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I Vathy

Publications and source records attributed to I Vathy.

5 recordsLinked to original sources
PubMed1992

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↗
PubMed1991

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↗
PubMed1988

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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