Abnormal behavior and neurotransmissions of tenascin gene knockout mouse

Biochem Biophys Res Commun. 1996 Apr 5;221(1):151-6. doi: 10.1006/bbrc.1996.0561.

Abstract

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.

MeSH terms

  • Animals
  • Behavior, Animal / drug effects*
  • Dopamine Agents / metabolism
  • Dopamine Agents / pharmacology
  • Mice
  • Mice, Knockout
  • Motor Activity / drug effects
  • Neurotransmitter Agents / metabolism*
  • Radioligand Assay
  • Serotonin Agents / metabolism
  • Serotonin Agents / pharmacology
  • Tenascin / genetics*

Substances

  • Dopamine Agents
  • Neurotransmitter Agents
  • Serotonin Agents
  • Tenascin