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Exercise induces BDNF and synapsin I to specific hippocampal subfields.
Shoshanna Vaynman1, Zhe Ying, Fernando Gómez-Pinilla
1Department of Physiological Science, UCLA, Los Angeles, California 90095, USA.
Journal of Neuroscience Research
|April 14, 2004
Summary
Exercise increases brain-derived neurotrophic factor (BDNF) and synapsin I in the hippocampus, impacting neural plasticity. This study reveals BDNF
Area of Science:
- Neuroscience
- Molecular Biology
- Exercise Physiology
Background:
- Brain-derived neurotrophic factor (BDNF) is crucial for neuronal plasticity and survival.
- Synapsin I is involved in synaptic vesicle regulation and neuronal function.
Purpose of the Study:
- To investigate the causal relationship between BDNF and exercise-induced synapsin I expression in the hippocampus.
- To map the distribution of BDNF and synapsin I in the rodent hippocampus following exercise.
Main Methods:
- A novel microsphere injection method was used to block BDNF's action via its tyrosine kinase (Trk) receptor.
- Real-time TaqMan RT-PCR was employed to quantify synapsin I mRNA levels.
- Quantitative immunohistochemistry was used to analyze protein distribution.
Main Results:
- Exercise-induced synapsin I mRNA levels were causally linked to BDNF.
- BDNF and synapsin I increased in the CA3 stratum lucidum and dentate gyrus.
- Synapsin I levels increased in the CA1 stratum radiatum and stratum lacunosum moleculare, independent of BDNF.
Conclusions:
- Exercise promotes plasticity in specific hippocampal circuits.
- BDNF plays a role in regulating synapsin I expression in response to exercise.
- The regulation of synapsin I by BDNF may be spatially restricted within the hippocampus.