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HIV, opiates, and enteric neuron dysfunction.

J J Galligan1

  • 1Neuroscience Program and the Department of Pharmacology and Toxicology, Michigan State University, East Lansing, MI, USA.

Neurogastroenterology and Motility
|March 31, 2015
PubMed
Summary
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Human immune deficiency virus (HIV) protein Tat enhances morphine

Area of Science:

  • Neurogastroenterology
  • Virology
  • Neuroimmunology

Background:

  • Human immune deficiency virus (HIV) targets CD4(+) T-lymphocytes, leading to immunosuppression.
  • HIV infection can cause central nervous system (CNS) dysfunction and enteric neural injury.
  • HIV-associated proteins, like Transactivator of transcription (Tat), contribute to neural injury.

Purpose of the Study:

  • To investigate the interaction between HIV Tat protein and morphine on enteric neurons.
  • To determine the effect of Tat and morphine on intestinal motility in vivo.

Main Methods:

  • Utilized a Tat-expressing transgenic mouse model.
  • Examined the effects on enteric neuron sodium channels and action potential generation.
  • Assessed alterations in propulsive intestinal motility.
Keywords:
Tatdiarrheaenteric nervous systementeric neuropathysodium channels

Related Experiment Videos

Main Results:

  • HIV Tat protein enhances the inhibitory effects of morphine on action potential generation in enteric neurons.
  • Tat potentiates morphine's inhibitory actions on intestinal propulsive motility.
  • Identified a specific interaction between Tat and morphine on Na(+) channels.

Conclusions:

  • HIV Tat protein plays a significant role in altering enteric neuron function and intestinal motility.
  • The interaction between Tat and morphine has implications for understanding HIV-associated diarrhea.
  • Findings may inform the use of opioid drugs in managing HIV-induced gastrointestinal issues.