title: Selective stimulation of striatal dopamine receptors of the D1- or D2-class causes opposite changes of fos expression in the rat cerebral cortex.
abstract: It has been suggested that activation of striatal neurons expressing D1 or D2 dopamine receptors elicits opposite changes in the net output of the basal ganglia circuitry and, consequently, in the functional interactions of the circuit with the cerebral cortex. In particular, it has been recently reported that striatal D1 receptors may regulate cortex function. To further address this issue, we mapped cerebral expression of Fos protein following intrastriatal stimulation of D1- or D2-class receptors in freely moving animals. Using permanent cannulas implanted in the right striatum, Sprague-Dawley rats received intrastriatal microinfusions of SKF 38393 (D1 agonist) or quinpirole (D2 agonist) or saline (controls), combined with systemic administration of D1 antagonist SCH 23390 or D2 antagonist eticlopride or saline. Animals treated with SKF 38393 showed dose-dependent, massive Fos increases in the motor, somatosensory, auditory, visual and limbic regions of the cerebral cortex, ipsilaterally to the injected striatum. Consistent Fos expression was also found in the injected striatum and, bilaterally, in the nucleus accumbens shell. These increases were effectively counteracted by systemic SCH 23390. Conversely, quinpirole did not induce significant cortical or striatal expression of Fos, which was instead observed after the systemic administration of eticlopride. Fos was not detected in any of the other basal ganglia nuclei, regardless of the dopamine agonists or antagonists used. Our results confirm that striatal D1 dopamine receptors play a central role in the modulation of cortical activity, thus providing additional information on the functional interaction between basal ganglia circuitry and cerebral cortex.
authors.affiliation: Laboratory of Functional Neurochemistry, IRCCS C Mondino, Pavia, Italy. abio.blandini@mondino.it
authors.forename: Fabio
authors.initials: F
authors.lastname: Blandini
authors.forename: Roberto
authors.initials: R
authors.lastname: Fancellu
authors.forename: Francesco
authors.initials: F
authors.lastname: Orzi
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Conti
authors.forename: Rosaria
authors.initials: R
authors.lastname: Greco
authors.forename: Cristina
authors.initials: C
authors.lastname: Tassorelli
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Nappi
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001522:Behavior, Animal; D002452:Cell Count; D002540:Cerebral Cortex / Q000033:anatomy & histology / Q000378:metabolism*; D003342:Corpus Striatum / Q000187:drug effects / Q000378:metabolism*; D018491:Dopamine Agonists / Q000494:pharmacology; D018492:Dopamine Antagonists / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D007839:Functional Laterality; D007150:Immunohistochemistry; D008297:Male; D016761:Oncogene Proteins v-fos / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017447:Receptors, Dopamine D1 / Q000502:physiology*; D017448:Receptors, Dopamine D2 / Q000502:physiology*; D012399:Rotation; D013239:Stereotyped Behavior / Q000187:drug effects
chemical_list: D018491:Dopamine Agonists; D018492:Dopamine Antagonists; D016761:Oncogene Proteins v-fos; D017447:Receptors, Dopamine D1; D017448:Receptors, Dopamine D2