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The Effects of HIV‐1 Gp120 on the Puncta Count and Expression of α5‐Containing GABA A Receptors in Cultured Rat Hippocampal Neurons
Author(s) -
Jo Adrienne,
Green Matthew,
Thayer Stanley
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.552.8
Subject(s) - microglia , hippocampal formation , neurotoxicity , receptor , neuroscience , immunocytochemistry , gabaa receptor , biology , neurocognitive , microbiology and biotechnology , medicine , pharmacology , immunology , cognition , endocrinology , toxicity , inflammation
Approximately 50% of the >30 million people worldwide affected by human immunodeficiency virus‐1 (HIV‐1) suffer from cognitive impairments known as HIV‐1‐associated neurocognitive disorders (HAND). HIV‐1 can infect microglia, leading to the release of toxic proteins, such as envelope glycoprotein 120 (gp120 IIIB ), which causes neurotoxicity and synaptodendritic damage. Gp120 is known to induce the release of interleukin‐1β (IL‐1β), a cytokine released by microglia. Previous work shows that IL‐1β increases the function of α5‐containing GABA A receptors (α5‐GABA A ‐Rs), which lowers cell excitability and may contribute to cognitive impairments. Thus, we tested whether gp120 would increase the expression of protein clusters of α5‐GABA A ‐Rs in primary hippocampal cultures derived from embryonic day 17 Sprague Dawley® rats. Immunocytochemistry was performed to examine the localization of α5‐GABA A ‐Rs relative to microtubule‐associated protein 2 (MAP2) immunoreactivity. Based on previous electrophysiology experiments on α5‐GABA A ‐Rs, we hypothesize that gp120 increases α5 puncta. Preliminary data demonstrates that gp120 leads to a trending increase in α5 puncta, which might explain the increased neuronal inhibition and decreased cell excitability seen in vitro. Altered excitability may lead to the cognitive impairments found in HAND patients. Thus, inhibition of α5‐GABA A ‐Rs may be a novel target for the treatment of HAND. Support or Funding Information This investigation was supported by DA07304 and the National Institute on Drug Abuse of the National Institutes of Health under Award Number 1R25DA039074‐01A1 through the Summer Research Program for Diversity Students in PharmacoNeuroImmunology (PNI) under Life Sciences Summer Undergraduate Research Programs. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .