Sodium Chloride and Dextrose Appetite of Un-Treated and Treated Adrenalectomized Rats

Richter, Curt P.; Bunch, George H.; Wooden, Howard E.

doi:10.1210/endo-29-1-115

Cited by 81 publications

(24 citation statements)

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“…Magnesium-deprived rats did not differ from controls in their saccharin intake in a prior study (Tordoff, 1992), but a reduced consumption of sweet compounds also accompanies deficiencies of sodium (Richter, 1941) and calcium (Tordoff and Rabusa, 1998). It is not clear why these mineral deficits should influence the intake of sweet solutions, although one possibility is that imbalances of magnesium and other ions interfere with the action of opioids that would normally mediate the ingestion of sweet compounds (Lujan et al, 1978;MarksKaufman et al, 1989;Kroin et al, 2000;Yamamoto et al, 2000).…”

Section: Discussionmentioning

confidence: 69%

Magnesium appetite in the rat

McCaughey

Tordoff

2002

Appetite

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Section: Discussionmentioning

confidence: 69%

Magnesium appetite in the rat

McCaughey

Tordoff

2002

Appetite

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“…Because after ADX some animals continue to produce corticosterone (CORT) from accessory tissues (Richter, 1941), and thereby may prevent degeneration (e.g. McNeill et al, 1991), 3 measures were used to determine efficacy of the ADX: saline versus water intake, weight gain, and determination of plasma CORT levels.…”

Section: Determination Of Efficacy Of Adrenalectomymentioning

confidence: 99%

Androgens Are Neuroprotective in the Dentate Gyrus of Adrenalectomized Female Rats

Frye

McCormick

2000

Stress

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Neuroprotective effects of androgens have not been well-characterized, but there is evidence that 5 alpha-androstane-3 alpha, 17 beta-diol (3 alpha-diol) has anti-seizure effects. To further examine androgens' neuroprotective effects, testosterone (T), dihydrotestosterone (DHT), 3 alpha-diol (1.0 mg/kg SC daily), or sesame oil vehicle was administered to adrenalectomized or sham-operated, young, female Long Evans rats (N = 52). After seven days, animals were perfused and trunk blood was collected for radioimmunoassay of plasma corticosterone and androgens. No pyknotic cells were seen in the dentate of the sham-operated animals or those animals that had incomplete adrenalectomies (n = 20); however, cresyl violet and TUNEL stains revealed pyknotic cells in the granule layer of the dentate gyrus of adrenalectomized rats (n = 28). Testosterone, DHT, or 3 alpha-diol significantly reduced the number of pyknotic cells in the dentate gyrus compared to vehicle administered, adrenalectomized rats. Steroid-administered animals had levels of T, DHT, or 3 alpha-diol within physiological concentrations. These findings suggest that T, DHT, or 3 alpha-diol may have neuroprotective effects via a common mechanism of action.

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“…Whether our results accurately reflect the change of GR mRNA in the long-term ADX rat forebrain is dependent on whether we rightly chose completely adrenalectomized rats, since many ADX rats do not in fact show hormone deficiency after chronic ADX (Richter, 1941;Sloviter et al, 1993). It is generally accepted that hippocampal granule cell loss, undetectable serum corticosterone and body weight loss are direct evidence for identifying the most hormone-deficient animals (Sloviter ef al., 1989(Sloviter ef al., , 1993McNeill er al., 1991).…”

Section: Discussionmentioning

confidence: 95%

Chronic Loss of Glucocorticoids Following Adrenalectomy Down‐regulates the Expression of Glucocorticoid Receptor mRNA in the Rat Forebrain

Yuri

Morimoto

et al. 1997

Eur J of Neuroscience

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In the negative feedback model, loss of endogenous glucocorticoids up-regulates the expression of glucocorticoid receptor mRNA. To elucidate further the effect of chronic lack of glucocorticoids on the expression of glucocorticoid receptor mRNA and protein, in situ hybridization and immunohistochemical methods were used to examine the long-term alteration of glucocorticoid receptor mRNA and its immunoreactivity in the forebrain of adrenalectomized rats. Constant lack of glucocorticoids resulted in marked decrease in the expression of glucocorticoid receptor mRNA and disappearance of glucocorticoid receptor immunoreactivity in many forebrain structures. In particular, in the suprapyramidal blade of the hippocampal granule cell layer and cerebral cortex, many cells showed almost no glucocorticoid receptor mRNA signals. These results suggest that long-term loss of endogenous glucocorticoids down-regulates the levels of glucocorticoid receptor mRNA, leading to reduction in the synthesis of glucocorticoid receptors in the rat forebrain. Therefore, the presence of endogenous glucocorticoids is vital to the continued expression of glucocorticoid receptor mRNA.

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Sodium Chloride and Dextrose Appetite of Un-Treated and Treated Adrenalectomized Rats

Cited by 81 publications

References 0 publications

Magnesium appetite in the rat

Magnesium appetite in the rat

Androgens Are Neuroprotective in the Dentate Gyrus of Adrenalectomized Female Rats

Chronic Loss of Glucocorticoids Following Adrenalectomy Down‐regulates the Expression of Glucocorticoid Receptor mRNA in the Rat Forebrain

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