Memantine prevents memory consolidation failure induced by soluble beta amyloid in rats.

摘要: It has been well documented that β-amyloid peptide accumulation and aggregation in the brain plays a crucial role pathophysiology of Alzheimer’s disease (AD). However, new orientation amyloid cascade hypothesis evidenced soluble forms (sAβ) are involved Aβ-induced cognitive impairment cause rapid disruption synaptic mechanisms underlying memory. The primary aim this study was to elucidate effects sAβ, acutely injected intracerebrally (i.c.v., 4 µM), on short term long memory young adult male rats, by using novel object recognition task. Glutamatergic receptors have proposed as mediating effect Aβ plasticity Thus, we also investigated sAβ prefrontal cortex (PFC) glutamate release specific contribution N-methyl-D-aspartate (NMDA) receptor modulation administration parameters evaluated. We found single i.c.v. injection 2h before testing did not alter ability rats differentiate between familiar object, test, while it able negatively affect consolidation/retrieval Moreover, significant increase levels PFC treated with 2 h earlier. Interestingly, deficit induced reversed NMDA-receptor antagonist, memantine (5 mg/kg i.p), administered immediately after familiarization trial (T1). On contrary, 30 min T1 trial, rescue impairment. Taken together, our results suggest an acute interferes such sAβ-induced indicates involvement glutamatergic system, proposing NMDA inhibition might prevent or lead recovery early