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Inflammation is implicated in the pathogenesis of cardiovascular disease. However,
whether and how inflammation contributes to autonomic dysfunction remain poorly characterized.
We previously demonstrated that IFNγ causes retraction of dendritic processes in cultures
of sympathetic neurons dissociated from rat superior cervical ganglia. Based on these
observations, we hypothesized that IFNγ similarly disrupts connectivity of postganglionic
sympathetic neurons in vivo. To test this hypothesis, young adult male Sprague Dawley rats were administered
purified recombinant rat IFNγ to at levels reported during acute or chronic neuroinflammatory
states. Relative to vehicle controls, dendritic arborization and synapse density were
significantly reduced in sympathetic neurons of SCG from IFNγ-treated animals. IFNγ-induced
loss of receptive surface in the SCG occurred in the absence of reduced neuronal cell
viability or decreased trophic interactions between SCG neurons and target tissues.
Decreased dendritic complexity and synapse loss was coincident with impaired ganglionic
neurotransmission as evidenced by an attenuated baroreflex in animals treated with
IFNγ. Based on these observations we propose a novel pathogenic mechanism of neuroinflammatory
cardiovascular disease in which IFNγ disrupts neuronal connectivity via selective
retraction of dendrites of autonomic neurons, leading to decreased sympathetic excitability.
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