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I Tucci

Publications and source records attributed to I Tucci.

5 recordsLinked to original sources

Supersensitivity to a D-1 dopamine receptor agonist and subsensitivity to a D-2 receptor agonist following chronic D-1 receptor blockade.

The effect of chronic D-1 dopamine (DA) receptor blockade on D-1 DA receptors and DA-mediated behaviors was studied in rats with unilateral, quinolinic acid-induced striatal lesions. Administration of the selective D-1 antagonist SCH 23390 for 15 days increased D-1 receptor numbers in the unlesioned striatum as indicated by [125I]SCH 23982 binding; ipsilateral turning initiated by the D-2 receptor agonist LY 171555 decreased, while grooming produced by the D-1 receptor agonist SKF 38393 intensified. There was, however, no change in the ability of the D-1 agonist to potentiate D-2 agonist-mediated rotation. The observed behavioral subsensitivity in response to a D-2 agonist may reflect D-1 receptor upregulation and the consequent imbalance of D-1/D-2 receptor interactions in the striatum where these two receptor subtypes appear to play opposite functional roles; potentiation of grooming, primarily a D-1 receptor-mediated behavior, may also reflect the increase in D-1 receptor numbers.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

Attenuation of D-1 antagonist-induced D-1 receptor upregulation by concomitant D-2 receptor blockade.

The effect of chronic selective D-1 and/or D-2 dopamine receptor blockade on regional D-1 receptor binding was studied in rat brain following chronic treatment with the specific D-1 antagonist SCH 23390 and/or the predominantly D-2 antagonist haloperidol. D-1 receptor density and affinity were evaluated by quantitative autoradiography using 125I-SCH 23982. Chronic SCH 23390 treatment increased D-1 receptor density by 30 to 40% in the striatum, accumbens and tuberculum olfactorium; receptor affinity remained unchanged. Haloperidol had no effect on D-1 receptor Bmax or Kd values, although, when administered with SCH 23390, reduced the D-1 receptor upregulation induced by the D-1 antagonist in striatum and tuberculum olfactorium, but not in nucleus accumbens. These results may be attributable to D-1/D-2 dopamine receptor interactions occurring in the striatum and tuberculum olfactorium and may have implications for the prevention and treatment of drug-induced extrapyramidal disorders.

Animals↗

D-1 dopamine receptor changes after striatal quinolinic acid lesion.

Regional changes in the distribution of D-1 dopamine receptors produced by unilateral striatal lesions were evaluated in rat brain by quantitative autoradiography. Lesions were induced by local infusion of quinolinic acid, an endogenous excitotoxin that destroys intrinsic neurons, but spares fibers of passage. D-1 receptor density, as determined by [125I]SCH 23982 binding, was reduced in caudate-putamen, globus pallidus, substantia nigra, nucleus entopeduncularis on the lesioned side. These results confirm the presence of D-1 receptors on striatal cell bodies and provide direct evidence for the existence of presynaptic D-1 receptors on the terminals of striatal projections.

Animals↗