Long term elevations in plasma thyrotropin, but not growth hormone, concentrations associated with lesion-induced depletion of median eminence somatostatin.

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.