ABSTRACT
Microglia-mediated synaptic plasticity after CNS injury varies depending on injury severity, but the mechanisms that adjust synaptic plasticity according to injury differences are largely unknown. This study investigates differential actions of microglia on essential spinal motor synaptic circuits following different kinds of nerve injuries. Following nerve transection, microglia and C-C chemokine receptor type 2 signaling permanently remove Ia axons and synapses from the ventral horn, degrading proprioceptive feedback during motor actions and abolishing stretch reflexes. However, Ia synapses and reflexes recover after milder injuries (nerve crush). These different outcomes are related to the length of microglia activation, being longer after nerve cuts, with slower motor-axon regeneration and extended expression of colony-stimulating factor type 1 in injured motoneurons. Prolonged microglia activation induces CCL2 expression, and Ia synapses recover after ccl2 is deleted from microglia. Thus, microglia Ia synapse removal requires the induction of specific microglia phenotypes modulated by nerve regeneration efficiencies. However, synapse preservation was not sufficient to restore the stretch-reflex function.
Subject(s)
Axons , Microglia , Nerve Regeneration , Receptors, Chemokine , Signal TransductionABSTRACT
A 39-year-old Caucasian woman presented to the emergency department with worsening abdominal pain, localised to the right lower quadrant, and diarrhoea for a week. Stool tested negative for Clostridium difficile, Giardialamblia and Cryptosporidium Following an abdominal CT, she was diagnosed with appendicitis. The histological preparation, along with the acute inflammatory changes of the vermiform appendix, was notable for clusters of small, basophilic spherical bodies most consistent with Cryptosporidium parvum infection. Ultimately, the patient was diagnosed with appendicitis secondary to C. parvum infection. This is exceedingly rare and only one other case has been previously reported.
