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To study the importance of neural connections of the medial basal hypothalamus (MBH) in mediating the prolactin (Prl) response to stress, adult male rats were subjected to complete, anterior or posterior surgical disconnection of the MBH. Complete MBH disconnection blocked, while anterior MBH disconnection significantly attenuated the effects of leg restraint and ether exposure on Prl responses. Similar effects were noted with regard to Prl responses to morphine and chlorpromazine, two potent stimulators of Prl secretion, indicating that the deficits were not specific for stressful stimuli. None of the surgical procedures significantly compromised the response of growth hormone or corticosterone to morphine, ruling out the possibility of surgically-induced panhypopituitarism. Pituitary stores of Prl were reduced in the groups with complete and anterior MBH disconnection at autopsy at 18 weeks. These results indicate that anterolateral neural connections of the MBH are important for maintaining adequate levels of pituitary Prl or mediating the stimuli for Prl secretory responses. These effects may involve alterations in the regulation of Prl-inhibiting factor or Prl-stimulating factor.

These studies examined the effects of surgical interruption of anterolateral neural connections of the medial basal hypothalamus (MBH) on the subsequent ability of the perifused anterior pituitary (AP) to release prolactin (Prl). Anterolateral MBH cuts were made in adult male rats; sham-operated rats served as controls. An in vivo experiment performed at 5 weeks after the two types of surgery showed that the MBH cuts did not alter non-stress plasma Prl concentrations, but this surgery reduced (P less than 0.05) the Prl response to stress. At 4 months after surgery, the perifused APs from rats with MBH cuts released less (P less than 0.001) Prl under basal conditions and when perifused in series with blocks of preoptic-hypothalamic tissue than did APs from the sham-operated controls. The APs from the MBH-cut and control groups released similar amounts of Prl in response to an initial administration of 56 mM potassium (high K+). After 6 h of perifusion, the APs of the group with MBH cuts contained less (P less than 0.001) Prl than did those of the control group. These findings suggest that transecting anterolateral connections of the MBH causes a reduction in Prl synthesis and steady-state release without affecting the pool of Prl that is released in response to high K+.

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.

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.