D.C. and S.R. contributed equally to this work.
Adaptations of glutamatergic synapses in the striatum contribute to recovery from cerebellar damage
Article first published online: 11 APR 2008
© The Authors (2008). Journal Compilation © Federation of European Neuroscience Societies and Blackwell Publishing Ltd
European Journal of Neuroscience
Volume 27, Issue 8, pages 2188–2196, April 2008
How to Cite
Centonze, D., Rossi, S., Bartolo, P. D., De Chiara, V., Foti, F., Musella, A., Mataluni, G., Rossi, S., Bernardi, G., Koch, G. and Petrosini, L. (2008), Adaptations of glutamatergic synapses in the striatum contribute to recovery from cerebellar damage. European Journal of Neuroscience, 27: 2188–2196. doi: 10.1111/j.1460-9568.2008.06182.x
- Issue published online: 11 APR 2008
- Article first published online: 11 APR 2008
- Received 7 August 2007, revised 21 February 2008, accepted 28 February 2008
- cerebellar deficits;
- glutamate transmission;
- recovery of function
Recent findings proposed that the cerebellum and the striatum, key structures in motor control, are more interconnected than commonly believed, and that the cerebellum may influence striatal activity. In the present study, the possible changes of synaptic transmission in the striatum of hemicerebellectomized rats have been investigated. Neurophysiological recordings showed a significant facilitation of glutamate transmission in the contralateral striatum occurring early following hemicerebellectomy. This process of synaptic adaptation appears to be relevant for the compensation of cerebellar deficits. Accordingly, pharmacological blockade of glutamate N-methyl-d-aspartate (NMDA) receptors with MK-801 prevented the rearrangement of excitatory synapses in the striatum and interfered with the recovery from motor disturbances in rats with cerebellar lesions. Hemicerebellectomy also perturbed γ-aminobutyric acid (GABA) transmission in contralateral but not ipsilateral striatum. The present findings advance the role of striatal excitatory transmission in the compensation of cerebellar deficits, providing support to the notion that adaptations of striatal function exert a role in the recovery of cerebellar symptoms.