile GH secretion.

These experiments were designed to determine whether brain lesions which elevate nonstress plasma levels of GH and disrupt stress-induced suppression of GH secretion in female rats affect the median eminence content of somatostatin. Some rats received lesions in the medial or lateral preoptic-anterior hypothalamic area (PO-AHA), while others received anterior hypothalamic cuts. Sham-operated and intact rats served as controls. GH and somatostatin were measured by RIA. Medial but not lateral PO-AHA lesions caused elevated nonstress plasma GH levels at 2, 14, 17, and 23 weeks after surgery, but normal levels were obtained at autopsy at 27 weeks. These lesions compromised GH responses to stress at 14 and 23 weeks. Rats with anterior hypothalamic cuts showed elevated nonstress GH levels at 17, 23, and 27 weeks after surgery and loss of the GH response to stress at 14 and 23 weeks. Median eminence content of somatostatin was reduced approximately 80% in rats with medial PO-AHA lesions or anterior cuts. Whereas medial PO-AHA lesions were associated with normal body length and weight and evidence of estrogen secretion, anterior hypothalamic cuts produced increased linear growth and body weight and signs of functional castration. These results suggest that the effects of lesions which cause prolonged elevation of nonstress GH levels and disruption of the GH stress response are due to interference with somatostatin neurons located in the medial PO-AHA. Somatostatin content of the median eminence seems to depend largely on connections originating in or traversing the medial PO-AHA.

To determine whether residual inhibitory control of growth hormone (GH) secretion in rats with lesions of the periventricular nucleus (PVN) and depleted median eminence content of somatostatin (SRIF) is due to SRIF, PVN-lesioned rats were treated with SRIF antiserum. Such treatment, in contrast to normal sheep serum, caused increased (P less than 0.0001) plasma GH in lesioned and control groups. These results indicate that biologically important amounts of SRIF are available in the PVN-lesioned rat.