• Neuroscience · Nov 2006

    Deficits of glutamate transmission in the striatum of experimental hemiballism.

    • D Centonze, S Rossi, P Gubellini, V De Chiara, A Tscherter, C Prosperetti, B Picconi, G Bernardi, P Calabresi, and C Baunez.
    • Clinica Neurologica, Dipartimento di Neuroscienze, Università di Roma Tor Vergata, Via Montpellier 1, 00133 Rome, Italy. centonze@uniroma2.it
    • Neuroscience. 2006 Nov 17; 143 (1): 213-21.

    AbstractHemiballism (HB) is a quite rare disorder, generally secondary to stroke, neoplasms or demyelinating plaques, classically considered as almost pathognomonic of a lesion in the subthalamic nucleus (STN). This alteration causes involuntary movements in the chorea-ballism spectrum. One theory is that the output nuclei of the basal ganglia are overinhibited in HB, while little is known about the physiological state of the striatum, the major input structure of the basal ganglia. In the present study, we recorded spontaneous and miniature excitatory and inhibitory postsynaptic currents (sEPSCs, mEPSCs, sIPSCs, mIPSCs) from projection neurons of the striatum of experimental HB. We found a selective reduction of striatal sEPSC and mEPSC frequency following chemical lesion of the STN of the rat, suggesting that reduced synaptic excitation of the input structure of the basal ganglia represents a physiological correlate of HB.

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