Streptozotocin-(STZ) treated diabetic male rats have significant repro
ductive endocrinopathy. To determine the functional responsiveness of
luteinizing hormone-releasing hormone (LHRH) neurons in STZ-treated di
abetic male rats, stimulated LHRH release was assessed using hypothala
mi from short-term STZ-treated, STZ-treated insulin-replaced, and cont
rol male rats. LHRH release from control, STZ-treated, and STZ-treated
, insulin-replaced explants in response to an initial and second 30-mi
n pulse of phenylephrine were not different. A terminal pulse, contain
ing 45 mM KCI, a general secretogogue, also revealed no differences be
tween groups in stimulated LHRH release. Glucose and testosterone leve
ls in the controls and the diabetic rats were significantly different.
Cell counts on serial brain sections processed for LHRH immunohistoch
emistry suggested that the number of LHRH neurons in the preoptic area
r (POA) and septal areas were not different between control and STZ-tr
eated rats. Thus, the short-term STZ-treated rats of this study were d
iabetic, and they displayed associated endocrinopathy; however, explan
ts obtained from control and STZ-treated rats exhibited a typical LHRH
responsiveness to both phenylephrine and KCI, and appeared similar in
LHRH neuron number. Therefore, these findings suggest that reproducti
ve endocrinopathy accompanying short-term STZ-induced diabetes in male
rats does not result from deficiency in LHRH neurons per se.