Methamphetamine-induced decrease in neural glucocorticoid receptors: relationship to monoamine levels

Lowy, Martin T.; Novotney, Susan

doi:10.1016/0006-8993(94)90647-5

Cited by 20 publications

(7 citation statements)

References 36 publications

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“…At neuroendocrine level AMPH increased in a dose-dependent manner plasma corticosterone levels but had no effects on circulating catecholamine levels. Effects of chronic AMPH on 5-HT and 5-HIAA contents in the hypothalamus are in agreement to previously reported for methamphetamine (MA) (15,16) or AMPH (13) and several observations suggest that serotonergic neurons are responsible of the corticosterone. Serotonin would stimulate CRF release from hypothalamic neurons producing an increase of plasma ACTH and corticosterone (13).…”

Section: Discussionsupporting

confidence: 80%

Hematological, immunological and neurochemical effects of chronic amphetamine treatment in male rats

Llorente-García

Abreu-González

González-Hernández

2009

J. Physiol. Biochem.

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In the present study, we have analyzed the effect of chronic amphetamine sulfate (AMPH) treatment on haematological, immunological and neurochemical parameters in the male rat. AMPH increased the total peripheral leukocyte count, and altered its differential counts, decreasing lymphocytes and increasing neutrophils. Flow cytometry study showed that the decline in circulating lymphocytes was caused by the loss of a particular lymphocyte subset, B-cell, which reduced both in percentage and in absolute number by 50%. T-cell population increased by 15% but not in absolute number, however there was no difference in either CD4+ or CD8+ T lymphocyte subsets between experimental groups. Neurochemically, AMPH reduced norepinephrine (NE) and serotonin (5-HT) contents in the hypothalamus and increased dopamine (DA) content in the striatum. Chronic AMPH increased in a dose-dependent manner serum corticosterone levels, had no effect on circulating catecholamines, reduced adrenal weights, and did not affect spleen weights although reduced their cellularities. These results show that chronic AMPH have important effects on immune function, particularly on humoral immune response because it reduced the circulating B cell population by half. In addition, AMPH plays an important role in the redistribution and trafficking of leukocytes, and both effects seem to be mediated by sympathetic innervation of the lymphoid organs.

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Section: Discussionsupporting

confidence: 80%

Hematological, immunological and neurochemical effects of chronic amphetamine treatment in male rats

Llorente-García

Abreu-González

González-Hernández

2009

J. Physiol. Biochem.

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“…Kabbaj et al [54] reported that chronic MA treatment in adult rats alters GR mRNA levels in the hippocampus in one strain (Fischer 344) but not another (Lewis). In another study, repeated administration of MA to Sprague-Dawley rats significantly decreased GR mRNA levels in the hippocampus and hypothalamus 6 days after treatment [55]. The absence of an effect of MA on GR immunoreactivity in the hippocampus and PVN reported here may therefore indicate that the genetic background might modulate sensitivity to MA.…”

Section: Discussionmentioning

confidence: 59%

Developmental Methamphetamine Exposure Results in Short- and Long-Term Alterations in Hypothalamic-Pituitary-Adrenal-Axis-Associated Proteins

Zuloaga¹,

Siegel²,

Acevedo³

et al. 2013

Dev Neurosci

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Developmental exposure to methamphetamine (MA) causes long-term behavioral and cognitive deficits. One pathway through which MA might induce these deficits is by elevating glucocorticoid levels. Glucocorticoid overexposure during brain development can lead to long-term disruptions in the hypothalamic-pituitary-adrenal (HPA) axis. These disruptions affect the regulation of stress responses and may contribute to behavioral and cognitive deficits reported following developmental MA exposure. Furthermore, alterations in proteins associated with the HPA axis, including vasopressin, oxytocin, and glucocorticoid receptors (GR), are correlated with disruptions in mood and cognition. We therefore hypothesized that early MA exposure will result in short- and long-term alterations in the expression of HPA axis-associated proteins. Male mice were treated with MA (5 mg/kg daily) or saline from postnatal day (P) 11 to P20. At P20 and P90, mice were perfused and their brains processed for vasopressin, oxytocin, and GR immunoreactivity within HPA axis-associated regions. At P20, there was a significant decrease in the number of vasopressin-immunoreactive cells and the area occupied by vasopressin immunoreactivity in the paraventricular nucleus (PVN) of MA-treated mice, but no difference in oxytocin immunoreactivity in the PVN, or GR immunoreactivity in the hippocampus or PVN. In the central nucleus of the amygdala, the area occupied by GR immunoreactivity was decreased by MA. At P90, the number of vasopressin-immunoreactive cells was still decreased, but the area occupied by vasopressin immunoreactivity no longer differed from saline controls. No effects of MA were found on oxytocin or GR immunoreactivity at P90. Thus developmental MA exposure has short- and long-term effects on vasopressin immunoreactivity and short-term effects on GR immunoreactivity.

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“…In animal studies, we have shown that the dentate gyrus and nucleus accumbens have a reduction in dendritic spines in adulthood when the animals were exposed to MA as neonates (Williams et al 2004a). Adult rats administered a neurotoxic regimen of MA have dose-dependent reductions in glucocorticoid receptor binding in the hippocampus and striatum but no changes in mineralocorticoid receptor binding (Lowy and Novotney 1994); comparable studies in the neonate are not available. The hippocampus has a rich supply of mineralocorticoid and glucocorticoid receptors that are important in inhibiting the stress response through negative feedback (Mizoguchi et al 2003).…”

Section: Discussionmentioning

confidence: 97%

Ontogeny of the adrenal response to (+)-methamphetamine in neonatal rats: The effect of prior drug exposure

Williams

Schaefer

Furay

et al. 2006

Stress

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We examined the ontogeny of the corticosterone response to (+)-methamphetamine in neonatal rats. In experiment-1, animals were injected with 10 mg/kg of (+)-methamphetamine or saline and plasma corticosterone levels were examined in separate groups 30 or 105 min later on postnatal day (P) 1, 3, 5, 7, 9, 11, 13, 15, 17, or 19. The adrenal response to methamphetamine was best described by a U-shaped function with the nadir of corticosterone release occurring between P7 and P13. Experiment-2 was similar except that the effect of four consecutive days of exposure to (+)-methamphetamine (four times daily at 2 h intervals with 10 mg/kg) was assessed with a single final dose early on the fifth day (i.e. P1-5, 3-7, 5-9, 7-11, 9-13, 11-15, 13-17, 15-19). The 30 min corticosterone response after multiple methamphetamine doses was augmented compared to single exposures, with the exception of the two earliest dosing intervals ending on P5 and P7, where the responses were lower. In addition, at 105 min, the levels of corticosterone were attenuated relative to a single drug administration. With the exception of animals receiving methamphetamine from P15 to P19, thymus weights were unaffected. The data demonstrate that (+)-methamphetamine is a robust activator of corticosterone release in developing animals and this release is extensively modified by age and previous drug exposure.

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Methamphetamine-induced decrease in neural glucocorticoid receptors: relationship to monoamine levels

Cited by 20 publications

References 36 publications

Hematological, immunological and neurochemical effects of chronic amphetamine treatment in male rats

Hematological, immunological and neurochemical effects of chronic amphetamine treatment in male rats

Developmental Methamphetamine Exposure Results in Short- and Long-Term Alterations in Hypothalamic-Pituitary-Adrenal-Axis-Associated Proteins

Ontogeny of the adrenal response to (+)-methamphetamine in neonatal rats: The effect of prior drug exposure

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