Abstract
Administration of L-dopa to unilaterally 6-hydroxydopamine-lesioned rats, activates the early gene c-fos in the lesioned caudate-putamen. D-1 receptor blockade by SCH 23390, prevented L-dopa-induced Fos-like immunoreactivity in the whole caudate-putamen, while D-2 receptor blockade by raclopride reduced Fos-like immunoreactivity only in the dorso-lateral portion. The results suggest that L-dopa induces c-fos primarily through an activation of D-1 receptors, while D-2 receptor stimulation plays a facilitatory influence on D-1-mediated c-fos expression.
MeSH terms
-
Animals
-
Benzazepines / pharmacology
-
Corpus Striatum / metabolism*
-
Denervation
-
Dopamine / metabolism*
-
Dopamine D2 Receptor Antagonists
-
Levodopa / pharmacology*
-
Male
-
Proto-Oncogene Proteins c-fos / metabolism*
-
Raclopride
-
Rats
-
Rats, Sprague-Dawley
-
Receptors, Dopamine / physiology*
-
Receptors, Dopamine D1 / antagonists & inhibitors
-
Receptors, Dopamine D1 / physiology
-
Receptors, Dopamine D2 / physiology
-
Salicylamides / pharmacology
Substances
-
Benzazepines
-
Dopamine D2 Receptor Antagonists
-
Proto-Oncogene Proteins c-fos
-
Receptors, Dopamine
-
Receptors, Dopamine D1
-
Receptors, Dopamine D2
-
Salicylamides
-
Raclopride
-
Levodopa
-
Dopamine