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Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive cognitive decline. Pathologic accumulation of soluble amyloid- β  (A β ) oligomers impairs synaptic plasticity and causes epileptic seizures, both of which contribute to cognitive dysfunction in AD. However, whether seizures could regulate A β -induced synaptic weakening remains unclear. Here we show that a single episode of electroconvulsive seizures (ECS) increased protein expression of membrane-associated STriatal-Enriched protein tyrosine Phosphatase (STEP 61 ) and decreased tyrosine-phosphorylation of its substrates N-methyl D-aspartate receptor (NMDAR) subunit GluN2B and extracellular signal regulated kinase 1/2 (ERK1/2) in the rat hippocampus at 2 days following a single ECS. Interestingly, a significant decrease in ERK1/2 expression and an increase in APP and A β  levels were observed at 3-4 days following a single ECS when STEP 61  level returned to the baseline. Given that pathologic levels of A β  increase STEP 61  activity and STEP 61 -mediated dephosphorylation of GluN2B and ERK1/2 leads to NMDAR internalization and ERK1/2 inactivation, we propose that upregulation of STEP 61  and downregulation of GluN2B and ERK1/2 phosphorylation mediate compensatory weakening of synaptic strength in response to acute enhancement of hippocampal network activity, whereas delayed decrease in ERK1/2 expression and increase in APP and A β  expression may contribute to the maintenance of this synaptic weakening.

Seizure-Induced Regulations of Amyloid-β, STEP61, and STEP61Substrates Involved in Hippocampal Synaptic Plasticity

Seizure-Induced Regulations of Amyloid-β, STEP₆₁, and STEP₆₁Substrates Involved in Hippocampal Synaptic Plasticity