Spatial learning induces neurotrophin receptor and synapsin I in the hippocampus

Citation
F. Gomez-pinilla et al., Spatial learning induces neurotrophin receptor and synapsin I in the hippocampus, BRAIN RES, 904(1), 2001, pp. 13-19
Citations number
27
Categorie Soggetti
Neurosciences & Behavoir
Journal title
BRAIN RESEARCH
ISSN journal
00068993 → ACNP
Volume
904
Issue
1
Year of publication
2001
Pages
13 - 19
Database
ISI
SICI code
0006-8993(20010615)904:1<13:SLINRA>2.0.ZU;2-S
Abstract
We report that rats learning a spatial memory task in the Morris water maze show elevated expression of the signal transduction receptor for BDNF and the synaptic associated protein synapsin I in the hippocampus. Nuclease pro tection assays showed maximal levels of TrkB and synapsin I mRNAs in the hi ppocampus by the time that asymptotic learning performance had been reached (Day 6). Increases in synapsin I mRNA were matched by changes in synapsin I protein as revealed by western blot analysis. Synapsin I is a downstream effector for the BDNF tyrosine kinase cascade pathway which has important r oles in synaptic remodeling and function. Therefore, parallel changes in Tr kB and synapsin I mRNAs suggest a role of the BDNF system in synaptic funct ion or adaptation. Levels of TrkB mRNA in the hippocampus were attenuated a fter learning acquisition (Day 20), but synapsin I mRNA was still elevated, suggesting that the BDNF system may participate in events secondary to lea rning, such as strengthening of neural circuits. TrkB and synapsin I mRNAs showed an increasing trend in the cerebellum of learning rats and no change s were observed in the caudal cerebral cortex. The selectivity of the chang es in trkB and synapsin I, affecting the hippocampus, is in agreement with the role of this structure in processing of spatial information. Behavioral regulation of neurotrophins may provide a molecular basis for the enhanced cognitive function associated with active lifestyles, and guide developmen t of strategies to promote neural healing after CNS injury or disease. (C) 2001 Elsevier Science B.V. All rights reserved.