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Title: Neurochemical and behavioral deficits consequent to expression of a dominant negative EphA5 receptor.

Authors: Halladay, A K; Tessarollo, L; Zhou, R; Wagner, G C

Published In Brain Res Mol Brain Res, (2004 Apr 7)

Abstract: The Eph family tyrosine kinase receptors and their ligands have been linked to axon guidance and topographic mapping of the developing central nervous system. More specifically, the EphA5 receptor has been shown to play a role in development of hippocamposeptal, retinotectal and thalamocortical projections. Recently, a line of transgenic mice was developed which expresses a truncated EphA5 receptor lacking a functional tyrosine kinase domain. In a previous study, axonal tracing revealed that medial hippocampal axons in this strain projected laterally and ventrally away from their normal target area. In the current study, both transgenic and wild-type controls were evaluated in unconditioned (rotorod and locomotor activity) and conditioned (water maze and active avoidance) behavior tasks which tested hippocampal and striatal functioning. Compared to controls, the transgenic strain did not show differences in rotorod motor activity but did show a transient deficit in spatial navigation ability and a consistent impairment in active avoidance. The dominant-negative mutant receptor also resulted in a decrease in striatal dopamine and serotonin concentrations with no change in hippocampal monoamines. Collectively, these data suggest that animals expressing a truncated EphA5 receptor show deficits related to striatal functioning.

PubMed ID: 15046871 Exiting the NIEHS site

MeSH Terms: Animals; Avoidance Learning/physiology; Brain Chemistry/genetics*; Brain/metabolism*; Brain/physiopathology; Corpus Striatum/metabolism; Corpus Striatum/physiopathology; Dopamine/metabolism*; Down-Regulation/genetics; Female; Genes, Dominant/genetics*; Hippocampus/metabolism; Hippocampus/physiopathology; Learning Disorders/genetics; Learning Disorders/metabolism; Learning Disorders/physiopathology; Male; Maze Learning/physiology; Memory Disorders/genetics; Memory Disorders/metabolism; Memory Disorders/physiopathology; Mice; Mice, Transgenic; Motor Activity/genetics; Mutation/genetics; Receptor, EphA5/biosynthesis*; Receptor, EphA5/genetics; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Serotonin/metabolism*

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