ArticleNeurochemical research2026
Neto2 Phosphorylation Promotes Neuronal Loss in KA-Induced Epileptic Rat Hippocampus by Upregulating the Interaction with GluK2.
Article in Neurochemical research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Kainate receptor, especially containing GluK2, hyperactivation plays an important role in epileptic excitotoxicity and neuronal damage, but the function of their key regulatory protein, neuropilin and tolloid-like protein 2 (Neto2), in this process is unclear. This study aimed to elucidate the role and molecular mechanism of Neto2 in regulating GluK2-mediate hippocampal neuronal damage. Our findings indicated that in kainic acid-induced epileptic rats, the level of phosphorylation in Neto2 and GluK2 elevated, and their interaction enhanced, accompanying the loss of neurons in the hippocampal cornu ammonis 3 / dentate gyrus regions. Remarkably, the calcium/calmodulin-dependent protein kinase II (CaMKII) inhibitor effectively reduced this protein phosphorylation and the interaction of the GluK2-Neto2. In addition, in HEK293T cells, the interference peptide (Tat-GluK2) targeting to the M3-S2 domain of GluK2 specifically blocked GluK2-Neto2 binding, and significantly reduced calcium influx. Importantly, CaMKII inhibitor and Tat-GluK2 both significantly improved the pathological status related to epilepsy including the abatement of hippocampal long-term potentiation, the reduced loss in hippocampal neurons, and the recovery of learning and memory. Collectively, our findings suggest that CaMKII-mediated increase in GluK2-Neto2 interaction is a primary driver of hippocampal neuronal loss in kainic acid-induced epileptic rats, targeting the GluK2-Neto2 binding domain may be a potential therapy-target for epilepsy.
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