Adaptations of glutamatergic synapses in the striatum contribute to recovery from cerebellar damage

Recent findings proposed that the cerebellum and the striatum, key structures in motor control, are more interconnected thancommonly believed, and that the cerebellum may influence striatal activity. In the present study, the possible changes of synaptictransmission in the striatum of hemicerebellectomized rats have been investigated. Neurophysiological recordings showed asignificant facilitation of glutamate transmission in the contralateral striatum occurring early following hemicerebellectomy. Thisprocess of synaptic adaptation appears to be relevant for the compensation of cerebellar deficits. Accordingly, pharmacologicalblockade of glutamate N-methyl-d-aspartate (NMDA) receptors with MK-801 prevented the rearrangement of excitatory synapses inthe striatum and interfered with the recovery from motor disturbances in rats with cerebellar lesions. Hemicerebellectomy alsoperturbed c-aminobutyric acid (GABA) transmission in contralateral but not ipsilateral striatum. The present findings advance the roleof striatal excitatory transmission in the compensation of cerebellar deficits, providing support to the notion that adaptations of striatalfunction exert a role in the recovery of cerebellar symptoms.