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Author Notes:

Jose A. Obeso, Neuroscience Area, Center for Applied Medical Research (CIMA), Pio XII Avenue, No. 55, 31008 Pamplona, Spain. jobeso@unav.es.

Expert technical assistance in tissue handling and preparation was provided by our technician Ms. Elvira Roda.

Subject:

Research Funding:

Supported by grants from the Michael J. Fox Foundation; Ministerio de Educación y Ciencia refs: BFU2006-06744 and SAF2005-08416-C02-01; FIS refs: PI051037 and 013/2003; Fundación de Investigación Médica Mutua Madrilenña; and by the agreement between FIMA and the “UTE project FIMA.”

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Clinical Neurology
  • Neurosciences & Neurology
  • intralaminar thalamic nuclei
  • MPTP monkey model
  • kainic acid lesion
  • Parkinson's disease
  • DEEP BRAIN-STIMULATION
  • MEDIAN-PARAFASCICULAR COMPLEX
  • PARKINSONS-DISEASE
  • SUBTHALAMIC NUCLEUS
  • BASAL GANGLIA
  • TOURETTES-SYNDROME
  • SQUIRREL-MONKEY
  • EFFERENT CONNECTIONS
  • GLOBUS-PALLIDUS
  • POSSIBLE INVOLVEMENT

Lesion of the centromedian thalamic nucleus in MPTP-treated monkeys

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Journal Title:

Movement Disorders

Volume:

Volume 23, Number 5

Publisher:

, Pages 708-715

Type of Work:

Article | Post-print: After Peer Review

Abstract:

The caudal intralaminar nuclei are a major source of glutamatergic afferents to the basal ganglia. Experiments in the 6-hydroxydopamine rat model have shown that the parafascicular nucleus is overactive and its lesion alleviates basal ganglia neurochemical abnormalities associated with dopamine depletion. Accordingly, removal of this excitatory innervation of the basal ganglia could have a beneficial value in the parkinsonian state. To test this hypothesis, unilateral kainate-induced chemical ablation of the centromedian thalamic nucleus (CM) has been performed in MPTP-treated monkeys. Successful lesions restricted to the CM boundaries (n = 2) without spreading over other neighboring thalamic nuclei showed an initial, short-lasting, and mild change in the parkinsonian motor scale but no effect against levodopa-induced dyskinesias. The lack of significant and persistent motor improvement leads us to conclude that unilateral selective lesion of the CM alone cannot be considered as a suitable surgical approach for the treatment of PD or levodopa-induced dyskinesias. The role of the caudal intralaminar nuclei in the pathophysiology of movement disorders of basal ganglia origin remains to be clarified.

Copyright information:

© 2008 Movement Disorder Society.

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