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  4. Prior pathology in the basal forebrain cholinergic system predisposes to inflammation-induced working memory deficits: Reconciling inflammatory and cholinergic hypotheses of delirium.

Prior pathology in the basal forebrain cholinergic system predisposes to inflammation-induced working memory deficits: Reconciling inflammatory and cholinergic hypotheses of delirium.

Field RH, Gossen A, Cunningham C (2012) Prior pathology in the basal forebrain cholinergic system predisposes to inflammation-induced working memory deficits: Reconciling inflammatory and cholinergic hypotheses of delirium. J Neurosci 32(18):6288-6294. doi: 10.1523/JNEUROSCI.4673-11.2012

Summary: The authors lesioned the basal forebrain of mice with 0.08 μg or 0.4 μg icv injections of mu p75-SAP (Cat. #IT-16) to establish an early dementia-associated cholinergic loss model. The mice were then challenged with systemic inflammation using low-dose lipopolysaccharide (LPS). The mu p75-SAP lesion left hippocampal-dependent reference and working memory relatively intact. LPS-induced inflammation created acute working memory deficits; an aceytlcholinesterase inhibitor protected against this deficit.

Related Products: mu p75-SAP (Cat. #IT-16)

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