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Biomedical subjects

I Vathy

Publications and source records attributed to I Vathy.

7 recordsLinked to original sources

Sex dimorphic alterations in postnatal brain catecholamines after gestational morphine.

The concentration of brain catecholamines was measured in the hypothalamus, preoptic area (POA), frontal cortex, cerebellum, and striatum of rats exposed in utero to morphine (5-10 mg/kg/twice daily) during gestation days 11-18. Prenatal morphine induced regionally specific, sexually dimorphic alterations in male and female norepinephrine (NE), and dopamine (DA) content at different postnatal ages. Prenatal morphine significantly increased NE content in the hypothalamus of both sexes at postnatal day (PND) 23. In the POA, on the other hand, morphine increased NE content in exposed males at PND 23 and in females at PND 33. In the cerebellum, the NE content of both sexes was significantly elevated at PND 45. In the striatum, NE content was increased by the prenatal morphine only in females at PND 16. The concentration of DA was also affected in a sexually dimorphic manner. At PND 16, prenatal morphine increased the levels of hypothalamic DA only in males, and it reduced the content of DA in female but not male POA. At PND 45, prenatal morphine increased DA in the hypothalamus of females and decreased it in males. In the cerebellum of 16-day-old morphine-exposed animals, DA levels were increased only in males; at PND 45, the levels of DA were still increased in males but had not changed in females. In the striatum, the DA content was reduced only in males at PND 16. Thus, prenatal morphine alters the development of both NE and DA neurotransmitter systems in the hypothalamus, POA, striatum, and cerebellum in a sexually dimorphic manner.

Animals

Modulation of catecholamine turnover rate in brain regions of rats exposed prenatally to morphine.

The concentration and turnover rate of brain catecholamines were measured in the hypothalamus, preoptic area (POA), frontal cortex, striatum and cerebellum of adult male and female rats exposed in utero to morphine (5-10 mg/kg/twice a day) during gestation days 11-18. Norepinephrine (NE) and dopamine (DA) turnover rates were estimated following alpha-methylparatyrosine (AMPT) administration. Prenatal morphine altered NE content and turnover in male and female rats in a regionally specific, sexually dimorphic manner. Basal NE content increased approximately 60% in the hypothalamus of male rats, but it decreased about 30% in the hypothalamus of female rats. NE turnover in the hypothalamus of morphine-exposed rats increased 50% in males and decreased 50% in females. Prenatal morphine had no effects on NE turnover in the male POA, but in female rats NE turnover decreased approximately 60%. Alterations in the frontal cortex of morphine-exposed male and female rats resembled the pattern in the hypothalamus; however, the differences did not reach statistical significance. In addition, prenatal morphine had no effect on striatal or cerebellar NE or on basal levels or turnover of DA in any brain regions. These results demonstrate that prenatal morphine alters the content and turnover of NE in a sexually dimorphic manner in specific brain regions of male and female rats, suggesting alterations in the density of terminals and/or utilization of NE. These sexually dimorphic alterations in hypothalamic NE induced by prenatal morphine may be related to the changes observed in adult male and female sexual behavior in our previous work.

Animals

Effects of prenatal morphine on adult sexual behavior and brain catecholamines in rats.

Female rats exposed to morphine in utero (5-10 mg/kg twice a day on days 11-18 of gestation) were significantly inhibited in their sexual behavior when compared to saline-exposed controls. In contrast, males exposed prenatally to morphine had shorter post-ejaculatory intromission latencies and, after the first test, exhibited increased mounting and intromitting activity relative to controls. Examination of the brain catecholamine content revealed that morphine in utero may permanently alter adult hypothalamic norepinephrine levels in male and female rats. The morphine-induced alterations in hypothalamic norepinephrine levels were sexually dimorphic. In the hypothalamus of male rats, norepinephrine content was increased 95%, whereas in the hypothalamus of female rats it was decreased 57% relative to controls. These results suggest that prenatal morphine exposure, which differentially affects adult male and female sexual behavior, also alters hypothalamic norepinephrine content in a sexually dimorphic fashion.

Animals

Intracranial dialysis and microinfusion studies suggest that morphine may act in the ventromedial hypothalamus to inhibit female rat sexual behavior.

The present investigation examined the neural sites and mechanisms of opiate inhibition of female sexual behavior. Systemic administration of morphine (10 mg/kg) significantly reduced ovarian steroid-induced estrous behavior in female rats. This behavioral inhibition was prevented when the opiate receptor antagonist naloxone (5 mg/kg) was administered 30 min prior to morphine. Bilateral infusion of morphine directly into the ventromedial hypothalamus (VMH) also inhibited hormone-dependent estrous behavior for at least 2 hr. Furthermore, naloxone infusion into the VMH 20 min before behavior testing reduced the inhibitory effects of systemically administered morphine on lordosis. These results suggest that morphine may inhibit female sexual behavior by acting directly on the VMH, the primary site at which ovarian steroids facilitate this behavior. In a separate experiment we used in vivo brain microdialysis to test the hypothesis that morphine inhibits lordosis by interfering with norepinephrine (NE) neurotransmission in the VMH. In control rats, the onset of mating was associated with increased NE release in the VMH. Morphine-treated animals displayed neither behavioral estrus nor elevated NE release from the VMH when tested with stimulus males. These data are consistent with the hypothesis that morphine suppresses NE release in the VMH. Nevertheless, mechanisms other than or in addition to attenuation of hypothalamic NE release may contribute to the inhibitory effects of morphine on lordosis.

Animals

Ovarian steroids and hypothalamic norepinephrine release: studies using in vivo brain microdialysis.

This study employed microdialysis in urethane-anesthetized female rats to monitor ovarian steroid-dependent changes in KCl-evoked levels of extracellular norepinephrine (NE) in the ventromedial hypothalamus. An initial KCl stimulus (Sl) increased NE from low or undetectable levels in all animals. A second KCl stimulus (S2) given several hr later evoked 40% less NE release than did Sl in ovariectomized (OVX) females or OVX females given only estrogen or progestin. In contrast, the two KCl-evoked NE releases were equivalent in OVX females administered both estrogen and progestin. These results suggest that ovarian steroids may act as presynaptic modulators of NE release in the ventromedial hypothalamus.

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