title: Reduced eticlopride-induced Fos expression in caudate-putamen and globus pallidus after unilateral frontal cortex injury: relation to neglect.
abstract: Unilateral ablation of medial agranular cortex in rats results in neglect of contralateral stimuli and reductions in amphetamine-induced expression of the immediate early gene, c-fos, in both caudate-putamen and globus pallidus. Both unilateral neglect and the reductions in dopamine agonist induction of subcortical Fos immunoreactivity dissipate over a matter of weeks. Dopamine agonism induces Fos predominantly in striatonigral cells and in globus pallidus via striatopallidal disinhibition, whereas Fos is induced in striatopallidal cells by administration of antagonists of the D2 dopamine receptor subfamily. To examine more directly effects of cortical injury on striatopallidal function, induction of striatal Fos by the D2 antagonist eticlopride (0.1 mg/kg, s.c.) was examined in rats with medial agranular cortex ablation. In the same animals, eticlopride-induced Fos in globus pallidus was also examined. Five days after unilateral cortex injury, in rats showing neglect, the numbers of Fos immunoreactive nuclei induced by eticlopride were reduced by 50% in caudate-putamen and 25% in globus pallidus of the ipsilateral hemisphere. These lesion effects were restricted to dorsolateral caudate-putamen and dorsal pallidum. Three or more weeks after cortical injury, in rats recovered from neglect, eticlopride-induced Fos was normalized in caudate-putamen, but still decreased by 20% in globus pallidus. Along with previous findings, these results suggest that behavioral recovery from neglect produced by cortical injury may be at least partially mediated by normalizations of function of both striatopallidal and striatonigral neurons. In addition, the present findings suggest that normalization of function of pallidal cells activated by eticlopride is not necessary for behavioral recovery from frontal cortex ablation. Lingering reductions in excitatory cortico-subthalamo-pallidal input may be responsible for the longer-lasting dysfunctions of these pallidal cells.
authors.affiliation: Department of Psychobiology, University of California, Irvine 92717-4550, USA.
authors.forename: J M
authors.initials: JM
authors.lastname: Vargo
authors.forename: J F
authors.initials: JF
authors.lastname: Marshall
mesh_terms: D000818:Animals; D002421:Caudate Nucleus / Q000187:drug effects / Q000378:metabolism*; D003072:Cognition Disorders / Q000188:drug therapy / Q000378:metabolism*; D018491:Dopamine Agonists / Q000494:pharmacology; D018492:Dopamine Antagonists / Q000494:pharmacology*; D005625:Frontal Lobe / Q000293:injuries*; D005917:Globus Pallidus / Q000187:drug effects / Q000378:metabolism*; D007150:Immunohistochemistry; D009949:Orientation / Q000502:physiology; D016760:Proto-Oncogene Proteins c-fos / Q000096:biosynthesis*; D011699:Putamen / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D017448:Receptors, Dopamine D2 / Q000819:agonists; D012457:Salicylamides / Q000494:pharmacology*; D013534:Survival
chemical_list: D018491:Dopamine Agonists; D018492:Dopamine Antagonists; D016760:Proto-Oncogene Proteins c-fos; D017448:Receptors, Dopamine D2; D012457:Salicylamides; C045989:eticlopride