Clare Fadden

Neurohypophyseal vasopressin in the Syrian hamster: response to short photoperiod, pinealectomy, melatonin treatment, or osmotic stimulation.

In the present study, the effect of photoperiod on vasopressin content in the pituitary neurointermediate lobe (NIL), as well as the ability of pinealectomy to prevent and melatonin to mimic the short photoperiod-induced changes in NIL vasopressin were studied in male Syrian hamsters. The ability of melatonin to modify the hyperosmotically stimulated vasopressin release was also determined. Exposure to short photoperiod (SD) for 4 or 10 weeks increased vasopressin content in the hamster NIL. In long photoperiod (LD)-exposed hamsters, pinealectomy induced a decrease in NIL vasopressin content, whereas no effect of melatonin injections on vasopressin storage in the NIL was detected. In SD-exposed animals, pineal removal failed to alter vasopressin content in the NIL. Hypertonic saline administration led to the expected decrease in vasopressin content in the NIL both in vehicle- and melatonin-treated animals. The hyperosmotically stimulated release of vasopressin was not modified by previous treatment with melatonin. The data from the present study show that, in male Syrian hamsters, exposure of animals to SD increases the vasopressin content in the posterior pituitary, but these changes appear not to be mediated by SD-induced changes in melatonin secretion. Furthermore, the exposure of animals to SD prevents the pinealectomy-induced changes in NIL vasopressin content. Melatonin does not modify the hyperosmotically stimulated vasopressin release in the male Syrian hamster.

Influence of Diabetes on the Gonadotropin Response to the Negative Feedback Effect of Testosterone and Hypothalamic Neurotransmitter Turnover in Adult Male Rats

The influence of diabetes on the gonadotropin response to the negative feedback effect of testosterone (T) and hypothalamic neurotransmitter turnover rates in adult male rats was evaluated. Adult male Sprague-Dawley rats were made diabetic by an intraperitoneal injection of streptozotocin (STZ; 5 mg/100 g body weight) in citrate buffer. Vehicle-injected rats served as controls. On day 9, all rats were bilaterally castrated and treated subcutaneously on alternate days with either peanut oil or T propionate (TP) in peanut oil (100 micrograms/rat). Plasma follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL), and T concentrations were measured by specific radioimmunoassays from blood samples collected on day 1 (before castration) and 2, 4, 6, and 7 days after castration. On day 7 after castration (day 15 after vehicle or STZ treatment), 1 h before autopsy, the rats were injected intraperitoneally with saline or a tyrosine hydroxylase inhibitor, alpha-methyl-p-tyrosine (25 mg/100 g BW), for the measurement of norepinephrine (NE) and dopamine turnover in median eminence and medial basal hypothalamus (MBH). Circulating FSH, LH, PRL, and T levels were significantly lower (FSH and T: p less than 0.001; LH and PRL: p less than 0.05) in gonad-intact rats treated with STZ than in vehicle-injected animals. The castration-induced increase in plasma LH levels was attenuated in diabetic rats. The suppressive effect of T on LH secretion was significantly greater (p less than 0.001) in STZ-treated rats relative to TP-treated nondiabetic controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Streptozotocin-induced diabetes blocks the positive feedback release of luteinizing hormone in the female rat

The effects of streptozotocin-induced (STZ) diabetes on the release of gonadotropins was studied in female rats. In the first experiment, rats were ovariectomized and 2 days later were injected with STZ. Three weeks later rats were treated with estrogen and progesterone and blood samples were taken via intraatrial cannulae for luteinizing hormone (LH) assay. Afternoon surges of LH were seen in 4/5 control but 0/8 STZ rats. Pituitary responses to LH-releasing hormone in vitro did not differ. In the 2nd experiment, ovariectomized estrogen-primed rats were killed prior to and during a progesterone-induced LH surge. As in Experiment 1, STZ-treatment inhibited the LH surge but did not effect the afternoon rise in median eminence norepinephrine turnover which has previously been shown to be important in stimulating LH release. Turnover of norepinephrine in the anterior hypothalamus was depressed in the diabetic rats both prior to and during the expected time of the LH surge. Dopamine turnover was depressed in all three brain regions studied. It can be concluded that the positive feedback control of LH release is severely attenuated in diabetic rats but the mechanism explaining the loss is not clear. Diabetes-induced alterations in hypothalamic catecholamine metabolism may be involved but further work is needed to more carefully define these relationships.

The Effects of Short Photoperiod, Pinealectomy, and Melatonin Treatment on Oxytocin Synthesis and Release in the Male Syrian Hamster

The pineal gland has been shown to affect plasma oxytocin (OT) levels, but the mechanism of this action is not apparent. In the present study, the ability of the photoperiod to affect plasma OT levels, neurointermediate lobe (NIL) OT content, and hypothalamic OT mRNA levels was studied in male Syrian hamsters. In addition, the ability of pinealectomy to prevent and melatonin (MEL) to mimic the short photoperiod-induced changes were also determined. Exposure to short days (SD) led to the expected decrease in testes weight and plasma PRL levels, but plasma OT levels were unchanged. However, NIL OT content was increased in the SD-exposed animals. Hypothalamic OT mRNA levels were not significantly altered by SD exposure. Pinealectomy blocked the effects of SD on testes weight, whereas afternoon MEL injections mimicked the effects of SD. In long day (LD)-exposed hamsters, pinealectomy induced a decrease in NIL OT content without altering hypothalamic OT mRNA levels. In SD-exposed animals, NIL OT content was not affected by pinealectomy. Melatonin injections had no significant effect on NIL OT content or hypothalamic OT mRNA levels. The data from the present study suggest that exposure of male Syrian hamsters to short photoperiods influences some aspects of OT synthesis and/or transport to produce its increased accumulation in the NIL, but does not affect OT release. These changes are apparently not the result of SD-induced changes in MEL secretion, but conceivably could be related to the previously documented effects of SD on hypothalamic catecholamine turnover.

Diabetes disrupts copulatory behavior and neuroendocrine responses of male rats to female conspecifics

Streptozotocin-induced diabetes disrupts copulatory behavior in the male rat. The increase in serum luteinizing hormone (LH) that occurs in the male rat in response to the presence of a receptive female is absent in most diabetic rats. A female-induced testosterone rise is not seen in diabetic male rats, including those showing an increase in LH. The female-induced LH rise appears to be secondary to increased hypothalamic norepinephrine metabolism, which is severely attenuated in diabetic rats not exhibiting an LH rise in response to a female.

Effects of streptozotocin-induced diabetes on the response of male rats to immobilization stress

The effects of streptozotocin-induced (STZ) diabetes on the response to immobilization stress were evaluated in adult male rats. Rats were injected with STZ or vehicle and handled daily to minimize stress. Four weeks later, half of the animals were lightly anesthetized with ether and immobilized for 20 min. At that time the stressed and nonstressed controls were sacrificed, and blood and tissue collected for hormone and amine determinations. Immobilization caused an increase in plasma glucose levels in the controls, but caused no further increase in the already high levels seen in the diabetic rats. Basal corticosterone levels did not differ between the STZ and control rats, and the increase after immobilization was of similar magnitude. The stress-induced increase in prolactin was attenuated in the diabetic rats. Immobilization caused a significant rise in plasma norepinephrine (NE) levels in control, but not in diabetic rats. Adrenal NE content and tyrosine hydroxylase activity were not significantly affected by stress or STZ treatment. Dopamine (DA) and NE content was increased in the hypothalamus of immobilized diabetic rats as compared to nondiabetic immobilized controls. These results demonstrate that diabetic rats respond to immobilization stress, but the endocrine and sympathetic nervous system response is impaired. Changes in the stress response may be related to changes in hypothalamic amine metabolism.