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The role of the subthalamic nucleus in ‘compulsive’ behavior in rats
Author(s) -
Winter Christine,
Flash Shira,
Klavir Oded,
Klein Julia,
Sohr Reinhard,
Joel Daphna
Publication year - 2008
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/j.1460-9568.2008.06148.x
Subject(s) - subthalamic nucleus , nucleus accumbens , basal ganglia , ventral tegmental area , putamen , neuroscience , caudate nucleus , psychology , ventral pallidum , dopamine , globus pallidus , ventral striatum , infralimbic cortex , 5 ht4 receptor , deep brain stimulation , parkinson's disease , medicine , prefrontal cortex , striatum , agonist , dopaminergic , central nervous system , cognition , receptor , disease
Different lines of evidence point to dysfunction of basal ganglia‐thalamocortical circuits in obsessive‐compulsive disorder (OCD). It has been hypothesized that the circuits' dysfunction in OCD may be characterized by a relative under‐activity of the indirect compared with the direct pathway within these circuits. The present study tested whether lesions of the subthalamic nucleus (STN), a major node of the indirect pathway, would affect compulsive behavior, using the signal attenuation rat model of OCD. In this model, compulsive lever‐pressing is induced by the attenuation of an external signal of reward delivery; an attenuation that is hypothesized to simulate the deficient response feedback suggested to underlie obsessions and compulsions in patients with OCD. Rats sustaining lesions to the STN showed a selective increase in compulsive lever‐pressing compared with sham‐operated rats. A post mortem biochemical analysis revealed a decrease in serotonin content in the prelimbic and infralimbic cortices, caudate‐putamen (but not nucleus accumbens), globus pallidus and substantia nigra‐ventral tegmental area, as well as a decrease in dopamine content in the caudate‐putamen in STN‐lesioned compared with sham rats. A comparison to recent findings that lesions to the orbitofrontal cortex, which also result in a selective increase in compulsive lever‐pressing, lead to a decrease in serotonin and dopamine content in the caudate‐putamen suggests that there may be a final common pathway by which different brain pathologies may lead to a pro‐compulsive state.