Interneuron NMDA receptors change the gear of motor learning in the cerebellar machine

Fekete, Ádám; Wang, Lu-Yang

doi:10.1113/jp277376

Cited by 1 publication

(1 citation statement)

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“… 63 , 64 , 65 Glutamate is an excitatory neurotransmitter, a major ligand for NMDA receptors in the central nervous system, and has a key role in synaptic plasticity. It has been shown that MIA affects the expression and function of NMDA receptors in the developing brain of the offspring, 66 and that inhibition or over‐activation of NMDA receptors can cause neurotoxic effects and induce apoptosis, 67 , 68 , 69 , 70 while moderate activation of NMDA receptors has been shown to benefit learning and memory functions. 71 In two different developmental stages of the hippocampus, we analyzed three NMDA receptor subunits and found increased expression of NMDAR1, NMDAR2A and NMDAR2B subunits mainly in adulthood not in adolescence.…”

Section: Discussionmentioning

confidence: 99%

Impaired erythropoietin‐producing hepatocellular B receptors signaling in the prefrontal cortex and hippocampus following maternal immune activation in male rats

Shao

Cai

Chen

et al. 2023

Genes Brain and Behavior

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An environmental risk factor for schizophrenia (SZ) is maternal infection, which exerts longstanding effects on the neurodevelopment of offspring. Accumulating evidence suggests that synaptic disturbances may contribute to the pathology of the disease, but the underlying molecular mechanisms remain poorly understood. Erythropoietin‐producing hepatocellular B (EphB) receptor signaling plays an important role in synaptic plasticity by regulating the formation and maturation of dendritic spines and regulating excitatory neurotransmission. We examined whether EphB receptors and downstream associated proteins are susceptible to environmental risk factors implicated in the etiology of synaptic disturbances in SZ. Using an established rodent model, which closely imitates the characteristics of SZ, we observed the behavioral performance and synaptic structure of male offspring in adolescence and early adulthood. We then analyzed the expression of EphB receptors and associated proteins in the prefrontal cortex and hippocampus. Maternal immune activation offspring showed significantly progressive cognitive impairment and pre‐pulse inhibition deficits together with an increase in the expression of EphB2 receptors and NMDA receptor subunits. We also found changes in EphB receptor downstream signaling, in particular, a decrease in phospho‐cofilin levels which may explain the reduced dendritic spine density. Besides, we found that the AMPA glutamate, another glutamate ionic receptor associated with cofilin, decreased significantly in maternal immune activation offspring. Thus, alterations in EphB signaling induced by immune activation during pregnancy may underlie disruptions in synaptic plasticity and function in the prefrontal cortex and hippocampus associated with behavioral and cognitive impairment. These findings may provide insight into the mechanisms underlying SZ.

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