ArticleThe Journal of biological chemistry2026
Prenatal cannabinoid exposure alters excitation-inhibition balance through glutamate and GABA receptor-mediated signaling.
Article in The Journal of biological chemistry, 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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15 authors.
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Abstract
The growing perception that marijuana is safe during pregnancy has led to a marked increase in prenatal cannabis use, raising concerns about its long-term effects on brain development and cognition. This study investigated the consequences of prenatal delta-9-tetrahydrocannabinol (THC) exposure on hippocampal circuit function, synaptic plasticity, and memory in adolescent offspring using a rodent model. We found that prenatal THC exposure resulted in persistent deficits in hippocampal-dependent memory and significant disruptions in synaptic plasticity, including impaired long-term potentiation and increased long-term depression. Electrophysiological analyses revealed reduced AMPAR-mediated synaptic transmission and a shift toward increased inhibitory signaling, suggesting an excitation/inhibition (E/I) imbalance in the hippocampus. These functional changes were accompanied by selective downregulation of postsynaptic glutamatergic proteins (GluA1, GluN2A, GluN2B, and PSD95), while presynaptic glutamate markers remained unchanged. Notably, immunohistochemical and anatomical analyses demonstrated region-specific reorganization of inhibitory networks, including altered distribution and colocalization of cannabinoid 1 receptor (CB
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