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MHC class I upregulation is not sufficient to rescue neonatal alpha motoneurons after peripheral axotomy.
Brain Res. 2008 Oct 31; 1238:23-30.BR

Abstract

Associated with neuronal death, profound synaptic changes occur in the spinal cord during the apoptotic process triggered after axotomy in neonatal rats. With respect to this, the major histocompatibility complex of class I (MHC class I) has recently emerged as a new mechanism related to synaptic stripping and plasticity. The present study investigated the impact of upregulating MHC class I expression by treatment with beta interferon (beta INF) on motoneuron survival, synaptic plasticity and astrogliosis after neonatal sciatic nerve injury. P2 rats were subjected to unilateral axotomy followed by three days of beta INF treatment. The results were analyzed by counting Nissl stained motoneurons, immunohistochemistry (anti-synaptophysin, MHC class I, GFAP and Iba-1) and transmission electron microscopy. INF treatment induced an increased expression of MHC class I, which resulted in a stronger synaptic elimination process in the spinal cord, as seen by the synaptophysin labeling. GFAP and Iba-1 upregulation were not significantly altered by the INF treatment, displaying the same degree of enhanced reactivity as compared to the placebo group. The ultrastructural analysis showed that, apart from the overall reduction of inputs in the neuropil, no statistical differences were present when comparing the INF and placebo treated animals. Also, neuronal survival was not altered by cytokine administration. The present results provide evidence that MHC class I upregulation after neonatal injury does not change the fate of lesioned motoneurons. In this way, the lack of neurotrophic support may cause broader synaptic loss, which superposes the more subtle effects of the upregulation of MHC class I.

Authors+Show Affiliations

Department of Anatomy, Institute of Biology, University of Campinas, Campinas, SP, Brazil.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

18775685

Citation

Payés, Ana Carolina Linardi Munguia, et al. "MHC Class I Upregulation Is Not Sufficient to Rescue Neonatal Alpha Motoneurons After Peripheral Axotomy." Brain Research, vol. 1238, 2008, pp. 23-30.
Payés AC, Zanon RG, Pierucci A, et al. MHC class I upregulation is not sufficient to rescue neonatal alpha motoneurons after peripheral axotomy. Brain Res. 2008;1238:23-30.
Payés, A. C., Zanon, R. G., Pierucci, A., & Oliveira, A. L. (2008). MHC class I upregulation is not sufficient to rescue neonatal alpha motoneurons after peripheral axotomy. Brain Research, 1238, 23-30. https://doi.org/10.1016/j.brainres.2008.08.032
Payés AC, et al. MHC Class I Upregulation Is Not Sufficient to Rescue Neonatal Alpha Motoneurons After Peripheral Axotomy. Brain Res. 2008 Oct 31;1238:23-30. PubMed PMID: 18775685.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - MHC class I upregulation is not sufficient to rescue neonatal alpha motoneurons after peripheral axotomy. AU - Payés,Ana Carolina Linardi Munguia, AU - Zanon,Renata Graciele, AU - Pierucci,Amauri, AU - Oliveira,Alexandre L R, Y1 - 2008/08/23/ PY - 2008/07/04/received PY - 2008/08/13/revised PY - 2008/08/13/accepted PY - 2008/9/9/pubmed PY - 2009/2/10/medline PY - 2008/9/9/entrez SP - 23 EP - 30 JF - Brain research JO - Brain Res. VL - 1238 N2 - Associated with neuronal death, profound synaptic changes occur in the spinal cord during the apoptotic process triggered after axotomy in neonatal rats. With respect to this, the major histocompatibility complex of class I (MHC class I) has recently emerged as a new mechanism related to synaptic stripping and plasticity. The present study investigated the impact of upregulating MHC class I expression by treatment with beta interferon (beta INF) on motoneuron survival, synaptic plasticity and astrogliosis after neonatal sciatic nerve injury. P2 rats were subjected to unilateral axotomy followed by three days of beta INF treatment. The results were analyzed by counting Nissl stained motoneurons, immunohistochemistry (anti-synaptophysin, MHC class I, GFAP and Iba-1) and transmission electron microscopy. INF treatment induced an increased expression of MHC class I, which resulted in a stronger synaptic elimination process in the spinal cord, as seen by the synaptophysin labeling. GFAP and Iba-1 upregulation were not significantly altered by the INF treatment, displaying the same degree of enhanced reactivity as compared to the placebo group. The ultrastructural analysis showed that, apart from the overall reduction of inputs in the neuropil, no statistical differences were present when comparing the INF and placebo treated animals. Also, neuronal survival was not altered by cytokine administration. The present results provide evidence that MHC class I upregulation after neonatal injury does not change the fate of lesioned motoneurons. In this way, the lack of neurotrophic support may cause broader synaptic loss, which superposes the more subtle effects of the upregulation of MHC class I. SN - 1872-6240 UR - https://www.unboundmedicine.com/medline/citation/18775685/MHC_class_I_upregulation_is_not_sufficient_to_rescue_neonatal_alpha_motoneurons_after_peripheral_axotomy_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-8993(08)02040-4 DB - PRIME DP - Unbound Medicine ER -