Cortical-striatal synaptic dysfunction, including enhanced toxic signaling by extrasynaptic N-methyl-d-aspartate receptors (eNMDARs), precedes neurodegeneration in Huntington disease (HD).A previous study showed Activin A, whose transcription is upregulated by calcium influx via synaptic NMDARs, suppresses eNMDAR signaling.Therefore, we examined the role of 2012 honda civic si coilovers Activin A in the YAC128 HD mouse model, comparing it to wild-type controls.We found decreased Activin A secretion in YAC128 cortical-striatal co-cultures, while Activin bar-vac 7/somnus A overexpression in this model rescued altered eNMDAR expression.
Striatal overexpression of Activin A in vivo improved motor learning on the rotarod task, and normalized striatal neuronal eNMDAR-mediated currents, membrane capacitance and spontaneous excitatory postsynaptic current frequency in the YAC128 mice.These results support the therapeutic potential of Activin A signaling and targeting eNMDARs to restore striatal neuronal health and ameliorate behavioral deficits in HD.