Loss of vasopressin-immunoreactive neurons in alcoholics is dose-related and time-dependent

Harding, Anthony John; Halliday, Glenda M.; Ng, Joanne; Harper, Clive; Kril, Jillian J.

doi:10.1016/0306-4522(95)00577-3

Cited by 139 publications

(63 citation statements)

References 50 publications

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“…Others have described decreases in vasopressin mRNA and vasopressin neurons as a result of chronic alcohol exposure (Sanna et al, 1993;Gulya et al, 1991;Harding et al, 1996;Ishizawa et al, 1990). Our preliminary results thus far confirm this reduction of vasopressin mRNA in the brain, and also reveal a suppression of VI receptor mRNA in the brain as well.…”

Section: Measurement Of Brain Vasopressin and Vasopressin Receptor Mrnasupporting

confidence: 88%

Vasopressin Regulation and Renal Fluid and Electrolyte Handling in Rat Model of Acute and Chronic Alcohol Exposure

Uyehara¹

2002

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Public reporting burden for this collection of information is estimated to average 1 liour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Washington Headquarters Services, Directorate Catherine F. T. Uyehara, Ph.D. PERFORMING ORGANIZATION NAMEIS) AND ADDRESS(ES)Tripler Army Medical Center Tripler AMC Hawaii 96859-5000 ^3. ABSTRACT (Maximum200 words)We have previously shown that after effects of short term alcohol exposure cause rats to have an mcreased water diuresis m response to a water load whereas after long term alcohol exposure, rats exhibit an impaired ability to excrete a water load. Our latest data indicate that in a 4-week withdrawal phase from chronic alcohol exposure, water excretion impairment begins to return towards control levels. The up-and down-regulation of renal vasopressin V2 receptors appear to be behind differentially altered renal function in different phases of alcohol exposure. Prolonged diuresis during the acute phase of alcohol exposure is associated with a decrease in V2 receptor mRNA and a down-regulation of V2 receptors. During chronic alcohol exposure, renal V2 receptor mRNA is up-regulated, indicating that increased synthesis of V2 receptors causes increased renal efficacy of vasopressin despite similar circulating vasopressin levels between alcohol-exposed and control rats. During the withdrawal phase, V2 receptor mRNA returns towaid normal levels, demonstrating that chronic alcohol-induced impairment of renal water excretion is reversible. Results suggest fliat alcohol-induced changes in renal responsiveness to vasopressin causes the pattern of diuresis, impaired water excretion, and recovery in the different phases of alcohol exposure.

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Section: Measurement Of Brain Vasopressin and Vasopressin Receptor Mrnasupporting

confidence: 88%

Vasopressin Regulation and Renal Fluid and Electrolyte Handling in Rat Model of Acute and Chronic Alcohol Exposure

Uyehara¹

2002

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“…For instance, chronic alcohol exposure has been shown to damage AVP-producing cells in adult animals and humans (19,13), and also morphological alterations had been reported in AVPproducing cells of the hypothalamus as a result of PE exposure (26). An alternative explanation may, however, involve the influence of the hypothalamic-pituitary-adrenal (HPA) axis.…”

Section: Discussionmentioning

confidence: 99%

“…fetal alcohol syndrome; vasopressin; plasma osmolality; thirst; vasopressin messenger ribonucleic acid; neurohypophysis CHRONIC CONSUMPTION of alcohol has been shown to significantly reduce the number of AVP-producing neurons in the rat supraoptic nucleus (19). More recently, chronic alcoholism in humans has also been shown to reduce AVP-producing neurons in a dose-related and time-dependent manner (13). Furthermore, AVP synthesis is reduced, as evidenced by reduced AVP mRNA in the hypothalamus of rats chronically administered alcohol, and there is a reduced AVP mRNA response to an osmotic stimulus in similarly treated rats (28).…”

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confidence: 99%

Prenatal exposure to ethanol causes partial diabetes insipidus in adult rats

Knee¹,

Sato²,

Uyehara³

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

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ethanol in adult rats and humans leads to reduced AVP-producing neurons, and prenatal ethanol (PE) exposure has been reported to cause changes in the morphology of AVP-producing cells in the suprachiasmatic nucleus of young rats. The present studies further characterize the effects of PE exposure on AVP in the young adult rat, its hypothalamic synthesis, pituitary storage, and osmotically stimulated release. Pregnant rats were fed a liquid diet with 35% of the calories from ethanol or a control liquid diet for days 7-22 of pregnancy. Water consumption and urine excretion rate were measured in the offspring at 60 -68 days of age. Subsequently, the offspring were infused with 5% NaCl at 0.05 ml ⅐ kg Ϫ1 ⅐ min Ϫ1 with plasma samples taken before and at three 40-min intervals during infusion for measurement of AVP and osmolality. Urine output and water intake were ϳ20% greater in PEexposed rats than in rats with no PE exposure, and female rats had a greater water intake than males. The relationship between plasma osmolality and AVP in PE-exposed rats was parallel to, but shifted to the right of, the control rats, indicating an increase in osmotic threshold for AVP release. Pituitary AVP was reduced by 13% and hypothalamic AVP mRNA content was reduced by 35% in PEexposed rats. Our data suggest that PE exposure can cause a permanent condition of a mild partial central diabetes insipidus. fetal alcohol syndrome; vasopressin; plasma osmolality; thirst; vasopressin messenger ribonucleic acid; neurohypophysis CHRONIC CONSUMPTION of alcohol has been shown to significantly reduce the number of AVP-producing neurons in the rat supraoptic nucleus (19). More recently, chronic alcoholism in humans has also been shown to reduce AVP-producing neurons in a dose-related and time-dependent manner (13). Furthermore, AVP synthesis is reduced, as evidenced by reduced AVP mRNA in the hypothalamus of rats chronically administered alcohol, and there is a reduced AVP mRNA response to an osmotic stimulus in similarly treated rats (28). Correspondingly, chronic exposure to alcohol in humans has been reported to reduce plasma levels of AVP (7, 14) and cerebrospinal fluid levels of AVP (23). Thus the AVP system would appear to be impaired by chronic alcohol exposure in adult rats and humans.Previous work has also demonstrated that brain weight is reduced in adult rats that were prenatally exposed to ethanol during the second half of pregnancy (29), and other studies have demonstrated a dose dependence of alcohol-induced brain damage and that some brain structures are more sensitive to the damage than others (21). More specifically, Rojas-Castaneda et al. (26) have reported evidence of morphological changes in the AVP-producing cells of the suprachiasmatic nucleus of 15-dayold rats that were prenatally exposed to ethanol. However, the number of AVP-producing cells was not observed to be significantly reduced in similar studies by the same group (27).Last, there is evidence that AVP systems are nearly fully developed during gestation. AVP has bee...

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“…Several studies have also reported significant noradrenergic cell loss in the locus coeruleus (2,5,60), although not all studies have found this loss (36). Recent studies have also indicated that certain neurons that contain the peptide vasopressin may be sensitive to chronic ethanol-induced neurotoxicity in both rats and humans (34,62). Damage to hypothalamic vasopressin and other peptide-containing neurons could disrupt a variety of hormone functions as well as daily rhythms that are important for healthy living.…”

mentioning

confidence: 99%