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Differential spine loss and regrowth of striatal neurons following multiple forms of deafferentation: a Golgi study
H W Cheng1, J A Rafols, H G Goshgarian
1Division of Neurogerontology, Andrus Gerontology Center, University of Southern California, Los Angeles 90089-0191, USA.
Abstract:
Golgi-Cox method and morphometric analyses were used to study the plasticity of striatal medium spiny I neurons in 6-month-old C57BL/6N mice after unilateral or bilateral lesion of the cerebral cortex or combined lesions of the ipsilateral cerebral cortex and intralaminar thalamus. In adult mouse, unilateral lesions of the cerebral cortex did not result in a net gain or loss of linear dendritic length in a randomly selected population of striatal medium spiny I neurons. In addition, there was a well-defined time course of striatal spine loss and replacement occurring after a unilateral cortical lesion. By day 3 postlesion the average 20-microm dendritic segment had lost 30% of the unlesioned control spine value, reached its nadir, lost 45.5%, at 10 days postlesion, and recovered to 80% of unlesioned control levels by 20 days postlesion. The recovery of spines was blocked by a secondary lesion on the contralateral cortex but not on the ipsilateral intralaminar thalamus. These data suggest that striatal medium spiny I neurons of adult mice have a remarkable capacity for plasticity and reactive synaptogenesis following a decortication. The recovery of spine density is primarily induced by axonal sprouting of survival homologous afferent fibers from the contralateral cortex.
Insights
Adult mouse striatal neurons show remarkable plasticity after cortical lesions. Spine density recovers due to contralateral cortical input, highlighting reactive synaptogenesis in the striatum.
Area of Science:
- Neuroscience
- Neuroplasticity
- Synaptogenesis
Background:
- Striatal medium spiny neurons (MSNs) are crucial for motor control and reward processing.
- Understanding MSN plasticity is key to deciphering brain repair mechanisms.
Purpose of the Study:
- To investigate the plasticity of striatal MSNs following cortical lesions in adult mice.
- To determine the time course and influencing factors of spine dynamics post-lesion.
Main Methods:
- Golgi-Cox staining and morphometric analysis were employed.
- Unilateral and bilateral cortical lesions, as well as combined lesions, were induced in C57BL/6N mice.
- Dendritic spine density was quantified over time post-lesion.
Main Results:
- Unilateral cortical lesions did not alter overall dendritic length but induced significant spine loss and subsequent recovery.
- Spine density decreased by 45.5% at 10 days post-lesion, recovering to 80% by 20 days.
- Contralateral cortical lesions blocked spine recovery, while ipsilateral thalamic lesions did not.
Conclusions:
- Adult mouse striatal MSNs exhibit substantial plasticity and reactive synaptogenesis after decortication.
- Axonal sprouting from contralateral cortical afferents is the primary driver of spine recovery.
- This plasticity demonstrates the brain's capacity for structural reorganization following injury.