Literature DB >> 11596046

Two types of projection neurons in the internal pallidum of primates: single-axon tracing and three-dimensional reconstruction.

M Parent1, M Lévesque, A Parent.   

Abstract

The axonal projections of the internal pallidum (GPi) in cynomolgus monkeys (Macaca fascicularis) were studied by labeling small pools of neurons with biotinylated dextran amine. Fifty-two axons were reconstructed entirely from serial sections with a camera lucida. Two types of projection neurons were identified in the GPi on the basis of their target sites. The abundant and centrally located type I neurons gave rise to a long axonal branch that descended directly to the pedunculopontine tegmental nucleus, where it arborized discretely. Other branches ascended to the thalamus and broke into 10-15 thinner collaterals that ran through most of the ventral anterior nucleus, where they terminated as typical plexuses. About half of these axons gave rise to collaterals that arborized in both components of the centre médian/parafascicular thalamic complex. The less numerous and peripherally located type II neurons had an axon that climbed the rostral thalamic pole, coursed along the stria medullaris, and arborized profusely within the lateral habenular nucleus, which stood out as the most densely innervated pallidal target. Some type II axons provided collaterals to the anterior thalamic nuclei. A small proportion of axons of both types had branches that crossed the midline and terminated in contralateral GPi target structures. Three-dimensional reconstruction showed that type I axons arborized principally along the sagittal plane. These data reveal that GPi neurons of type I act through a widely distributed axonal network upon thalamic and brainstem premotor neurons, whereas type II neurons act in a much more focused manner upon lateral habenular neurons. Copyright 2001 Wiley-Liss, Inc.

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Year:  2001        PMID: 11596046     DOI: 10.1002/cne.1340

Source DB:  PubMed          Journal:  J Comp Neurol        ISSN: 0021-9967            Impact factor:   3.215


  63 in total

1.  Diversity of axonal ramifications belonging to single lateral and medial olivocochlear neurons.

Authors:  W Bruce Warr; Jo Ellen Boche
Journal:  Exp Brain Res       Date:  2003-10-14       Impact factor: 1.972

2.  Integration of cortical and pallidal inputs in the basal ganglia-recipient thalamus of singing birds.

Authors:  Jesse H Goldberg; Michael A Farries; Michale S Fee
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Review 3.  The pedunculopontine nucleus as a target for deep brain stimulation.

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Review 4.  Functional connectivity and integrative properties of globus pallidus neurons.

Authors:  D Jaeger; H Kita
Journal:  Neuroscience       Date:  2011-07-27       Impact factor: 3.590

Review 5.  Reward processing by the lateral habenula in normal and depressive behaviors.

Authors:  Christophe D Proulx; Okihide Hikosaka; Roberto Malinow
Journal:  Nat Neurosci       Date:  2014-09       Impact factor: 24.884

6.  Deep brain stimulation of the globus pallidus internus in the parkinsonian primate: local entrainment and suppression of low-frequency oscillations.

Authors:  Kevin W McCairn; Robert S Turner
Journal:  J Neurophysiol       Date:  2009-01-21       Impact factor: 2.714

7.  Independent circuits in the basal ganglia for the evaluation and selection of actions.

Authors:  Marcus Stephenson-Jones; Andreas A Kardamakis; Brita Robertson; Sten Grillner
Journal:  Proc Natl Acad Sci U S A       Date:  2013-09-03       Impact factor: 11.205

8.  Evolutionary conservation of the habenular nuclei and their circuitry controlling the dopamine and 5-hydroxytryptophan (5-HT) systems.

Authors:  Marcus Stephenson-Jones; Orestis Floros; Brita Robertson; Sten Grillner
Journal:  Proc Natl Acad Sci U S A       Date:  2011-12-27       Impact factor: 11.205

Review 9.  Deep Brain Stimulation for Movement Disorders of Basal Ganglia Origin: Restoring Function or Functionality?

Authors:  Thomas Wichmann; Mahlon R DeLong
Journal:  Neurotherapeutics       Date:  2016-04       Impact factor: 7.620

10.  New hypotheses about postural control support the notion that all dystonias are manifestations of excessive brain postural function.

Authors:  Anne J Blood
Journal:  Biosci Hypotheses       Date:  2008
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