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

• Published in: The European journal of neuroscience Vol. 13; no. 1; pp. 179 - 189
• Main Authors: Nakamura, Kazuhiro, Manabe, Toshiya, Watanabe, Masahiko, Mamiya, Takayoshi, Ichikawa, Ryoichi, Kiyama, Yuji, Sanbo, Makoto, Yagi, Takeshi, Inoue, Yoshiro, Nabeshima, Toshitaka, Mori, Hisashi, Mishina, Masayoshi
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Science Ltd 01.01.2001; Wiley Subscription Services, Inc
• Subjects: Animals; Brain - pathology; Chimera; Hippocampus - physiology; learning; Long-Term Potentiation - physiology; Maze Learning - physiology; Membrane Glycoproteins - deficiency; Membrane Glycoproteins - genetics; Memory - physiology; Mice; Mice, Inbred Strains; Mice, Knockout - genetics; Motor Activity - physiology; Nerve Tissue Proteins - deficiency; Nerve Tissue Proteins - genetics; Neural Inhibition - physiology; Neuronal Plasticity; prepulse inhibition; Reference Values; Reflex, Startle - physiology; Sensation - physiology; Synapses - physiology; synaptic plasticity; telencephalin
• ISSN: 0953-816X; 1460-9568
• DOI: 10.1046/j.0953-816X.2000.01366.x

Telencephalin (TLCN) is a cell adhesion molecule selectively expressed in the telencephalon of the mammalian brain. The mutant mice lacking TLCN had no detectable abnormalities in their neural development and synaptic structures. Ablation of TLCN increased the hippocampal long‐term potentiation and its saturation level. The TLCN mutation selectively enhanced the performance of the radial maze and water‐finding tasks, learning tasks with appetitive reinforcers, but not the contextual fear conditioning and Morris water maze tasks with aversive stimuli for conditioning. Furthermore, the TLCN mutant mice showed an increase of prepulse inhibition of the acoustic startle response. These results suggest that TLCN is a determinant of the dynamic range of synaptic plasticity and plays roles in reward‐motivated learning and memory and sensorimotor gating.