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Evidence and possible mechanism for the permanent decline in tuberoinfundibular dopaminergic neuronal activity after chronic estradiol administration in Fischer 233 rats

Thesis/Dissertation ·
OSTI ID:6717663
The objective of these studies was to determine if the decline in tuberoinfundibular dopaminergic (TIDA) neuronal function observed during chronic estradiol-17-..beta.. (E/sub 2/) administration persisted after E/sub 2/ was removed. Ovariectomized (OVX) Fischer 344 rats were implanted with an E/sub 2/-containing Silastic capsule for 4 weeks. Anterior pituitary (AP) weight and serum prolactin was greatly increased at the end of the E/sub 2/ treatment, that persisted 4 and 26 weeks after E/sub 2/ was withdrawn. Ag the end of E/sub 2/ treatment and 4 weeks after E/sub 2/ was withdrawn, TIDA function, as evaluated by electrical stimulation of median eminence tissue in vitro after allowing for uptake of /sup 3/H-DA, was decreased compared to OVX controls. In an attempt to elucidate the mechanism by which E/sub 2/ results in a permanent decline in TIDA function, F344 rats were given daily bromocryptine injections in addition to a 30-day E/sub 2/ treatment. TIDA neuronal release was reduced in both E/sub 2/ and E/sub 2/ and bromocryptine treated groups. However, by 30 days after discontinuing treatment only rats given E/sub 2/ alone showed a persistent decline in TIDA function. Since permanent damage to hypothalamic neurons by an enlarged AP was speculated to be the result of E/sub 2/ treatment, neurons which regulate other AP hormones may also be damaged. To evaluate this possibility, pulsatile release of prolactin, growth hormone (GH) and luteinizing hormone (LH) was evaluated in OVX control rats, chronically E/sub 2/-treated rats, and rats 120 days after chronic E/sub 2/ treatment. Only the frequency of prolactin pulses, but not the frequency of GH and LH pulses, was reduced in rats 120 days after E/sub 2/ treatment. This suggests selectivity in the hypothalamic damage produced by the enlarged AP.
Research Organization:
Michigan State Univ., East Lansing (USA)
OSTI ID:
6717663
Country of Publication:
United States
Language:
English