Neuroscience
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Recent studies have demonstrated that Camk2b expression is modified in neuropsychiatric illnesses and potentially affects synaptic plasticity. However, the molecular events arising from Camk2b dysregulation are not fully elucidated and need to be comprehensively explored. In the present study, we first induced over-expression and under-expression of Camk2b in cultured rat hippocampal neurons through transfection with lentivirus plasmids. ⋯ Through cross comparison, several candidate target proteins regulated directly by Camk2b were revealed. Further network and immunoblot analyses demonstrated that Mapk3 could be an important linker and Camk2b-Mapk3 might serve as a new potential pathway affecting the expression of synaptic proteins in hippocampal neurons. Collectively, the present results offer a new comprehension of the regulatory molecular mechanism of Camk2b and thereby increase our understanding of Camk2b-mediated synaptogenesis in synaptic plasticity.
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We studied the effects of inflammatory pain on working memory and correlated the pain effects with changes in dendritic spine density and glutamate signaling in the medial prefrontal cortex (mPFC) of male and female mice. Injection of Complete Freund's Adjuvant (CFA) into the hind paw modeled inflammatory pain. The CFA equally decreased the mechanical thresholds in both sexes. ⋯ Furthermore, while the CFA injection decreased the expression of the glutamate transporter VGlut1 on the soma of mPFC neurons in both sexes, the decrease was sex dependent. We concluded that inflammatory pain, which increases sensory input into the mPFC neurons, may impair working memory by altering the glutamate signaling. The glutamate deficit that develops as a result of the pain is more pronounced in male mice in comparison to female mice.