TNFα Levels and Macrophages Expression Reflect an Inflammatory Potential of Trigeminal Ganglia in a Mouse Model of Familial Hemiplegic Migraine

• DOI: 10.1371/journal.pone.0052394
• Publication Date: 2013-01-12T00:06:37Z
• Authors: Alessia Franceschini; Sandra Vilotti; Michel D. Ferrari; Arn M. J. M. van ...; Andrea Nistri; Elsa Fabbretti
• Keywords: Familial hemiplegic migraine

Latent changes in trigeminal ganglion structure and function resembling inflammatory conditions may predispose to acute attacks of migraine pain. Here, we investigated whether, sensory ganglia, cytokines such as TNFα might contribute a local phenotype transgenic knock-in (KI) mouse model familial hemiplegic type-1 (FHM-1). To this end, macrophage occurrence cytokine expression ganglia were compared between wild type (WT) R192Q mutant CaV2.1 Ca2+ channel (R192Q KI) mice, genetic FHM-1. Cellular molecular characterization was performed using combination confocal immunohistochemistry assays. With respect WT, KI enriched activated macrophages suggested by their morphology immunoreactivity the markers Iba1, CD11b, ED1. constitutively expressed higher mRNA levels IL1β, IL6, IL10 MCP-1 chemokine. Consistent with report that is major factor sensitize observed that, following an reaction evoked LPS injection, significantly WT ganglia. Our data suggest complex cellular environment could support new tissue compatible neuroinflammatory profile. We propose FHM patients, condition pain pathophysiology through release soluble mediators, including TNFα, modulate crosstalk neurons resident glia, underlying process neuronal sensitisation.