Enhancement of hippocampal LTP, reference memory and sensorimotor gating in mutant mice lacking a telencephalon-specific cell adhesion molecule

Telencephalin (TLCN) is a cell adhesion molecule selectively expressed in t he telencephalon of the mammalian brain. The mutant mice lacking TLCN had n o detectable abnormalities in their neural development and synaptic structu res. Ablation of TLCN increased the hippocampal long-term potentiation and its saturation level. The TLCN mutation selectively enhanced the performanc e of the radial maze and water-finding tasks, learning tasks with appetitiv e reinforcers, but not the contextual fear conditioning and Morris water ma ze tasks with aversive stimuli for conditioning. Furthermore, the TLCN muta nt mice showed an increase of prepulse inhibition of the acoustic startle r esponse. These results suggest that TLCN is a determinant of the dynamic ra nge of synaptic plasticity and plays roles in reward-motivated learning and memory and sensorimotor gating.