Peripheral nerve lesions are followed by an increase in expression of immune molecules, such as the Major Histocompatibility Complex Class I (MHC-I). The MHC-I upregulation is directly related to the synaptic plasticity process, glial cell activity modulation and functional recovery. Knockout mice for the MHC-I obligatory chain ²2 microglobulin (²2m), show increased reduction in synaptic density and deficit in axonal regeneration after peripheral lesion. There are other receptors that share MHC-I domains, such as paired-immunoglobulin receptors (PIR-A and B) and Killer-cell immunoglobulin-like receptors (KIR), specifically KIR3DL2. Such receptors have an inhibitory role in axonal growth after lesion. In the same way, Toll-like receptors 2 and 4 (TLR 2 and TLR 4) are activated in the spinal cord after lesion, relating TLR 4 to mediate synaptic stability and TLR 2, synaptic elimination. The present project aims to evaluate the synaptic plasticity process and functional recovery after ventral root crush (VRC) in knockout mice for ²2m, TLR 4 and TLR 2, correlating morphological findings with glial reactivity and expression of proteins related to the signaling pathways involving immune system components.
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