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Publication : Abnormal behavior and neurotransmissions of tenascin gene knockout mouse.

First Author  Fukamauchi F Year  1996
Journal  Biochem Biophys Res Commun Volume  221
Issue  1 Pages  151-6
PubMed ID  8660327 Mgi Jnum  J:32517
Mgi Id  MGI:80011 Doi  10.1006/bbrc.1996.0561
Citation  Fukamauchi F, et al. (1996) Abnormal behavior and neurotransmissions of tenascin gene knockout mouse. Biochem Biophys Res Commun 221(1):151-6
abstractText  To examine the role of tenascin (TN) in vivo, we have produced mice in which the TN gene is inactivated. In behavioral studies, TN-knockout mice showed abnormal behavior such as hyperlocomotion and poor swimming ability. Biochemical analysis revealed that serotonin (5-HT) and dopamine (DA) transmission was decreased in the cerebral cortex, the hippocampus, or the striatum of TN-knockout mouse brain. The intraperitoneal administration of the DA receptor agonist, LY171555 (0.5 mg/kg, BW), inhibited the hyperlocomotion, and swimming behavior was transiently improved by the treatment with the 5-HT receptor agonist, 1-(4-iodo-2,5-dimethoxyphenyl)-2-aminopropane hydrochloride. These findings suggest that TN may play an important role in neurotransmissions related to behavior.
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