Premium
Contribution of Noradrenergic Neurons to the Regulation of Dopaminergic (D 1 ) Receptor Denervation Supersensitivity in Rat Prefrontal Cortex
Author(s) -
Tassin J. P.,
Studler J. M.,
Hervé D.,
Blanc G.,
Glowinski J.
Publication year - 1986
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1986.tb12953.x
Subject(s) - prefrontal cortex , dopaminergic , endocrinology , medicine , chemistry , dopamine , receptor , denervation , adenylate kinase , neuroscience , biology , cognition
3,4‐Dihydroxyphenylethylamine (DA, dopamine) levels in the rat prefrontal cortex were selectively decreased by 52%, leaving noradrenaline (NA) levels unaffected, 4 weeks following restricted bilateral electrolytic lesions of the ventral mesencephalic tegmentum (VMT). These lesions also induced a significant increase in DA‐sensitive, but not isoproterenol‐sensitive, adenylate cyclase activity in tissue homogenates (+ 38%). We had shown previously that chemical (6‐hydroxydo‐pamine, 6‐OHDA) lesions of the VMT destroy both ascending DA and NA fibers but do not alter the D 1 ‐receptor density in the prefrontal cortex. In this study, electrolytic lesions of the VMT were combined with bilateral injections of 6‐OHDA made laterally in the pedunculus cerebellaris superior to assess the role of NA fibers in the development of D 1 ‐receptor supersensitivity. This combined treatment produces a large decrease of cortical NA levels (‐95%), an increase in β‐adrenergic‐sensitive adenylate cyclase activity (+110%), and a decrease in DA levels (‐ 60%), but does not alter D 1 ‐receptor density in the prefrontal cortex. These results indicate that the development of D 1 ‐receptor supersensitivity in the prefrontal cortex following electrolytic lesion of the VMT depends on the presence of an intact NA innervation.