Behavioral effects of L-tryptophan and p-chlorophenylalanine after adrenalectomy or dexamethasone administration in rats

Effects of acute administration of L-tryptophan (L-TRP. 250.0 mg/kg, i.p.) on active avoidance conditioning and "open-field" behavior were studied in male rats after adrenalectomy of dexamethasone administration. L-TRP inhibited the acquisition and reproduction of active avoidance reaction in adrenalectomized and dexamethasone-treated rats. Moreover, L-TRP decreased horizontal locomotor activity and grooming behavior in the "open field" on adrenalectomized rats. On the contrary, p-CPA restored the active avoidance conditioning in adrenalectomized rats and rats with excess of glucocorticoids. Also, p-CPA increased the total locomotor activity and grooming behavior in the "open field" in adrenalectomized rats, but decreased horizontal locomotor activity and enhanced emotional reaction in dexamethasone-treated rats in the "open field".     

Effect of adrenalectomy and corticosterone on cocaine-induced sensitization in rats.

Effects of adrenalectomy (ADX) and corticosterone (CORT) on the development and expression of sensitization to the locomotor effect of cocaine (COC) were studied in rats. Sensitization was evoked by 5 daily injections of COC (10 mg/kg) and measured after a challenge dose of the drug (10 mg/kg) after a 5-day withdrawal (on day 10 of the experiment). ADX, performed before the start of COC administration, completely blocked the manifestation of COC-induced sensitization. In contrast, ADX performed on animals already sensitized to COC did not affect the sensitized locomotor activity response to a challenge dose of COC (on day 18). Pretreatment with CORT, 10 mg/kg, but not 5 mg/kg, before each of the 5 daily COC injections facilitated the development of COC sensitization, tested after a 5-day withdrawal. When pretreated with CORT alone (10 mg/kg), the challenge dose of COC administered on day 10 induced cross-sensitization to CORT. CORT (10 mg/kg) injected acutely before COC on day 10, potentiated the expression of COC sensitization. When given alone, on day 10 CORT (5-10 mg/kg) induced an increase in the locomotor activity of rats pretreated daily (5 injections) with COC. No drug treatment induced conditioned locomotion, as measured after saline challenge on day 8. Our results indicate that CORT facilitates the development and expression of COC sensitization, while ADX blocks the initiation of the behavioral phenomenon only. Moreover, there takes place cross-sensitization between CORT and COC, which indicates a close relationship between the drug-related mechanism and behavioral sensitization.     

Effects of ACTH, dexamethasone, adrenalectomy and stress on cAMP content of adenohypophysis and adrenals in rats.

The effects of adrenalectomy, ether-laparotomy stress and in vivo administration of either ACTH or dexamethasone on the cAMP levels in the anterior pituitary and the adrenal glands were investigated in male rats. After adrenalectomy or ether-laparotomy stress, an increase of the pituitary cAMP levels was observed. A prior administration of dexamethasone failed to inhibit the increase of the pituitary cAMP levels. Acute administration of dexamethasone increased the cAMP levels in the pituitary. Chronic administration of dexamethasone decreased the cAMP levels in the pituitary, but ACTH did not. These data suggest that cAMP might be involved in the mediation of the hypothalamo-pituitary-adrenal axis.     

The effect of adrenalectomy upon the absorption,distribution and metabolism of ethanol in the rat

There was an increase in blood ethanol levels following the intraperitoneal or intravenous administration of ethanol to rats 8 days after adrenalectomy, compared to control animals. This was due to a 20% decrease in total body water and an increased rate of absorption following intraperitoneal administration. There was no change in the rate of ethanol metabolism.     

Effect of ACTH, dexamethasone, and adrenalectomy on the secretion of testosterone in the rat

The effect of ACTH (100 micrograms/animal/day, i.p.), dexamethasone (75 micrograms/animal/day, s.c.), both for three consecutive days, and adrenalectomy, with or without dexamethasone, maintained according to the group, one, two or three days, on the plasmatic testosterone and corticosterone levels, has been studied in adult male Wistar rats. ACTH and adrenalectomy produced a high decrease in testosterone levels (p less than 0.001 for the three days studied). Dexamethasone produced lower testosterone levels in the first day followed by partial recuperation between the second and the third days of its administration. Dexamethasone produced the effects mentioned for intact animals. The changes in corticosterone levels were according to an adequate response of the hypothalamus-pituitary-adrenal system under these experimental circumstances. ACTH exerts an inhibitory effect on testosterone secretion in the rat, so that such an effect from the data obtained after adrenalectomy and simultaneous dexamethasone injections, does not seems to be mediated either by the presence of adrenals or high corticosterone levels.     

Type I and type II corticosteroid receptor gene expression in the rat: effect of adrenalectomy and dexamethasone administration

We have used 32P-labeled cRNA probes directed against Type I (mineralocorticoid, high affinity glucocorticoid) and Type II (classical glucocorticoid) receptor mRNA to screen various tissues, and have investigated the effect of adrenalectomy (ADX) and dexamethasone (DM) administration on their levels in hippocampus. Both Northern blot and S1 nuclease analysis showed Type I mRNA to be high in hippocampus, colon, and heart; low in liver; and undetectable in thymus. Type II mRNA was high in liver, thymus, and brain; and low in testis and parotid. A transient increase in both hippocampal Type I and Type II mRNA was noted at 1-3 days post ADX. DM similarly elicited a rise in hippocampal Type I mRNA at 2-4 days after ADX, but prevented the ADX-induced increment in Type II mRNA. In contrast to the transient increase in Type I receptor mRNA levels, hippocampal levels of Type I receptors measured by [3H]aldosterone binding were constant 1-16 days post ADX. DM administration caused a doubling in Type I receptor levels over 4 days, with plateau levels at 4-16 days; previously, DM has been shown to lower Type II receptor levels in the hippocampus.(ABSTRACT TRUNCATED AT 250 WORDS)