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HIV-1 Tat-induced changes in synaptically-driven network activity adapt during prolonged exposure.

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The HIV-1 Tat protein disrupts neural network activity, causing aberrant brain function linked to neurocognitive disorders. However, neural networks adapt to Tat exposure, potentially offering a protective response.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Virology

Background:

  • HIV-associated neurocognitive disorders (HAND) affect nearly half of HIV patients.
  • The HIV-1 transactivator of transcription (Tat) protein is implicated in HAND pathogenesis.
  • Mechanisms underlying Tat's neurotoxicity are not fully understood.

Purpose of the Study:

  • To investigate the effects of HIV-1 Tat protein on spontaneous synaptic activity in cultured rat hippocampal neurons.
  • To elucidate the role of the low-density lipoprotein receptor-related protein (LRP) in Tat-induced network alterations.

Main Methods:

  • Utilized fura-2-based Ca(2+) imaging to monitor intracellular calcium levels.
  • Employed whole-cell patch-clamp recording to assess neuronal electrical activity.
  • Cultured networked rat hippocampal neurons for in vitro experiments.

Main Results:

  • Tat exposure led to decreased frequency and increased duration of spontaneous action potential bursts and Ca(2+) spikes.
  • These Tat-induced network changes were dependent on the low-density lipoprotein receptor-related protein (LRP).
  • Neural network activity adapted to control levels during prolonged (24 h) Tat exposure.

Conclusions:

  • HIV-1 Tat protein induces aberrant network activity in hippocampal neurons via LRP.
  • Neural network adaptation to sustained Tat exposure may represent a neuroprotective mechanism.
  • Altered network excitability and adaptation are potential contributors to HAND and seizure disorders.