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

被引:22
作者
Centonze, Diego [1 ,2 ]
Rossi, Silvia [1 ,2 ]
De Bartolo, Paola [2 ,3 ]
De Chiara, Valentina [1 ,2 ]
Foti, Francesca [2 ,3 ]
Musella, Alessandra [1 ,2 ]
Mataluni, Giorgia [1 ,2 ]
Rossi, Stefano [4 ]
Bernardi, Giorgio [1 ,2 ]
Koch, Giacomo [1 ,2 ]
Petrosini, Laura [2 ,3 ]
机构
[1] Univ Roma Tor Vergata, Dipartimento Neurosci, Rome, Italy
[2] Fdn Santa Lucia, CERC, Rome, Italy
[3] Univ Roma La Sapienza, Dipartimento Psicol, Rome, Italy
[4] Univ Roma La Sapienza, Dipartimento Meccan & Aeronaut, Rome, Italy
关键词
cerebellar deficits; EPSC; glutamate transmission; rat; recovery of function;
D O I
10.1111/j.1460-9568.2008.06182.x
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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 gamma-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.
引用
收藏
页码:2188 / 2196
页数:9
相关论文
共 34 条
  • [1] [Anonymous], 1958, PHYSL PATHOLOGY CERE
  • [2] Blum D, 2003, J NEUROSCI, V23, P5361
  • [3] Deficits of glutamate transmission in the striatum of experimental hemiballism
    Centonze, D.
    Rossi, S.
    Gubellini, P.
    De Chiara, V.
    Tschertier, A.
    Prosperetti, C.
    Picconi, B.
    Bernardi, G.
    Calabresi, P.
    Baunez, C.
    [J]. NEUROSCIENCE, 2006, 143 (01) : 213 - 221
  • [4] Abnormal sensitivity to cannabinoid receptor stimulation might contribute to altered gamma-aminobutyric acid transmission in the striaturn of R6/2 Huntington's disease mice
    Centonze, D
    Rossi, S
    Prosperetti, C
    Tscherter, A
    Bernardi, G
    Maccarrone, M
    Calabresi, P
    [J]. BIOLOGICAL PSYCHIATRY, 2005, 57 (12) : 1583 - 1589
  • [5] Cepeda C, 2003, J NEUROSCI, V23, P961
  • [6] The roles of the cerebellum and basal ganglia in timing and error prediction
    Dreher, JC
    Grafman, J
    [J]. EUROPEAN JOURNAL OF NEUROSCIENCE, 2002, 16 (08) : 1609 - 1619
  • [7] IDENTIFICATION OF SYNAPTIC TERMINALS OF THALAMIC OR CORTICAL ORIGIN IN CONTACT WITH DISTINCT MEDIUM-SIZE SPINY NEURONS IN THE RAT NEOSTRIATUM
    DUBE, L
    SMITH, AD
    BOLAM, JP
    [J]. JOURNAL OF COMPARATIVE NEUROLOGY, 1988, 267 (04) : 455 - 471
  • [8] From preparation to online control: Reappraisal of neural circuitry mediating internally generated and externally guided actions
    Elsinger, C. L.
    Harrington, D. L.
    Rao, S. M.
    [J]. NEUROIMAGE, 2006, 31 (03) : 1177 - 1187
  • [9] Federico F, 2006, RESTOR NEUROL NEUROS, V24, P1
  • [10] MOTOR PRACTICE AND NEUROPHYSIOLOGICAL ADAPTATION IN THE CEREBELLUM - A POSITRON TOMOGRAPHY STUDY
    FRISTON, KJ
    FRITH, CD
    PASSINGHAM, RE
    LIDDLE, PF
    FRACKOWIAK, RSJ
    [J]. PROCEEDINGS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES, 1992, 248 (1323) : 223 - 228