Quantitation of parvalbumin+ neurons and human immunodeficiency virus type 1 (HIV-1) regulatory gene expression in the HIV-1 transgenic rat: effects of vitamin A deficiency and morphine.
Quantitation of parvalbumin+ neurons and human immunodeficiency virus type 1 (HIV-1) regulatory gene expression in the HIV-1 transgenic rat: effects of vitamin A deficiency and morphine.
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DOI：
10.3109/13550280903555712
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发表时间：
2010-02
影响因子：
3.2
通讯作者：
Royal W
中科院分区：
文献类型：
--
作者：
Sultana S;Li H;Puche A;Jones O;Bryant JL;Royal W
Vitamin A (VA) deficiency in HIV infection has been associated with more progressive HIV disease which may be enhanced by opioid use. In these studies were examined the effects of VA deficiency and morphine on frontal cortex neuronal numbers in the HIV-1 transgenic (Tg) rat. These studies showed that totals numbers of neurons were similar for rats on the VA deficient diet as for rats on the normal diet and these numbers were not affected by treatment with morphine. In contrast, numbers of neurons that expressed the calcium-binding protein parvalbumin, which is a marker interneurons that express the inhibitory neurotransmitter gamma-amino butyric acid (GABAergic neurons) were decreased for wild-type (Wt) rats on the VA deficient diet and for Wt rats treated with morphine. In addition, parvalbumin+ neurons were also decreased for Tg rats on a normal diet but increased to normal levels when these animals were placed on the VA deficient diet and treated with morphine. Analysis of expression of HIV regulatory proteins vif, vpr, and nef in frontal cortex and adjacent subcortical white matter showed that expression of these genes was increased in the Tg rat on the normal diet as compared to a control housekeeping gene. Morphine treatment suppressed expression of the HIV genes; however, expression was increased by VA deficiency and by morphine plus deficiency. These studies therefore suggest that VA deficiency, opioid and HIV infection alone and in combination may either suppress neuronal metabolic activity or induce metabolic stress, resulting in the observed changes in levels of parvalbumin expression. The specific mechanisms that underlie these effects require further study.
