Journal
JOURNAL OF NEUROVIROLOGY
Volume 22, Issue 6, Pages 866-870Publisher
SPRINGER
DOI: 10.1007/s13365-016-0464-1
Keywords
beta-Adrenergic receptor; mu-Opioid receptor; Splice variant; Central nervous system; HIV-associated neurocognitive disorders; HIV encephalitis
Categories
Funding
- National Institutes of Health (NIH)-National Institute on Drug Abuse (NIDA) [F32 DA033898, R01 DA036154]
- NIH through the National Institute of Mental Health (NIMH)
- National Institute of Neurological Disorders and Stroke (NINDS) [U01 MH083501, R24 MH59724]
- Texas NeuroAIDS Research Center [U01 MH083507, R24 NS45491]
- National Neurological AIDS Bank [5U01 MH083500, NS38841]
- California NeuroAIDS Tissue Network [U01 MH083506, R24 MH59745]
- Statistics and Data Coordinating Center [U01 MH083545, N01 MH32002]
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We previously reported that mRNA expression of the unique alternatively spliced OPRM1 isoform mu-opioid receptor-1K (MOR-1K), which exhibits excitatory cellular signaling, is elevated in HIV-infected individuals with combined neurocognitive impairment (NCI) and HIV encephalitis (HIVE). It has recently been shown that the beta(2)-adrenergic receptor (beta(2)-AR) chaperones MOR-1K, normally localized intracellularly, to the cell surface. Here, we found mRNA expression of the adrenoceptor beta 2 (ADRB2) gene is also elevated in NCI-HIVE individuals, as well as that beta(2)-AR protein expression is elevated in HIV-1-infected primary human astrocytes treated with morphine, and discuss the implications for MOR-1K subcellular localization in this condition.
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