PLASTICITY OF SYNAPSES IN THE RAT NEOSTRIATUM AFTER UNILATERAL LESIONOF THE NIGROSTRIATAL DOPAMINERGIC PATHWAY

In the 6-hydroxydopamine model of Parkinson's disease in the rat, ther e is a significant reduction in the number of dendritic spines on the principal projection neurons in the neostriatum, presumably attributab le to loss of the nigrostriatal dopamine input. These spines invariabl y receive input from terminals forming asymmetric synapses that origin ate mainly from the cortex. The object of the present study was to det ermine the fate of those terminals after the loss of dendritic spines. Unbiased estimates of synaptic density and absolute numbers of synaps es in a defined volume of the neostriatum were made using the ''disect or'' and Cavalieri techniques. Numerical synaptic density of asymmetri c synaptic contacts was 17% lower in the neostriatum deprived of dopam ine innervation and, in absolute terms, there were 3 billion (19%) few er contacts. The numerical density of a subpopulation of asymmetric co ntacts on dendritic spines that have complex or perforated synaptic sp ecializations and normally make up 9% of the asymmetric population was 44% higher on the experimental side. Asymmetric synapses were found t o be enriched in glutamate using postembedding immunogold labeling. Th e present observations demonstrate that the loss of spines previously reported after 6-hydroxydopamine lesions is accompanied by a loss of a symmetric synapses rather than by the movement of synapses from spines to other postsynaptic targets. The study also demonstrates that there is an increase in complex synaptic interactions that have been implic ated in synaptic plasticity in other regions of the CNS after experime ntal manipulations.