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Anatomical evidence for glial activation after intrathecal lumbosacral HIV-1 glycoprotein; gp120-induced allodynia.

Holguin A, Armstrong CB, Twining CM, Milligan ED, Hansen MK, McGorry M, O’Connor KA, Quan N, Martin D, Lappi DA, Maier SF, Watkins LR (2000) Anatomical evidence for glial activation after intrathecal lumbosacral HIV-1 glycoprotein; gp120-induced allodynia. Neuroscience 2000 Abstracts 733.4. Society for Neuroscience, New Orleans, LA.

Summary: Intrathecal (IT) HIV-1 glycoprotein, gp120: (a) produces thermal hyperalgesia & low threshold mechanical allodynia, and (b) increases interleukin-1β (IL1β) protein levels in lumbosacral (LS) spinal cord tissue & surrounding cerebrospinal fluid (CSF). Activated astrocytes & microglia (glia) release IL1β in response to gp120, and IT IL1 receptor antagonist or glial metabolic inhibitors prevent IT gp120-induced allodynia and thermal hyperalgesia. We determined whether IT gp120 produces glial activation and increased expression of glial IL1β as well as allodynia. LS spinal cord was collected 1.5 & 3 hrs after IT gp120 injection & verification of allodynia for immunocytochemistry (ICC) & in situ analysis of IL1β protein & mRNA. ICC for glial activation markers was performed 4,8 & 18 hrs after IT gp120 in LS & cervical spinal cords, as upregulation of these markers is delayed relative to behavioral changes. IT gp120 produced allodynia & increased IL1β protein ICC expression in LS spinal white (astrocytes) & gray matter (cells not identifiable) at 1.5 but not 3 hrs after injection. Increases in in situ IL1β mRNA were not detected. RT-PCR analysis of IL1β mRNA is underway. Glial activation (ICC) was observed in LS tissue 8 & 18 hrs after IT gp120. We are examining IT gp120 allodynia & hyperalgesia after an IT microglia-specific toxin (Saporin-linked Mac-1 antibody) injection that disrupts glial function. ICC procedures will verify Mac-1 Saporin microglial toxicity.

Related Products: Mac-1-SAP mouse/human (Cat. #IT-06)

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