Plasticity of afferent fibers to striatal neurons bearing D1 dopamine receptors in Parkinson's disease
β Scribed by Marie-Paule Muriel; Yves Agid; Etienne Hirsch
- Publisher
- John Wiley and Sons
- Year
- 2001
- Tongue
- English
- Weight
- 135 KB
- Volume
- 16
- Category
- Article
- ISSN
- 0885-3185
- DOI
- 10.1002/mds.1103
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β¦ Synopsis
Abstract
The loss of dopaminergic neurons in the substantia nigra provokes a plasticity of corticostriatal synapses in Parkinson's disease (PD). The corticostriatal pathway nevertheless makes synapses with neurons bearing D1 dopamine receptors (D1R) and/or D2 dopamine receptors. At the ultrastructural level, we analyzed the morphological characteristics of synapses formed by afferent fibers making asymmetric contacts with the dendritic spines of neurons identified by D1R immunoreactivity, in the striatum of control subjects and PD patients. A quantitative analysis of the morphological characteristics of the synapses and of the number of perforated synapses (considered to be very active) was performed. In PD, a 50% increase in the number of perforated synapses making contact with D1R dendritic spines was observed, whereas no change in the number of perforated synapses on nonβD1R spines was observed. The change in the number of perforated synapses on D1R dendrites was associated with a slight but nonsignificant increase in the surface area of the corticostriatal afferent fibers and the surface of the mitochondria in these fibers (+29.0% and +34.6%, respectively). This suggests a hyperactivity of corticostriatal fibers in contact with D1Rβbearing neurons of the direct pathway in the basal ganglia circuitry. Since stimulation of the direct pathway is thought to alleviate the clinical symptoms of PD, this suggests that the differences observed may be involved in compensatory mechanisms. Β© 2001 Movement Disorder Society.
π SIMILAR VOLUMES
The time course of the loss in presynaptic dopamine transporters (DAT) and of the increase in postsynaptic dopamine D2 receptors (D2R) was studied in a rat model of Parkinson's disease. For this, in vitro autoradiographic experiments were performed in the striatum using (E)-N-(3-iodoprop-2-enyl)-2be