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This research aims to clarify how HIV-1 gp120 influences nociceptive signaling at synapses involving NMDA receptors.

HIV-1 gp120 induces nociceptive hypersensitivity via α2δ-1–bound NMDA receptors at primary afferent–excitatory neuron synapses

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This research aims to clarify how HIV-1 gp120 influences nociceptive signaling at synapses involving NMDA receptors.
Intrathecal gp120 administration in male and female mice to assess synaptic NMDAR activity.
Assessment of α2δ-1 and GluN1 expression in dorsal root ganglion and spinal cord.
Use of gabapentin and C-terminal peptide for inhibiting α2δ-1 interactions.
Gp120 increased presynaptic and postsynaptic NMDAR hyperactivity, enhancing nociceptive sensitivity.
Blocking α2δ-1 or disrupting α2δ-1–NMDAR interactions reversed gp120-induced hypersensitivity.
Genetic deletion of Cacna2d1 significantly reduced nociceptive hypersensitivity caused by gp120.

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Randomized trial examines gp120's role in enhancing nociceptive hypersensitivity, suggesting new treatment pathways for HIV-related chronic pain.

Gautam et al. (2026) studied this question.

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Randomized trial examines gp120's role in enhancing nociceptive hypersensitivity, suggesting new treatment pathways for HIV-related chronic pain.