Neuroplastin deletion in glutamatergic neurons impairs selective brain functions and calcium regulation: implication for cognitive deterioration.

ABSTRACT: The cell adhesion molecule neuroplastin (Np) is a novel candidate to influence human intelligence. Np-deficient mice display complex cognitive deficits and reduced levels of Plasma Membrane Ca²⁺ ATPases (PMCAs), an essential regulator of the intracellular Ca²⁺ concentration ([iCa²⁺]) and neuronal activity. We show abundant expression and conserved cellular and molecular features of Np in glutamatergic neurons in human hippocampal-cortical pathways as characterized for the rodent brain. In Nptn ^{lox/loxEmx1Cre} mice, glutamatergic neuron-selective Np ablation resulted in behavioral deficits indicating hippocampal, striatal, and sensorimotor dysfunction paralleled by highly altered activities in hippocampal CA1 area, sensorimotor cortex layers I-III/

SUBMITTER: Herrera-Molina R 

PROVIDER: S-EPMC5544750 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature