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The alpha7-nicotinic receptor contributes to gp120-induced neurotoxicity: implications in HIV-associated neurocognitive disorders
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The alpha7-nicotinic receptor contributes to gp120-induced neurotoxicity: implications in HIV-associated neurocognitive disorders
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Journal Article
The alpha7-nicotinic receptor contributes to gp120-induced neurotoxicity: implications in HIV-associated neurocognitive disorders
2018
Overview
Currently, there are no specific therapies to treat HIV-1 associated neurocognitive disorders (HAND). The HIV-1 envelope, gp120, induces neuropathological changes similar to those in HAND patients; furthermore, it triggers an upregulation of the α7-nicotinic acetylcholine receptor (α7-nAChR), facilitating intracellular calcium overload and neuronal cell death. Using a gp120
IIIB
-transgenic mouse (gp120-tgm) model, we demonstrate that α7-nAChRs are upregulated on striatal neurons. Activation of α7-nAChRs leads to an increase in both intracellular calcium and percentage of apoptotic cells, which can be abrogated by antagonizing the receptor, suggesting a role for α7-nAChRs in gp120-induced neurotoxicity. Moreover, we demonstrate for the first time that gp120-tgm have learning deficiencies on a striatum-dependent behavioral task. They also show locomotor deficiencies, which improved with α7-nAChR antagonists, further supporting a role for this receptor in gp120-induced neurotoxicity. Together, these results uncover a new mechanism through which gp120-induced modulation of α7-nAChRs in the striatum can contribute to HAND development.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 13/51
/ 14/19
/ 64/60
/ 82/80
/ 96/63
/ Acetylcholine receptors (nicotinic)
/ alpha7 Nicotinic Acetylcholine Receptor - metabolism
/ Animals
/ Calcium
/ Corpus Striatum - metabolism
/ Female
/ HIV Envelope Protein gp120 - metabolism
/ Humanities and Social Sciences
/ Male
/ Mice
/ Neurocognitive Disorders - metabolism
/ Neurotoxicity Syndromes - metabolism
/ Receptors, Nicotinic - metabolism
/ Rodents
/ Science
