Anatomical Investigations of the Pallidotegmental Pathway in Monkey and Man

  • David B. Rye
  • Robert S. Turner
  • Jerrold L. Vitek
  • Roy A. E. Bakay
  • Michael D. Crutcher
  • Mahlon R. DeLong
Part of the Advances in Behavioral Biology book series (ABBI, volume 47)


The targets of internal pallidal efferents have attracted considerable attention given the central role proposed for the internal segment of the globus pallidus (GPi) in models of normal and pathological movement.1–3 The previous emphasis of these models on basal ganglia-thalamocortical circuitry, has left pathways between the GPi and the midbrain tegmentum largely unexplored. In the primate, the size and functional import of pallidofugal projections upon the mesopontine tegmentum are nonetheless likely to be significant. A majority of neurons in the primate GPi contribute to this pathway via collateralization from pallidothalamic fibers,4–6 and its terminl zone has been described as “extensive”7. Experimental and pathophysiological observations implicate the mesopontine tegmental region in receipt of basal ganglia output as important in modulating normal and pathological movement. Electrical stimulation and micro infusions of substance-P or NMDA8 into the mesopontine tegmentum in decerebrate subprimate preparations elicit treadmill locomotion, while GABAergic pathways play an inhibitory role8, 9 (i. e. the “mesencephalic locomotor region” (MLR).10–12 In awake behaving subprimates, cytotoxic lesions including, but not restricted to, midbrain tegmental/basal ganglia circuitry produce incomplete hindlimb extension, bradykinesia and dyscoordination.13 Depending on the locus and the electrical or pharamacological stimulus parameters applied, motor effects ranging from decreased “postural support” to increased spontaneous motor activity have also been reported.14–21 Enhanced utilization of 2-deoxyglucose in the mesopontine tegmentum in primate models of Parkinsons disease (PD)22 suggests that excessive pallidotegmental inhibition might contribute to hypokinesia, while decreased utilization in a model of hemiballismus23 suggests that disinhibition of the mesopontine tegmentum might contribute to hyperkinetic disorders.


Subthalamic Nucleus Paradoxical Sleep Superior Cerebellar Peduncle Biotinylated Dextran Amine Pedunculopontine Nucleus 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


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Copyright information

© Springer Science+Business Media New York 1996

Authors and Affiliations

  • David B. Rye
    • 1
  • Robert S. Turner
    • 1
  • Jerrold L. Vitek
    • 1
  • Roy A. E. Bakay
    • 2
  • Michael D. Crutcher
    • 1
  • Mahlon R. DeLong
    • 1
  1. 1.Department of NeurologyEmory University School of MedicineAtlantaUSA
  2. 2.Department of NeurosurgeryEmory University School of MedicineAtlantaUSA

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