Differential spine loss and regrowth of striatal neurons following multiple forms of deafferentation: A Golgi study

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-μm 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.