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Craniofacial Res

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For instance, in preclinical models, long-term ketamine exposure increases the expression of GABA receptor subunits in the prefrontal cortex while simultaneously reducing glutamate receptor subunits, impairing synaptic signaling and cognitive function ( Ketamine also downregulates brain-derived neurotrophic factor, particularly in the hippocampus, exacerbating deficits in synaptic plasticity and cognitive functions

One of these mechanisms is through the activation of transcription factors, such as nuclear factor erythroid 2 (NRF2), which promotes the expression of genes involved in oxidative stress response