Impact of acute inflammation on spinal motoneuron synaptic plasticity following ventral root avulsion.
BACKGROUND
Ventral root avulsion is a proximal nerve root lesion in which ventral motor nerve rootlets are torn from surface of the spinal cord, resulting in extensive death of motoneurons. It has been previously shown that if such lesioning is performed in an animal with experimental autoimmune encephalomyelitis (EAE), a significant number of motoneurons can be rescued despite an intense inflammatory reaction. This rescue effect has been attributed to production of a number of neurotrophic factors by invading T cells. Synaptological changes may be involved in neuronal degeneration, and a better understanding of the role of these changes may be of importance for developing new strategies to promote neuronal survival. The objective of the present work was to evaluate neuronal survival, astroglial reaction and synaptic input changes in spinal cord anterior horn motor nuclei after ventral root avulsion in animals with EAE, both during peak disease and after remission.


METHODS
Lewis rats were subjected to unilateral avulsion of lumbar ventral roots (VRA) and divided into three groups: VRA control, VRA at peak of EAE, and VRA during EAE remission. The animals were sacrificed and their lumbar spinal cords processed for immunohistochemistry, transmission electron microscopy, and motoneuron counting.


RESULTS
The results indicate a reduction in astroglial reaction, a maintenance of microglial reactivity, and increases in synaptic covering of, and survival of, motoneurons in the VRA+EAE group as compared to VRA alone.


CONCLUSIONS
The present findings indicate that CNS inflammation may directly influence synaptic plasticity as well as the stability of neuronal networks, positively influencing the survival of lesioned neurons.
Barbizan
Roberta
R
Department of Anatomy, Cell Biology, Physiology and Biophysics, Institute of Biology, University of Campinas (UNICAMP), Campinas, SP, Brazil.
Oliveira
Alexandre L R
AL
D000818:Animals; D002452:Cell Count; D002470:Cell Survival / Q000502:physiology; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000473:pathology; D005260:Female; D005620:Freund's Adjuvant; D006168:Guinea Pigs; D007150:Immunohistochemistry; D007249:Inflammation / Q000473:pathology*; D046529:Microscopy, Electron, Transmission; D009046:Motor Neurons / Q000473:pathology* / Q000648:ultrastructure; D004676:Myelin Basic Protein / Q000378:metabolism; D009473:Neuronal Plasticity / Q000502:physiology*; D011843:Radiculopathy / Q000473:pathology*; D051381:Rats; D011917:Rats, Inbred Lew; D013116:Spinal Cord / Q000473:pathology* / Q000648:ultrastructure; D013569:Synapses / Q000473:pathology* / Q000648:ultrastructure; D013601:T-Lymphocytes / Q000502:physiology
D004676:Myelin Basic Protein; D005620:Freund's Adjuvant