Neuronal pentraxin 2 is required for facilitating excitatory synaptic inputs onto spinal neurons involved in pruriceptive transmission in a model of chronic itch.
Central nervous system-specific tamoxifen-induced and hippocampus-specific deletion demonstrate that the effects of Nptx2 deletion on anxiety-like behavior are hippocampus-specific and not developmentally related. In addition mice with Nptx2 deletion exhibit decreased hippocampal cell proliferation and increased stress-induced neuronal activity.
findings indicate that Narp contributes to the antidepressant action of Electroconvulsive Therapy and implicate the ability of Electroconvulsive Shock to induce dendritic arborization of differentiating granule cells as a relevant step in eliciting this response.
Early postnatal NPTX2(-/-)/NPTXR(-/-) mice exhibit delayed circuit maturation with a prolonged critical period permissive for giant depolarizing potentials
the results of this study indicated that Narp released from mPFC neurons plays a key role in mediating synaptic changes underlying instrumental reinforcer devaluation.
Narp prominently accumulated at excitatory synapses on parvalbumin-expressing interneurons propose that Narp recruits AMPARs at excitatory synapses onto interneurons to rebalance network excitation/inhibition dynamics following increased circuit activity
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