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BDNF Influence on Adult Terminal Axon Sprouting after Partial Deafferentation
Beatriz Benítez-Temiño1, Rosendo G Hernández1, Rosa R de la Cruz1
1Departamento de Fisiología, Facultad de Biología, Universidad de Sevilla, 41012 Seville, Spain.
Brain-derived neurotrophic factor (BDNF) promotes axon sprouting in the oculomotor system. Exogenous BDNF application restored synaptic coverage after partial deafferentation and stimulated growth in intact animals.
Area of Science:
- Neuroscience
- Molecular Biology
- Ophthalmology
Background:
- Brain-derived neurotrophic factor (BDNF) is crucial for neuronal survival, development, and synaptic plasticity.
- BDNF is present in the oculomotor system, regulating motoneuron afferent composition and firing patterns.
- BDNF expression and axonal sprouting increase after partial deafferentation of extraocular motoneurons.
Purpose of the Study:
- To investigate the active role of BDNF in promoting axon sprouting after partial deafferentation of medial rectus motoneurons.
- To determine if BDNF can stimulate axon sprouting in the absence of neuronal lesions.
Main Methods:
- Partial deafferentation of medial rectus motoneurons was induced by transecting the ascending tract of Deiters.
- Exogenous BDNF was injected into the medial rectus muscle.
- Axon terminal sprouting was assessed using calretinin immunostaining.
- Experiments were also conducted on intact animals without lesions.
Main Results:
- Exogenous BDNF significantly stimulated terminal axon growth, fully restoring synaptic coverage around motoneuron somata.
- Calretinin staining in the neuropil increased beyond control levels after BDNF treatment.
- BDNF demonstrated the ability to stimulate axonal sprouting even in intact nervous systems.
Conclusions:
- BDNF plays an active role in the plastic adaptations occurring after partial deafferentation of oculomotor neurons.
- BDNF can promote axonal sprouting and synaptic regeneration in the central nervous system.
- Targeted BDNF application may hold therapeutic potential for conditions involving neuronal damage or loss of synaptic function.
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