pituitrin and Nerve-Degeneration

Topics: Animals; Axons; Catecholamines; Circadian Rhythm; Diabetes Insipidus; Histocytochemistry; Hypothalamo-Hypophyseal System; Hypothalamus; Male; Microscopy, Electron; Nerve Degeneration; Nerve Regeneration; Neuroglia; Neurons; Testis; Time Factors; Vasopressins; Water

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

In males, long-term alcohol consumption provokes neurochemical changes in the medial parvocellular division of the PVN (PVNmp) that are partially reversed by withdrawal. Because gonadal steroids modulate the activity of the hypothalamo-pituitary-adrenal axis, we analyzed the possibility that the repercussions of chronic alcohol consumption and withdrawal on the anatomy and neurochemistry of the PVNmp might differ between the sexes. Male and female Wistar rats were examined after ingesting a 20% alcohol solution for 6 months or after 2 months of withdrawal from 6 months of alcohol consumption. The levels of gonadal steroids and the basal concentrations of corticosterone were also evaluated. Chronic alcohol consumption and withdrawal did not alter the global cytoarchitectonic features of the PVNmp in rats of both sexes. However, alcohol consumption was associated with a decrease in the number of vasopressin (VP) neurons only in females and of corticotropin releasing hormone (CRH) neurons in males and females. Further, the response to withdrawal was sexually dimorphic because in males there was a partial recovery of the number of CRH neurons whereas in females there was a further loss of VP and CRH neurons. Corticosterone levels were unchanged by alcohol consumption, but they were decreased by withdrawal in females. Alcohol consumption and withdrawal did not alter estrogen and progesterone concentrations in females, but decreased testosterone levels in males. These findings show that the response of CRH and VP neurons to excess alcohol is gender-specific, with females being more vulnerable during alcohol consumption and, most notably, after withdrawal.

Topics: Alcohol-Induced Disorders, Nervous System; Alcoholism; Animals; Cell Death; Chronic Disease; Corticosterone; Corticotropin-Releasing Hormone; Disease Models, Animal; Down-Regulation; Female; Gonadal Steroid Hormones; Gonads; Hypothalamo-Hypophyseal System; Male; Nerve Degeneration; Paraventricular Hypothalamic Nucleus; Pituitary-Adrenal System; Rats; Rats, Wistar; Sex Characteristics; Substance Withdrawal Syndrome; Vasopressins

It has been reported that various types of axonal injury of hypothalamo-neurohypophyseal tract can result in degeneration of the magnocellular neurons (MCNs) in hypothalamus and development of central diabetes insipidus (CDI). However, the mechanism of the degeneration and death of MCNs after hypophysectomy in vivo is still unclear. This present study was aimed to disclose it and to figure out the dynamic change of central diabetes insipidus after hypophysectomy.. The analysis on the dynamic change of daily water consumption (DWC), daily urine volume(DUV), specific gravity of urine(USG) and plasma vasopressin concentration showed that the change pattern of them was triphasic and neuron counting showed that the degeneration of vasopressin neurons began at 10 d, aggravated at 20 d and then stabilized at 30 d after hypophysectomy. There was marked upregulation of cleaved Caspase-3 expression of vasopressin neurons in hypophysectomy rats. A "ladder" pattern of migration of DNA internucleosomal fragments was detected and apoptotic ultrastructure was found in these neurons. There was time correlation among the occurrence of diabetes insipidus, the changes of plasma vasopressin concentration and the degeneration of vasopressin neurons after hypophysectomy.. This study firstly demonstrated that apoptosis was involved in degeneration of supraoptic vasopressin neurons after hypophysectomy in vivo and development of CDI. Our study on time course and correlations among water metabolism, degeneration and apoptosis of vasopressin neurons suggested that there should be an efficient therapeutic window in which irreversible CDI might be prevented by anti-apoptosis.

Topics: Animals; Apoptosis; Caspase 3; Cell Count; Diabetes Insipidus, Neurogenic; Drinking; Hypophysectomy; Male; Nerve Degeneration; Neurons; Rats; Rats, Sprague-Dawley; Supraoptic Nucleus; Urine; Vasopressins

Spontaneously hypertensive rats (SHR) pathologically elevate blood pressure with age. This elevation is accompanied by specific neuronal degeneration in the hypothalamus and enlargement of the lateral ventricles. The aim of this study was to assess the neuroprotective effect of the monoamine oxidase B (MAO-B) inhibitor, rasagiline on paraventricular (PVN) hypothalamic degeneration in SHR. The S-enantiomer of rasagiline, S-PAI, a much weaker MAO inhibitor, and two antihypertensive drugs, captopril and hydralazine were also tested. Normotensive Wistar Kyoto (WKY) rats served as controls. One month-old SHR or WKY rats were treated daily for 3-4 months. Systolic blood pressure was recorded, parvocellular vasopressin (VP) immunopositive cells were counted and the area of the third ventricle measured. In saline-treated SHR, blood pressure rose significantly and the number of VP parvocellular cells was reduced by about 60% relative to WKY. Rasagiline, 1 mg/kg/day, reduced PVN neuronal cell death in SHR up to 112% relative to saline-treated SHR; 0.3 mg/kg/day exerted a smaller but significant effect. These actions were accompanied by parallel reductions in systolic blood pressure. Captoril, hydralazine and S-PAI did not prevent death of VP neurons. In SHR, the volume of the third ventricle was about double that of WKY. Rasagiline significantly prevented this ventricular dilation. These results indicate than rasagiline protects from cell death in an in vivo animal model in a dose-dependant manner and could be of use as a neuroprotector in the central nervous system.

Topics: Animals; Antihypertensive Agents; Blood Pressure; Disease Models, Animal; Dose-Response Relationship, Drug; Hypertension; Indans; Male; Monoamine Oxidase Inhibitors; Nerve Degeneration; Neurodegenerative Diseases; Neurons; Neuroprotective Agents; Paraventricular Hypothalamic Nucleus; Rats; Rats, Inbred SHR; Rats, Wistar; Third Ventricle; Treatment Outcome; Vasopressins

The hyperosmolality associated with diabetes mellitus triggers an increase in neuronal activity and vasopressin production within magnocellular neurosecretory cells (MNCs) of the hypothalamic supraoptic nucleus (SON). In this study, we examined the effect of chronic diabetes on the function and survival of these neurons. After 6 months, but not 6 weeks, of streptozotocin (STZ)-induced diabetes, we observed an increase in the appearance of small hyperchromatic neurons and a decrease in SON neuronal density. A subpopulation of neurons within the SON at this time point demonstrated positive staining for cleaved caspase-3 and TUNEL, two markers of apoptosis. In addition, the number of vasopressin-positive neurons was decreased. Markers for apoptosis did not colocalize with vasopressin immunopositivity; this was probably due to a diabetes-induced degenerative process causing downregulation of vasopressin expression or depletion of neuropeptide. Although the phenotypes of the apoptotic neurons were not identified, other SON neurons including oxytocin-producing neurons are unlikely to be affected by chronic hyperglycemia. Microglial hypertrophy and condensation were also observed in the 6-month diabetic SON. Although upregulation of vasopressin production in response to acute hyperosmolality is adaptive, prolonged overstimulation of vasopressin-producing neurons in chronic diabetes results in neurodegeneration and apoptosis.

Topics: Animals; Antigens, CD; Antigens, Neoplasm; Antigens, Surface; Apoptosis; Avian Proteins; Basigin; Blood Proteins; Caspase 3; Caspases; Chronic Disease; Diabetes Mellitus, Experimental; Disease Models, Animal; Down-Regulation; Glial Fibrillary Acidic Protein; Gliosis; In Situ Nick-End Labeling; Male; Membrane Glycoproteins; Microglia; Nerve Degeneration; Neurons; Rats; Rats, Sprague-Dawley; Supraoptic Nucleus; Vasopressins; Water-Electrolyte Balance

Experimental evidence obtained in various animal models of brain injury indicates that vasopressin promotes the formation of cerebral edema. However, the molecular and cellular mechanisms underlying this vasopressin action are not fully understood. In the present study, we analyzed the temporal changes in expression of vasopressin V1a receptors after traumatic brain injury (TBI) in rats. In the intact brain, the V1a receptor was expressed in neurons located in all layers of the frontoparietal cortex. The V1a receptor-immunoreactive product was predominantly localized to neuronal nuclei and had both a diffused and punctate staining pattern. The V1a receptors were also expressed in astrocytes, especially in layer 1 of the frontoparietal cortex. In these cells, two distinctive patterns of immunopositive staining for V1a receptors were observed: a diffused cytosolic staining of cell bodies and processes and a clearly punctate staining pattern that was predominantly localized to the astrocytic cell bodies. The real-time reverse-transcriptase polymerase chain reaction analysis of changes in mRNA for the V1a receptor demonstrated that after TBI, there is an early (4 h post-TBI) increase in the number of transcripts in the ipsilateral frontoparietal cortex, when compared to the contralateral hemisphere or the sham-injured rats. This increase in the message was followed by the up-regulation of expression of the V1a receptors at the protein level. This was most evident in cortical astrocytes in the areas surrounding the lesion. The number of the V1a receptor-immunopositive astrocytes in the traumatized parenchyma gradually increased, starting at 8 h and peaking at 4-6 days after TBI. Furthermore, a redistribution of V1a receptors from the astrocytic cell bodies to the astrocytic processes was observed. In addition to astrocytes, an increased expression of V1a receptors was found in the endothelium of both blood microvessels and the large-diameter blood vessels in the frontoparietal cortex ipsilateral to injury. This increase in the V1a receptor expression was apparent between 2 and 4 days after TBI. As early as 1-2 h following the impact, there was also a striking increase in the number of the V1a receptor-immunopositive beaded axonal processes, with greatly enlarged varicosities, that were localized to various areas of the injured parenchyma. It is suggested that the increased expression of V1a receptors plays an important role in the vasopressin-mediated formatio

Topics: Animals; Astrocytes; Axons; Blood-Brain Barrier; Brain; Brain Edema; Brain Injuries; Cerebral Cortex; Disease Models, Animal; Disease Progression; Endothelium, Vascular; Male; Nerve Degeneration; Neurons; Rats; Rats, Sprague-Dawley; Receptors, Vasopressin; RNA, Messenger; Up-Regulation; Vasopressins

The ability of alcohol to activate the hypothalamic-pituitary-adrenal (HPA) axis is well documented in investigations based in acute and short-term experimental paradigms. Herein, we have addressed the possibility that the prolonged exposure to ethanol concentrations that are initially effective in stimulating corticosteroid secretion might induce alterations in the response of the HPA axis that cannot be evinced by shorter exposures. Using conventional histological techniques, immunohistochemistry and in situ hybridization, we have examined the medial parvocellular division of the paraventricular nucleus (PVNmp), and the synthesis and expression of corticotropin-releasing hormone (CRH) and vasopressin (VP) by its constituent neurons, in rats submitted to 6 months of ethanol treatment and to withdrawal (2 months after 6 months of alcohol intake). Ethanol treatment and withdrawal did not produce neuronal loss in the PVNmp. However, the total number of CRH- and VP-immunoreactive neurons and the CRH mRNA levels were significantly decreased by ethanol treatment. In withdrawn rats, the number of CRH- and VP-immunostained neurons and the gene expression of CRH were increased relative to ethanol-treated rats and did not differ from those of controls. No significant variations were detected in VP mRNA levels as a result of ethanol treatment or withdrawal. These results show that prolonged alcohol intake blunts the expression of CRH and VP in the parvocellular neurons of the PVN, and that this effect is, partially at least, reversible by withdrawal. They also suggest that the development of tolerance to the effects of ethanol involve changes that take place at the hypothalamic level.

Topics: Alcohol Drinking; Alcoholism; Animals; Central Nervous System Depressants; Corticotropin-Releasing Hormone; Ethanol; Gene Expression; Hypothalamo-Hypophyseal System; Immunohistochemistry; In Situ Hybridization; Male; Nerve Degeneration; Neurons; Paraventricular Hypothalamic Nucleus; Pituitary-Adrenal System; Rats; Rats, Wistar; RNA, Messenger; Substance Withdrawal Syndrome; Time Factors; 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

Selective death of magnocellular vasopressinergic neurons in the hypothalamus has been reported in cases of hereditary and idiopathic diabetes insipidus and after experimental lesions of the hypothalamo-neurohypophyseal pathway. To identify trophic factors that promote survival of these neurons, an in vitro model system was established in which organotypic cultures of the rat hypothalamic paraventricular nucleus were maintained in chemically-defined medium. We observe that the majority of magnocellular vasopressinergic neurons die in these cultures, while other cell populations such as corticotrophin-releasing factor producing parvicellular and oxytocin producing magnocellular cells retain a well preserved cytoarchitectonic organization. Degenerating vasopressinergic cells exhibit morphological signs of apoptosis and stained positively when analysed by the terminal deoxynucleotidyl transferase biotinylated dUTP nick end-labelling assay. Partial survival of vasopressinergic neurons occurred after co-culturing the paraventricular nucleus with neurohypophyseal explants, indicating that target-derived factors may be required for the survival of these neurons. Cell survival is dramatically increased by the administration of ciliary neurotrophic factor and leukemia inhibiting factor, but not by interleukin 6 or the members of the neurotrophin family. Reverse transcription-polymerase chain reaction followed by Southern analysis shows the presence of ciliary neurotrophic factor messenger RNA in the neurohypophysis. Thus, endogenous ciliary neurotrophic factor and leukemia inhibiting factor, produced by neurohypophyseal cells may function as a physiological survival factor for neurosecretory vasopressinergic neurons.

Topics: Animals; Apoptosis; Blotting, Southern; Brain Chemistry; Cell Survival; Cells, Cultured; Cerebral Ventricles; Ciliary Neurotrophic Factor; Gene Expression; Growth Inhibitors; In Situ Nick-End Labeling; Interleukin-6; Leukemia Inhibitory Factor; Lymphokines; Microscopy, Electron; Nerve Degeneration; Nerve Tissue Proteins; Neurons; Neurosecretory Systems; Paraventricular Hypothalamic Nucleus; Pituitary Gland, Posterior; Rats; Rats, Sprague-Dawley; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; 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

Central nervous system feedback loops centered on hypothalamic neurons control atrial natriuretic peptide (ANP). We evaluated the ANP response to arterial hypotension, isotonic blood volume expansion, and increase in plasma osmolality in 14 patients with multiple system atrophy (MSA). Seven of the patients were characterized by a lack of vasopressin response to hypotension (MSA type B), suggesting chronic sinoaortic denervation, and seven by a preserved response (MSA type A). Orthostatic hypotension decreased ANP in controls and type A patients, whereas ANP in type B was not affected. Isotonic saline infusion increased ANP and diuresis in controls and type A patients, whereas it did not affect ANP in type B. Osmotic load increased plasma osmolality and vasopressin in controls and MSA patients and ANP in controls and type A but not in type B patients. In MSA patients with altered afferent control of vasopressin, ANP secretion is not stimulated by blood volume expansion, osmotic load, or blood pressure, suggesting that afferent excitatory control plays a role in the release of ANP.

Topics: Atrial Natriuretic Factor; Blood Pressure; Blood Volume; Brain Diseases; Diuresis; Female; Humans; Hypertension; Isotonic Solutions; Male; Middle Aged; Nerve Degeneration; Osmolar Concentration; Posture; Saline Solution, Hypertonic; Sodium Chloride; Vasopressins

The vasopressin (VP) innervation of the human locus coeruleus (LC) was immunocytochemically investigated in Alzheimer's disease (AD) patients and non-demented controls. A dense innervation of VP fibers was present throughout the entire rostro-caudal length of the LC in both, controls and AD-patients. The VP immunoreactivity was confined to fibers; no signs of cell body staining could be found. Comparison of five non-demented control subjects and five AD patients on fifteen different levels throughout the LC revealed that the VP innervation of this nucleus remained intact in AD, even in the rostral part of the LC, which is the most affected region with respect to neuronal loss.

Topics: Aged; Aged, 80 and over; Alzheimer Disease; Female; Humans; Immunohistochemistry; Locus Coeruleus; Male; Nerve Degeneration; Nerve Fibers; Vasopressins

Luteinizing hormones-releasing hormone (LHRH), vasopressin, and corticotropin systems were examined by immunocytochemical methods in male rats 2 to 20 days after deafferentation of the basal hypothalamus. Axonal degeneration of the vasopressin system (whose perikarya lie rostral to the island) and the corticotropin system (whose perikarya lie within the island) was examined and compared with the response of the LHRH system. Vasopressin immunoreactive staining was absent in the internal zone of the median eminence 10 and 20 days after deafferentation. Disruption of the efferent projections of the opiocortin system caused the loss of almost all fiber staining outside the island by the 5th postoperative day. LHRH staining in the median eminence was modestly reduced in 5 days, considerably reduced in 10 days and negligible 20 days after deafferentation. At 10 and/or 20 days after deafferentation densely stained fibers of all three systems were observed on both sides of the cut. Invasive vasopressinergic fibers reached the lateral median eminence by the 20th postoperative day. This study reports on the response of three neuropeptide systems after complete deafferentation and demonstrates that regeneration can occur across the knife cut.

Topics: Adrenocorticotropic Hormone; Animals; Denervation; Gonadotropin-Releasing Hormone; Hypothalamus; Immunoenzyme Techniques; Male; Nerve Degeneration; Nerve Fibers; Nerve Regeneration; Rats; Vasopressins

Degenerative lesions in the superior vermis of the cerebellum were produced in 8 of 14 rats that were first made hyponatremic for three days with vasopressin and water and then given hypertonic saline. Within the superior vermis, lesions were predominantly localized to the crests of the folia. These lesions were characterized by demyelination of folial white matter and necrosis of granule cells at the junction with the white matter. In severe degeneration, the entire width of the granule cell layer was involved and Purkinje cell necrosis was found as well. Hyponatremia alone or administration of hypertonic saline to normonatremic rats did not result in lesions. Because of the topographical and histopathological similarity of these lesions to those of alcoholic cerebellar degeneration, our findings raise the possibility of a contribution of electrolyte-induced injury to the pathogenesis of alcoholic cerebellar degeneration.

Topics: Animals; Arginine Vasopressin; Cerebellum; Hyponatremia; Male; Myelin Sheath; Necrosis; Nerve Degeneration; Rats; Rats, Inbred Strains; Saline Solution, Hypertonic; Sodium; Sodium Chloride; Vasopressins

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

Fragments of the anterior hypothalamus that contain supraoptic nuclei and short axonal segments from adult guinea pigs have been kept in organ culture for up to 15 days. Electron micrographs displayed intact nuclei, Nissl substance, Golgi bodies, and an ultrastructure characteristic of viable neurosecretory cells; by contrast, the surrounding neurophil showed extensive degeneration. The cultured hypothalamic tissues of the guinea pig that were pulsed with [(3)H]uridine incorporated label into the RNA of neurosecretory neurons, as determined by radioautography and chemical analysis. Furthermore, and most important, these cells retained a complement of hormones and the ability to incorporate (3)H- and (35)S-labeled amino acids into vasopressin, neurophysin, and other polypeptides. This incorporation was inhibited by either puromycin or cycloheximide.

Topics: Animals; Autoradiography; Cycloheximide; Cystine; Depression, Chemical; Golgi Apparatus; Guinea Pigs; Hypothalamus; Male; Nerve Degeneration; Nerve Tissue Proteins; Neurons; Neurosecretory Systems; Nissl Bodies; Organ Culture Techniques; Peptide Biosynthesis; Puromycin; Sulfur Isotopes; Tritium; Uridine; Vasopressins

Topics: Breast Neoplasms; Cortisone; Desoxycorticosterone; Diabetes Insipidus; Female; Hematocrit; Humans; Hyponatremia; Hypothalamo-Hypophyseal System; Middle Aged; Neoplasm Metastasis; Nerve Degeneration; Nerve Regeneration; Neurons; Pituitary Gland; Pituitary Gland, Posterior; Postoperative Complications; Sodium; Sodium Chloride; Vasopressins; Water; Water-Electrolyte Balance

Topics: Animals; Animals, Newborn; Dehydration; Diabetes Insipidus; Hydrocephalus; Hypothalamo-Hypophyseal System; Hypothalamus; Nerve Degeneration; Rats; Vasopressins