Brief ethanol exposure and stress-related factors disorganize neonatal breathing plasticity during the brain growth spurt period in the rat.

Rationale: The effects of early ethanol exposure upon neonatal respiratory plasticity have received progressive attention given a multifactorial perspective related with sudden infant death syndrome or hypoxia-associated syndromes. The present preclinical study was performed in 3-9-day-old pups, a stage in development characterized by a brain growth spurt that partially overlaps with the 3rd human gestational trimester.

Methods: Breathing frequencies and apneas were examined in pups receiving vehicle or a relatively moderate ethanol dose (2.

Conditioned breathing depression during neonatal life as a function of associating ethanol odor and the drug's intoxicating effects.

Fetal and neonatal ethanol-related alterations upon the respiratory system have been described in different mammals. Studies also indicate that perinates learn about the sensory attributes of ethanol and associate them with diverse physiological effects of the state of intoxication. The present study was conducted in rat neonates during a developmental stage equivalent to the third human gestational trimester.

Effects of ethanol exposure in a familiar or isolated context during infancy on ethanol intake during adolescence.

Early exposure to ethanol affects ethanol intake later in life. This early experience encompasses exposure to social stimuli and the pharmacological and orosensory properties of ethanol. The specific contribution of each type of stimulus to subsequent ethanol intake remains unknown.

Neonatal sensitization to ethanol-induced breathing disruptions as a function of late prenatal exposure to the drug in the rat: modulatory effects of ethanol's chemosensory cues.

Preclinical and clinical studies have systematically demonstrated abrupt changes in fetal respiratory patterns when the unborn organism is exposed to the effects of maternal ethanol intoxication. In subprimates, chronic exposure to this drug during gestation and infancy results in marked alterations of the plasticity of the respiratory network. These alterations are manifested in terms of an early incapability to overcome deleterious effects of hypoxic events as well as in terms of sensitization to ethanol's depressant effects upon breathing patterns.

Social isolation and stress related hormones modulate the stimulating effect of ethanol in preweanling rats.

Preweanling rats are highly sensitive to the locomotor stimulation induced by relatively high ethanol doses. In adult mice this ethanol effect is modulated by stress. The goal of the present study was to analyze the role of stress and corticosterone in the stimulating effect of ethanol in preweanling rats.

Dual effect of electrochemical stimulation of the medial preoptic area on the release of LH: possible neurotransmitter involvement.

Electrochemical and electrical stimulation of the medial preoptic area (MPA) was shown to induce release of LH in rats. Owing to differences in cytoarchitecture and neural afferents between the medial (mMPA) and lateral (lMPA) parts of the MPA, we decided to explore whether this difference in organization would distinctly influence the secretion of gonadotropin. Both parts of the MPA were electrochemically stimulated on the day of proestrus in freely behaving rats bearing chronic implanted electrodes.

Intraventricular injection of agents that enhance cyclic adenosine monophosphate formation leads to inhibition of proestrous luteinizing hormone surge in rats.

The effect of increasing hypothalamic levels of 3',5'-cyclic adenosine monophosphate (cAMP) on the preovulatory surge of luteinizing hormone (LH) and ovulation was studied in cycling rats. Animals hearing chronically implanted guiding cannulae into the third ventricle were injected with agents known to enhance the cellular levels of cAMP. Hourly blood samples from the unanesthetized, unrestrained rats were obtained between 11.

Daily variations in the sensitivity of proestrous LH surge in the inhibitory effect of intraventricular injection of 5-HT or GABA in rats.

Intraventricular injection of 5-hydroxytryptamine (5-HT) into female rats at 11:00 h on the day of proestrus inhibited the preovulatory surge of luteinizing hormone (LH) and ovulation. A similar response was observed after the activation of the serotonergic system by stimulation of the median raphe nucleus. A diurnal rhythm of these responses was observed.

Further evidence of an opposite effect of dorsal and median raphe nuclei on the proestrous surge of LH.

The effect of stimulation or lesions of either the dorsal or the median raphe nucleus on the proestrous surge of LH and on ovulation was studied in rats kept under constant illumination. Electrochemical stimulation (anodic DC of 100 microA during 30 sec) was applied at noon on the day of proestrus through chronically implanted electrodes. Lesions of the raphe nuclei were made by passing a cathodic current of 1 mA for 20 sec through nichrome electrodes stereotaxically implanted.

Inhibition of proestrous LH surge and ovulation in rats evoked by stimulation of the medial raphe nucleus involves a GABA-mediated mechanism.

The neurotransmitters involved in the inhibition of luteinizing hormone (LH) release induced by electrochemical stimulation (anodic d.c., 100 microA/30 s) of the medial raphe nucleus (MRn) were studied.

The Pineal Gland Mediates the Inhibition of Proestrous Luteinizing Hormone Surge and Ovulation in Rats Resulting from Stimulation of the Medial Raphe Nucleus or Injection of 5-HT into the Third Ventricle.

Abstract In cycling rats, electrochemical stimulation of the medial raphe nucleus or injection of 5-HT into the third ventricle on the day of proestrus blocked the preovulatory surge of luteinizing hormone and inhibited ovulation. The inhibitory effect of these procedures on gonadotropin secretion failed to occur in rats that had been pinealectomized a few weeks earlier. In contrast, sham-pinealectomized rats exhibited a response similar to that of intact rats.