Event Abstract Back to Event Immune molecules in neurons and glia – implications for synaptic plasticity after nerve lesion Staffan Cullheim1* 1 Karolinska institutet, Department of Neuroscience, Sweden There is accumulating evidence that immune molecules are used by neurons and glia in the CNS to modulate synaptic function and plasticity during development and after nerve injury. Spinal motoneurons in rat and mouse constitutively express mRNAs for the major histocompatibility complex (MHC) class I and beta2-microglobulin (beta2m), which is necessary for surface expression of MHC class I. One classical response to lesion of motor axons is the shedding of synapses from the cell surface of severed motoneurons. We have shown that mice lacking the beta2m gene display a more extensive synaptic elimination from the cell bodies of axotomized spinal motoneurons compared with wild-type (WT) mice. This surplus elimination is directed towards synaptic terminals with a putative inhibitory function. (Oliveira et al., Proc Natl Acad Sci USA 101:17843-17848. 2004). The complement system is a part of the innate immune system. Mice lacking complement proteins C1q or C3 exhibit large defects in the organisation of synapses in the development of the retinogeniculate pathway, resembling the picture seen in the absence of MHC class I (Stevens et al., Cell 131:1164-1178. 2007). We therefore studied the synaptic elimination from axotomized motoneurons in mice deficient in C3. In these mice the elimination was much less prominent than in WT animals, which lends support to the idea that complement proteins are ‘tagging’ synapses to be eliminated. Astrocytes and, in particular, microglia have been attributed important roles in the synaptic elimination response after axon lesion. In mice, mRNAs for classical MHC class I (H2-Kb/Db) was upregulated in both motoneurons and microglia after lesion, while non-classical MHC class I (H2-T22) was upregulated only in motoneurons. In contrast, C1q mRNA was upregulated solely in activated microglia, with no neuronal expression. The general pattern of activation, as revealed by GFAP and Iba 1 immunoreactivity for astrocytes and microglia, respectively, did not reveal any major differences between WT animals and mice with gene deletions for MHC class I or complement proteins. We conclude that the effects exerted by the immune molecules are very specific, probably involves glia but are not mirrored by the general activation pattern of glia. Keywords: MHC-class proteins, motoneuron, nerve lesion, plasticity Conference: Karolinska Institutet 200 years anniversary Symposium on Traumatic Injuries in the Nervous System, Stockholm, Sweden, 15 Sep - 16 Sep, 2010. Presentation Type: Presentation Topic: Traumatic Injuries in the Nervous System Citation: Cullheim S (2010). Immune molecules in neurons and glia – implications for synaptic plasticity after nerve lesion. Front. Neurol. Conference Abstract: Karolinska Institutet 200 years anniversary Symposium on Traumatic Injuries in the Nervous System. doi: 10.3389/conf.fneur.2010.56.00018 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 10 Sep 2010; Published Online: 21 Sep 2010. * Correspondence: Prof. Staffan Cullheim, Karolinska institutet, Department of Neuroscience, Stockholm, Sweden, Staffan.Cullheim@ki.se Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Staffan Cullheim Google Staffan Cullheim Google Scholar Staffan Cullheim PubMed Staffan Cullheim Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.
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