ArticleFrontiers in cell and developmental biology2026
Nauclea officinalis extract rescues working memory deficits in adolescent maternal immune activation offspring by restoring cholinergic signaling.
Article in Frontiers in cell and developmental biology, 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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Abstract
Objective: Maternal immune activation (MIA) is a key risk factor for schizophrenia-related cognitive deficits, linked to prefrontal cholinergic dysfunction. Nauclea officinalis extract (NOE) possesses documented anti-inflammatory and neuroprotective properties, but its effects on MIA-induced cognitive and neuronal dysfunctions are unknown. This study aimed to investigate whether NOE ameliorates MIA-induced working memory deficits by modulating infralimbic medial prefrontal cortex (IL-mPFC) cholinergic signaling and neuronal activity. Methods: Using a poly (I:C)-induced MIA rat model, adolescent offspring were treated with NOE (5, 10 and 20 mg/kg). Behavioral tests, Results: NOE dose-dependently attenuated MIA-induced neuroinflammation (IL-1β, IL-6, TNF-α) in the IL-mPFC. It restored acetylcholine (ACh) levels, reduced acetylcholinesterase (AChE) activity, but did not alter M1/M3 receptor expression. NOE (20 mg/kg) significantly improved 30-s delay working memory performance, an effect blocked by the muscarinic receptor antagonist scopolamine (SCO) and mimicked by the AChE inhibitor physostigmine (PHY). Electrophysiologically, NOE rescued MIA-impaired long-term potentiation (LTP) and paired-pulse ratio (PPR), and enhanced delay-related firing of IL pyramidal neurons. These restorative effects were similarly replicated by PHY and antagonized by SCO. Conclusion: NOE alleviates MIA-induced working memory deficits by reducing neuroinflammation and, crucially, by functionally potentiating cholinergic transmission in the IL-mPFC. The findings highlight the IL cholinergic system as a critical therapeutic target and position NOE as a promising multi-target agent for cognitive impairments in neurodevelopmental disorders.
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