Synapto-protective effect of lithium on HIV-1 Tat-induced synapse loss in rat hippocampal cultures

Human immunodeficiency virus type I (HIV-1) infection of the CNS produces synapse loss which correlates with cognitive decline in patients with HIV-associated neurocognitive disorders (HAND). Lithium is mood stabilizer of unknown mechanism used to treat bipolar disorder and is known to exhibit neuro...

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Bibliographic Details
Published in:Animal cells and systems 2022, 26(1), , pp.1-9
Main Authors: Hong, Namgue, Park, Jeong-Soo, Kim, Hee Jung
Format: Article
Language:English
Subjects:
HIV-1 Tat
Lithium
neuronal cell death
PSD95
synapse loss
생물학
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Summary:Human immunodeficiency virus type I (HIV-1) infection of the CNS produces synapse loss which correlates with cognitive decline in patients with HIV-associated neurocognitive disorders (HAND). Lithium is mood stabilizer of unknown mechanism used to treat bipolar disorder and is known to exhibit neuroprotective properties. Here, we studied the effects of lithium on HIV-1 Tat-induced synapses between rat hippocampal neurons. The number of synapses was quantified to detect clusters of the scaffold protein postsynaptic density 95 (PSD95) which is clustered at glutamatergic synapses on cultured rat hippocampal neurons in vitro. Lithium protected synapses from HIV-1 Tat-induced synapse loss and subsequent neuronal death. This synaptic protection was prevented by both the activation of NMDA receptor leading to intracellular signaling and the regulatory pathway of lithium including inositol depletion and glycogen synthase kinase-3β (GSK-3β). These results suggest that mood stabilizers might be effective drugs to treat neurodegenerative disorders including HAND.
ISSN:1976-8354
2151-2485
DOI:10.1080/19768354.2021.2018044