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MHC Class I, β2 microglobulin, and the INF‐γ receptor are upregulated in aged motoneurons

During aging, spinal cord motoneurons show characteristic changes including the loss of afferent boutons, a selective process that associates with gliosis and behavioral motor impairment. Evidence suggests that the major histocompatibility complex Class I (MHC I) system may be involved in synaptic plasticity of neurons during development and regeneration. In search of a mechanism governing senescent changes in synaptic connectivity, we report evidence for increased expression of MHC I and β2 microglobulin (β2M) in motoneurons and glial‐like profiles of 30‐month‐old rats. The regulatory signal(s) for MHC I expression in normal neurons remains unresolved but among tentative molecules are cytokines such as interferon‐γ (INF‐γ) and tumor necrosis factor α (TNF‐α). Interestingly, aged motoneurons, overlapping with those showing increased levels of MHC I, contained increased levels of INF‐γ receptor message. INF‐γ mRNA was detected at low levels in most (8/9) of the aged spinal cords but only infrequently (2/9) in young adult spinal cords; however, the cellular localization of INF‐γ mRNA could not be determined. Our data also indicates that TNF‐α is upregulated in the senescent spinal cord but that TNF‐α immunoreactive protein does not associate with motoneurons. We report evidence for an increased expression of MHC I and β2M in senescent spinal motoneurons and discuss the possibility that this regulation associates with INF‐γ or changes in neurotrophin signaling and neuron activity in senescence. © 2004 Wiley‐Liss, Inc.