Yamazaki Y, Hamaue N, Sumikawa K (2002) Nicotine compensates for the loss of cholinergic function to enhance long-term potentiation induction. Brain Res 946(1):148-152. doi: 10.1016/s0006-8993(02)02935-9 PMID: 12133604
Objective: Investigate the mechanisms of how cholinergic lesions impair the induction of long-term potentiation (LTP) and how nicotine can reverse the effects.
Summary: LTP in the hippocampal CA1 region is involved in learning and memory and its induction depends on the activation of N-methyl-D-aspartate receptors (NMDARs). Nicotine is shown to reverse memory deficits caused by lesioning of the cholinergic system, but the mechanism for this observation is unknown. The authors use 192-IgG-SAP to induce cholinergic lesioning, which impairs LTP induction. The authors suggest the compensatory action of nicotine is a via enhancement of NMDAR responses mediated by nicotine-induced disinhibition of pyramidal cells.
Usage: 2 ug of 192-IgG-Saporin (Cat. IT-01) were injected into the lateral ventricle of rats.
Related Products: 192-IgG-SAP (Cat. #IT-01)