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HIV and opiates dysregulate K⁺- Cl^- cotransporter 2 (KCC2) to cause GABAergic dysfunction in primary human neurons and Tat-transgenic mice.

ABSTRACT: Approximately half of people infected with HIV (PWH) exhibit HIV-associated neuropathology (neuroHIV), even when receiving combined antiretroviral therapy. Opiate use is widespread in PWH and exacerbates neuroHIV. While neurons themselves are not infected, they incur sublethal damage and GABAergic disruption is selectively vulnerable to viral and inflammatory factors released by infected/affected glia. Here, we demonstrate diminished K⁺-Cl^- cotransporter 2 (KCC2) levels in primary human neurons after exposure to HIV-1 or HIV-1 proteins ± morphine. Resulting disruption of GABA_AR-mediated hyperpolarization/inhibition was shown using genetically-encoded voltage (Archon1) and calcium (GCaMP6f) indicators. The HIV proteins Tat (acting through NMDA receptors) and

SUBMITTER: Barbour AJ

PROVIDER: S-EPMC7685173 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature

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Dataset Information

HIV and opiates dysregulate K⁺- Cl^- cotransporter 2 (KCC2) to cause GABAergic dysfunction in primary human neurons and Tat-transgenic mice.

OmicsDI is part of the ELIXIR infrastructure

Tweets

Dataset Information

HIV and opiates dysregulate K+- Cl- cotransporter 2 (KCC2) to cause GABAergic dysfunction in primary human neurons and Tat-transgenic mice.

OmicsDI is part of the ELIXIR infrastructure

Tweets

HIV and opiates dysregulate K⁺- Cl^- cotransporter 2 (KCC2) to cause GABAergic dysfunction in primary human neurons and Tat-transgenic mice.