oxytocin and Nerve-Degeneration

Topics: Acetylcholinesterase; Adrenal Medulla; Animals; Catecholamines; Cerebellum; Ganglia, Autonomic; Histocytochemistry; Hypothalamo-Hypophyseal System; Macromolecular Substances; Microscopy, Electron; Nerve Degeneration; Neurophysins; Neurosecretion; Neurosecretory Systems; Norepinephrine; Oxytocin; Pituitary Hormones, Posterior; Receptors, Adrenergic; Receptors, Cholinergic; Staining and Labeling; Synapses; Synaptic Membranes; Synaptic Transmission; Synaptic Vesicles; Tyrosine 3-Monooxygenase; Vasopressins

Previous data revealed that numerous neurons in the supraoptic nucleus degenerate after prolonged ethanol exposure, and that the surviving neurons increase their activity in order to prevent dramatic changes in water metabolism. Conversely, excess alcohol does not induce cell death in the suprachiasmatic nucleus, but leads to depression of neuropeptide synthesis that is further aggravated by withdrawal. The aim of the present study is to characterize the effects of prolonged ethanol exposure on the magnocellular neurons of the paraventricular nucleus (PVN) in order to establish whether or not magnocellular neurons display a common pattern of reaction to excess alcohol, irrespective of the hypothalamic cell group they belong. Using conventional histological techniques, immunohistochemistry and in situ hybridization, the structural organization and the synthesis and expression of vasopressin (VP) and oxytocin (OXT) in the magnocellular component of the PVN were studied under normal conditions and following chronic ethanol treatment (6 or 10 months) and withdrawal (4 months after 6 months of alcohol intake). After ethanol treatment, there was a marked decrease in the number of VP- and OXT-immunoreactive magnocellular neurons that was attributable to cell death. The surviving neurons were hypertrophied and the VP and OXT mRNA levels in the PVN unchanged. Withdrawal did not alter the number of VP- and OXT-producing neurons or the gene expression of these peptides. These results substantiate the view that after prolonged ethanol exposure numerous neurons of the hypothalamic magnocellular system degenerate, but the mRNA levels of VP and OXT are not decreased due to compensatory changes undergone by the surviving neurons.

Topics: Alcohol Drinking; Alcoholism; Animals; Central Nervous System Depressants; Ethanol; Gene Expression; Immunohistochemistry; In Situ Hybridization; Male; Nerve Degeneration; Neurons; Organ Size; Oxytocin; Paraventricular Hypothalamic Nucleus; Rats; Rats, Wistar; RNA, Messenger; Substance Withdrawal Syndrome; Vasopressins

In this paper we have investigated the distribution of corticotropin releasing hormone (CRH)-, vasopressin- and oxytocin-immunoreactive (IR) neurones in the paraventricular nucleus in the senile compared to the adult human brain. We found a higher number of CRH-IR neurones in senile compared to adult subjects. Vasopressin- and oxytocin-IR neurones were instead more weakly stained in the former compared to latter. These results support a hypothalamic involvement in promoting the higher activity of the hypothalamus-pituitary-adrenal axis and, thus, higher glucocorticoid plasma levels which have been described in the elderly.

Topics: Aged; Aging; Brain; Brain Chemistry; Corticotropin-Releasing Hormone; Female; Glucocorticoids; Hormones; Humans; Male; Middle Aged; Nerve Degeneration; Neurons; Oxytocin; Paraventricular Hypothalamic Nucleus; Risk Factors; Thyroid Hormones; Vasopressins

Axonal injury to hypothalamic magnocellular vasopressin (AVP) and oxytocin (OT) neurons causes degeneration of a substantial subpopulation of these neurons. In this study, we investigated the influence of osmolality on this injury-induced cell death. Normonatremic, chronically hypernatremic, and chronically hyponatremic rats received pituitary stalk compression (SC), which causes degeneration of AVP and OT terminals in the neurohypophysis. Twenty-one days after SC, rats were perfused and hypothalami were serially sectioned and alternately stained for AVP-neurophysin and OT-neurophysin immunoreactivities. Normonatremic and hypernatremic rats exhibited a triphasic pattern of water intake after SC, with peak intakes 3 times higher than those exhibited by sham-operated normonatremic rats. In contrast, hyponatremic SC rats exhibited peak water intakes of 600 ml/24 hr, approximately 9-10 times the water intakes of sham-operated normonatremic rats. In normonatremic rats, SC caused degeneration of 65% of the AVP neuron population in the SON and 73% in the PVN, but only 31% of the OT neuron population in the SON and 35% in the PVN. Similar results were found in hypernatremic rats after SC. However, in hyponatremic rats SC caused degeneration of 97% of the AVP neuron population in the SON and 93% in the PVN, and 90% of the OT neuron population in the SON and 84% in the PVN. Our results, therefore, demonstrate that injury-induced degeneration of magnocellular AVP and OT neurons is markedly exacerbated by chronic hypo-osmolar conditions, but neuronal survival is not enhanced by chronic hyperosmolar conditions.

Topics: Animals; Axons; Cell Count; Cell Death; Cell Survival; Deamino Arginine Vasopressin; Drinking; Hypernatremia; Hyponatremia; Male; Nerve Degeneration; Neurons; Oxytocin; Rats; Rats, Sprague-Dawley; Sodium; Sodium Chloride; Time Factors; Vasopressins

This study describes ultrastructural and morphometric changes in the arginine vasopressin (AVP)-like immunoreactive and oxytocin (OT)-like immunoreactive neurons in the hypothalamic paraventricular nuclei (PVN) and supraoptic nuclei (SON) of streptozotocin-induced diabetic rats at 1-12 months post-diabetes. At 1-6 months post diabetes, both AVP-immunoreactive and OT-immunoreactive neuronal somata were hypertrophied in the PVN and SON. These neuronal somata contained highly dilated rough endoplasmic reticulum in the cytoplasm. The reaction product for AVP as well as OT localization was dispersed throughout the cytoplasm and cell nucleus, but not within the nucleolus. Moreover, the reaction product appeared to be studded onto the ribosomes on dilated cisterns of the endoplasmic reticulum. At 9-12 months post-diabetes, both AVP-immunoreactive and OT-immunoreactive dendrites contained dilated endoplasmic reticulum, autophagic vacuoles, lipid bodies, microtubules, membranous bodies and occasionally swollen mitochondria. Labelled hypertrophied axonal profiles containing neurosecretory granules, autophagic vacuoles, membranous bodies and tubulovesicular elements were also observed in the neuropil. Morphometric study showed that both AVP-immunoreactive and OT-immunoreactive neuronal somata of the PVN and SON in the diabetic rats were markedly hypertrophied at all the time intervals examined. It is concluded that the morphometric changes observed represent hyperactivity of both AVP- and OT-immunoreactive neurons, while the concurrent ultrastructural changes observed at later stages may be indicative of degeneration.

Topics: Animals; Arginine Vasopressin; Diabetes Mellitus, Experimental; Male; Microscopy, Electron; Nerve Degeneration; Neurons; Oxytocin; Paraventricular Hypothalamic Nucleus; Rats; Rats, Wistar; Streptozocin; Supraoptic Nucleus

Topics: Adrenal Cortex Hormones; Afferent Pathways; Animals; Atropine; Electric Stimulation; Ergot Alkaloids; Feedback; Female; Gonadal Steroid Hormones; Hypothalamo-Hypophyseal System; Milk Ejection; Nerve Degeneration; Neurotransmitter Agents; Oxytocin; Pituitary Gland, Posterior; Pregnancy; Rats; Reflex; Spinal Cord; Vasopressins

Topics: Animals; Blood Pressure; Corpus Callosum; Haplorhini; Hypothalamus; Mesencephalon; Microtomy; Nerve Degeneration; Neurons; Oxytocin; Staining and Labeling; Urinary Bladder