Effects of experimental autoimmune encephalomyelitis on properties and function of the mouse major pelvic ganglion neurons
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Experimental autoimmune encephalomyelitis (EAE) serves as a valuable mouse model for studying the pathophysiology of multiple sclerosis (MS), a chronic autoimmune disease characterized by inflammation and demyelination of the central nervous system (CNS). While EAE mimics many aspects of MS, its effects on the lower urinary tract (LUT) remain poorly understood. This study investigated alterations in lower urinary tract output, excitability of major pelvic ganglion (MPG) neurons, and expression profiles of MPG neurons in EAE. Adult female SJL/J mice were induced with EAE, and clinical scores were monitored daily. Real-time quantitative polymerase chain reaction (qPCR) was employed to analyze gene expression in MPGs, while functional bladder output and electrophysiological measurements of MPG neurons were conducted to evaluate lower urinary tract output and MPG neuron excitability. The results revealed significant changes in lower urinary tract output, with decreased urine output observed in EAE mice compared to controls. Furthermore, MPG neuron excitability was altered, with changes in passive membrane properties and action potential characteristics observed in EAE-induced animals. Analysis of gene expression profiles in MPG neurons revealed significant alterations in the mRNA levels of ion channels and receptors implicated in bladder control mechanisms. These findings provide valuable insights into the pathophysiological mechanisms underlying lower urinary tract dysfunction in EAE, suggesting potential targets for therapeutic intervention in MS-related bladder dysfunction. Further research is warranted to elucidate the complex interplay between immune-mediated CNS damage and LUT dysfunction in MS and related conditions.
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Ph. D.