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Deficits in motor performance after pedunculopontine lesions in rats – impairment depends on demands of task
Author(s) -
MacLaren Duncan A. A.,
Santini Joseph A.,
Russell Ashley L.,
Markovic Tamara,
Clark Stewart D.
Publication year - 2014
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.12666
Subject(s) - pedunculopontine tegmental nucleus , neuroscience , pedunculopontine nucleus , cholinergic , psychology , basal ganglia , lesion , parkinson's disease , medicine , disease , deep brain stimulation , central nervous system , pathology , psychiatry
Anatomically and functionally located between basal ganglia and brainstem circuitry, the pedunculopontine tegmental nucleus ( PPT g) is in a pivotal position to contribute to motor behavior. Studies in primates have reported akinesia and postural instability following destruction of the PPT g. In humans, the PPT g partially degenerates in Parkinson's disease and stimulation of this region is under investigation as a possible therapeutic. Studies in rats report no crude motor impairment following PPT g lesion, although a detailed assessment of the role of the PPT g in rat motor function has not been reported. Our studies applied motor tests generally used in rodent models of Parkinson's disease to rats bearing either excitotoxic damage to all neuronal populations within PPT g, or selective destruction of the cholinergic subpopulation created with the toxin Dtx‐ UII . Neither lesion type altered baseline locomotion. On the rotarod, excitotoxic lesions produced a persistent impairment on the accelerating, but not fixed speed, conditions. In the vermicelli handling task (a quantitative measure of fine motor control and effective behavioral sequencing) excitotoxic lesions produced no single impairment, but globally increased the number of normal and abnormal behaviors. In contrast, depletion of cholinergic PPT g neurons produced impairment on the accelerating rotarod but no changes in vermicelli handling. Together, these results show that while PPT g lesions produce no impairment in the execution of individual motor actions, impairments emerge when the demands of the task increase. Results are discussed in terms of PPT g acting as part of a rapid action selection system, which integrates sensory information into motor output.