Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sexual differentiation of the rat brain is affected by certain compounds administered during the neonatal period. We evaluated the effects of exposure to THC during the critical period of sexual differentiation of the female rat brain on postpubertal estrous cycles and brain neurotransmitter levels. Newborn female rats were injected either with vehicle (oil) or with different doses of THC (0.38; 1.9 or 3.8 mg/100 g) subcutaneously during the first 5 days after birth. The rats were examined daily by vaginal lavage smears from 3 to 10 months of life for phases of estrous cyclicity. The animals were then sacrificed and the anterior hypothalamus preoptic area (AHPOA) and medial basal hypothalami (MBH) were collected, processed and the methionine-enkephalin (met-enkephalin), beta-endorphin-like immunoreactivity (beta-end LI), LHRH and substance-P were measured by radioimmunoassays. In addition, serum LH and prolactin levels were measured by radioimmunoassay. Compared with the control rats, the rats perinatally exposed to THC exhibited either constant metestrus diestrus type vaginal smears or irregular estrous cycles. In the THC-treated animals, the met-enkephalin and beta-end LI levels were lower in the AHPOA and higher in the MBH. The LHRH levels of THC-treated rats were significantly lower in the MBH. The substance-P levels were significantly lower in the AHPOA of THC treated animals. In the THC-treated rats, serum LH was low but, the prolactin levels were not significantly different from the control animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Early exposure to delta 9-tetrahydrocannabinol influences neuroendocrine and reproductive functions in female rats. 243 39

Acute treatment with delta 1-tetrahydrocannabinol (delta 1-THC) elevated the concentration of beta-endorphin-like immunoreactivity (beta-ELIR) in plasma and in the hypothalamus, but not in the hippocampus of rats habituated to the injection procedure. These effects were not obtained with the psychotropically inert analog of delta 1-THC, cannabidiol. In animals that had not been habituated to the injection procedure, placebo treatment induced a decrease in hippocampal beta-ELIR.
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PMID:Effect of acute administration of delta 1-tetrahydrocannabinol on beta-endorphin levels in plasma and brain tissue of the rat. 303 70

The possible existence of an increased susceptibility to the reinforcing properties of morphine was analyzed in male and female rats born from mothers exposed to delta9-tetrahydrocannabinol (THC, 1, 5, or 20 mg/kg) during gestation and lactation. Maternal exposure to low doses of THC (1 and 5 mg/kg), relevant for human consumption, resulted in an increased response to the reinforcing effects of a moderate dose of morphine (350 microg/kg), as measured in the place-preference conditioning paradigm (CPP) in the adult male offspring. These animals also displayed an enhanced exploratory behavior in the defensive withdrawal test. However, only females born from mothers exposed to THC 1 mg/kg exhibited a small increment in the place conditioning induced by morphine. The possible implication of the hypothalamo-pituitary-adrenal axis (HPA) was analyzed by monitoring plasma levels of adrenocorticotropic hormone (ACTH) and corticosterone in basal and moderate-stress conditions (after the end of the CPP test). Female offspring perinatally exposed to THC (1 or 5 mg/kg) displayed high basal levels of corticosterone and a blunted adrenal response to the HPA-activating effects of the CPP test. However, male offspring born from mothers exposed to THC (1 or 5 mg/kg) displayed the opposite pattern: normal to low basal levels of corticosterone, and a sharp adrenal response to the CPP challenge. The present study reveals that maternal exposure to low doses of THC results in an increased sensitivity to the reinforcing effects of morphine in the adult male offspring, and in sexually dimorphic behavioral and endocrine alterations in the adaptative responses to stressors such as novelty or place-preference testing. These results support the growing evidence of the importance of monitoring the long-term consequences of maternal consumption of cannabis derivatives.
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PMID:Maternal exposure to low doses of delta9-tetrahydrocannabinol facilitates morphine-induced place conditioning in adult male offspring. 976 57

The purpose of this study was to investigate the cannabinoid and opioid mediated regulation on the effects of central Delta(9)-tetrahydrocannabinol (Delta(9)-THC) administration on hypothalamus-pituitary-adrenal (HPA) axis activity in the male rat. Intracerebroventricular (i.c.v.) administration of delta(9)-THC (25, 50, 100 microg/rat) markedly increased plasma adrenocorticotropin hormone (ACTH) and corticosterone concentrations. Time course effect studies revealed that both hormones secretion peaked at 60 min after Delta(9)-THC i.c.v. administration (50 microg/rat), decreased gradually and returned to baseline levels by 480 min. The i.c.v. administration of the specific cannabinoid receptor antagonist SR-141716A (3 microg/rat) significantly attenuated the increase of both hormones secretion induced by Delta(9)-THC (50 microg/rat). Nevertheless, higher doses (12.5 and 50 microg/rat) of this compound increased both ACTH and corticosterone plasma concentrations. Subcutaneous (s.c.) administration with the opiate receptor antagonist naloxone (0.3 mg/kg) was without effect but significantly diminished the increase of both hormones secretion induced by Delta(9)-THC (50 microg/rat). Taken together, these results indicate that opiate and cannabinoid receptors are involved in the activation of the HPA axis induced by Delta(9)-THC. Furthermore, the increase of ACTH and corticosterone secretion after the administration of higher doses of SR-141716A than those required to block such activation, suggests that endogenous cannabinoids are tonically inhibiting the release of both hormones or that this agonist-like activity may be part of an uncharacterized action of this compound not mediated by cannabinoid receptors.
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PMID:Opioid and cannabinoid receptor-mediated regulation of the increase in adrenocorticotropin hormone and corticosterone plasma concentrations induced by central administration of delta(9)-tetrahydrocannabinol in rats. 1048 10

Chronic exposure to Delta(9)-tetrahydrocannabinol (Delta(9)-THC) increases corticotropin-releasing hormone (CRH) and proopiomelanocortin (POMC) gene expression in the rat hypothalamus. The levels of circulating gonadal steroids concurrently modulate both neuropeptides in male and female rats. However, it remains unknown whether gonadal steroids regulate Delta(9)-THC effects on CRH and POMC gene expression in the hypothalamus of male and female rats. To explore this hypothesis, experiments were conducted on intact, 2-week-gonadectomized, 1-week-gonadectomized, 1-week-dihydrotestosterone (DHT)- or estradiol-replaced male and female rats. One week after hormonal replacement, animals were treated with vehicle or Delta(9)-THC (5 mg/kg/day, i.p. for 7 days). Administration of Delta(9)-THC to intact male rats increased CRH gene expression. Castration abolished Delta(9)-THC effects of CRH gene expression in males but not in females. On the other hand, POMC mRNA levels were reduced as a result of castration, and DHT treatment did not prevent this decrease. Delta(9)-THC treatment similarly increases POMC gene expression of intact, orchidectomized and DHT-replaced males. In females, ovariectomy decreased CRH gene expression. Delta(9)-THC administration increased CRH gene expression to the same extent in castrated and estradiol-replaced rats. On the other hand, POMC gene expression was increased by ovariectomy, and Delta(9)-THC administration did only increase POMC transcript levels in the estradiol-replaced group. These data show that gonadal steroids differentially regulate the effects of Delta(9)-THC on both CRH and POMC gene expression in the hypothalamus of male and female rats, suggesting gender differences in the reaction to cannabinoids.
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PMID:Role of gonadal steroids in the corticotropin-releasing hormone and proopiomelanocortin gene expression response to Delta(9)-tetrahydrocannabinol in the hypothalamus of the rat. 1152 20

Recently, we demonstrated that prenatal Delta(9)-tetrahydrocannabinol (Delta(9)-THC) exposure alters proenkephalin mRNA levels in several brain regions of rat fetuses. In the present study, we analyzed mRNA levels of the two other opioid peptide precursors, prodynorphin and pro-opiomelanocortin (POMC), in several brain nuclei of rat fetuses which were exposed daily to Delta(9)-THC from day 5 of gestation. Prenatal Delta(9)-THC exposure altered POMC and prodynorphin mRNA levels in most of the brain areas studied at different fetal ages, but the effects were sex-dependent. Thus, POMC mRNA levels increased in Delta(9)-THC-exposed females, but decreased in Delta(9)-THC-exposed males at GD21 in the arcuate nucleus, cerebral cortex and habenular nuclei. POMC mRNA levels also increased in the arcuate nucleus and cerebral cortex of Delta(9)-THC-exposed fetuses at GD18. Prodynorphin mRNA levels were not altered by the prenatal Delta(9)-THC exposure in the striatum, cerebral cortex, hippocampus and hypothalamic structures of fetuses at GD16 and GD18, but a sexually dimorphic response was observed at GD21. Thus, prodynorphin mRNA levels increased in the cerebral cortex, hippocampus and paraventricular hypothalamic nucleus of Delta(9)-THC-exposed females, whereas no changes were observed in Delta(9)-THC-exposed males. In summary, Delta(9)-THC exposure altered the prenatal development of POMC and prodynorphin mRNA levels in several brain structures. Changes in POMC were similar to those reported previously for proenkephalin, increases in females but decreases in males, whereas changes in prodynorphin were only observed in females.
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PMID:Changes in prodynorphin and POMC gene expression in several brain regions of rat fetuses prenatally exposed to Delta(9)-tetrahydrocannabinol. 1282 1

Although drugs of abuse have different acute mechanisms of action, their brain pathways of reward exhibit common functional effects upon both acute and chronic administration. Long known for its analgesic effect, the opioid beta-endorphin is now shown to induce euphoria, and to have rewarding and reinforcing properties. In this review, we will summarize the present neurobiological and behavioral evidences that support involvement of beta-endorphin in drug-induced reward and reinforcement. Currently, evidence supports a prominent role for beta-endorphin in the reward pathways of cocaine and alcohol. The existing information indicating the importance of beta-endorphin neurotransmission in mediating the reward pathways of nicotine and THC, is thus far circumstantial. The studies described herein employed diverse techniques, such as biochemical measurements of beta-endorphin in various brain sites and plasma, and behavioral measurements, conducted following elimination (via administration of anti-beta-endorphin antibodies or using mutant mice) or augmentation (by intracerebral administration) of beta-endorphin. We suggest that the reward pathways for different addictive drugs converge to a common pathway in which beta-endorphin is a modulating element. Beta-endorphin is involved also with distress. However, reviewing the data collected so far implies a discrete role, beyond that of a stress response, for beta-endorphin in mediating the substance of abuse reward pathway. This may occur via interacting with the mesolimbic dopaminergic system and also by its interesting effects on learning and memory. The functional meaning of beta-endorphin in the process of drug-seeking behavior is discussed.
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PMID:Beta-endorphin and drug-induced reward and reinforcement. 1860 44