[3H]SCH 23390 binding sites increase after chronic blockade of D-1 dopamine receptors

Porceddu, M.L.; Ongini, Ennio; Biggio, Giovanni

doi:10.1016/0014-2999(85)90151-7

Cited by 98 publications

(25 citation statements)

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“…Consistent with the latter is our previous finding that the behavioral response to signal attenuation is increased following termination of repeated administration of SCH 23390 . Since chronic treatment with SCH 23390 leads to an increase in the density of D 1 receptors in the striatum (Creese and Chen, 1985;Giorgi et al, 1993;Hess et al, 1986Hess et al, , 1988Lappalainen et al, 1992;Memo et al, 1987;O'Boyle et al, 1993;Porceddu et al, 1985), the signaling of a phasic DA decrease is expected to be amplified by the larger number of D 1 receptors, leading to an abnormally high level of compulsive lever-pressing.…”

Section: Kg Haloperidol In Regular Extinctionmentioning

confidence: 99%

“…Thus, compounds that abolish phasic DA responses or their detection (eg D 1 agonists) may attenuate compulsions. A potential advantage of treatment with D 1 agonists rather than antagonists is that chronic administration of antagonists (but not agonists) may result in exaggeration of symptoms following treatment termination, as a result of treatment-induced increase in the density of D 1 receptors (Creese and Chen, 1985;Giorgi et al, 1993;Hess et al, 1986Hess et al, , 1988Lappalainen et al, 1992;Memo et al, 1987;O'Boyle et al, 1993;Porceddu et al, 1985). Indeed, repeated administration of SCH 23390 in rats led to an increase in compulsive behavior following the termination of drug administration .…”

Section: Kg Haloperidol In Regular Extinctionmentioning

confidence: 99%

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Selective Alleviation of Compulsive Lever-Pressing in Rats by D1, but not D2, Blockade: Possible Implications for the Involvement of D1 Receptors in Obsessive–Compulsive Disorder

Joel

Doljansky

2003

Neuropsychopharmacol

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Rats undergoing extinction of lever-pressing for food after the attenuation of an external feedback for this behavior exhibit excessive lever-pressing unaccompanied by an attempt to collect a reward. This behavior may be analogous to the excessive and unreasonable behavior seen in obsessive-compulsive disorder. In the present study, we tested the hypothesis that the compulsive behavior induced by signal attenuation is mediated via D 1 rather than D 2 receptors. Administration of 0.005, 0.01 and 0.03 mg/kg of the D 1 antagonist SCH 23390 reduced the number of compulsive lever-presses without affecting the number of lever-presses followed by an attempt to collect a reward. In contrast, administration of 0.005, 0.01, 0.024, 0.036 and 0.05 of the D 2 antagonist haloperidol dose-dependently decreased both types of lever-presses. In addition, haloperidol at doses that decreased lever-pressing in the post-training signal attenuation procedure (0.036 and 0.05 mg/kg) had a similar effect in regular extinction, whereas an SCH 23390 dose that decreased compulsive lever-pressing in the post-training signal attenuation procedure (0.01 mg/kg) had no effect on regular extinction. On the basis of electrophysiological data on the response of dopamine neurons to the omission of an expected reward, these results were interpreted as suggesting that compulsive lever-pressing depends on a phasic decrease in the stimulation of D 1 receptors. The implications of these results for the pathophysiology and treatment of obsessive-compulsive disorder are discussed.

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Section: Kg Haloperidol In Regular Extinctionmentioning

confidence: 99%

Section: Kg Haloperidol In Regular Extinctionmentioning

confidence: 99%

Selective Alleviation of Compulsive Lever-Pressing in Rats by D1, but not D2, Blockade: Possible Implications for the Involvement of D1 Receptors in Obsessive–Compulsive Disorder

Joel

Doljansky

2003

Neuropsychopharmacol

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“…These findings are consistent with the results reported here, indicating that a 94% increase of D 1 receptor density was associated with the administration of the selective antagonist SCH23390. It is interesting to note that both acute (Gupta and Mishra, 1993) and chronic administration (Creese and Chen, 1985;Dawson et al, 1986;Porceddu et al, 1985) of dopamine agonists or antagonists has also been associated with significant alterations in D 1 receptor density, without any appreciable change in receptor affinity. It is possible that alterations of receptor number may be the primary mechanism through which neurons adapt to blockade of D 1 receptors.…”

Section: Discussionmentioning

confidence: 98%

“…APDs usually require two or more weeks to achieve their full effects and, for this reason, subchronic or chronic drug administration over a period of weeks to months is generally employed to model their effects on dopamine receptor subtypes (Creese and Chen, 1985;Dawson et al, 1986;Giorgi et al, 1993;Lappalainen et al, 1992;Porceddu et al, 1985;See et al, 1990). Prior studies in which low-resolution autoradiography was employed demonstrated that chronic administration of either a D 1 or D 2 antagonist increases the B max , but does not alter the K d , for each of these receptor subtypes (Creese and Chen, 1985;Dawson et al, 1986;Mc-Gonigle et al, 1989;Parashos et al, 1987;Porceddu et al, 1985). It is important to emphasize, however, that changes in receptor populations occurring as a result of prolonged APD administration are likely to involve secondary and perhaps even tertiary downstream changes in complex neural circuits.…”

Section: Introductionmentioning

confidence: 99%

Acute administration of SCH23390 increases D1 receptors on nonpyramidal neurons in rat mPFC

Davidoff

Chu

Beneš

2000

Synapse

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Atypical antipsychotic drugs (APDs) such as clozapine and olanzapine antagonize both D(1) and D(2) receptors; however, little is known regarding their pharmacologic effect on specific neuronal elements within the local circuitry of corticolimbic regions, such as medial prefrontal cortex (mPFC). To characterize the effect of short-term antagonism of the D(1) receptor a high-resolution autoradiographic technique was used to assess the density (B(max)) and affinity (K(d)) of this receptor on pyramidal cells (i.e., large neurons (LNs, >/=100 microm(2))), nonpyramidal cells (i.e., small neurons (SNs, <100 microm(2))) and in the surrounding neuropil (NPL) of layer VI in rat mPFC. Either normal saline or the selective D(1) antagonist SCH23390 (1.0 mg/kg/day) were administered for 48 h via Alzet osmotic pumps. Frozen sections were incubated in [(3)H]SCH23390 (1-8 nM) in the presence or absence of the competitive inhibitor SKF38393 (10 microM). A microscopic adaptation to Scatchard analysis revealed a significant increase (82%) in B(max) for neuronal cell bodies (P < 0.05), but not for neuropil of drug-treated animals. Further analysis indicated that the increase in B(max) was present on SNs (94%, P < 0.05), but not LNs in SCH23390-treated rats. In contrast, K(d) values for LNs, SNs, and NPL were not significantly altered by drug treatment. Since the vast majority of SNs are nonpyramidal in nature, short-term administration of a selective D(1) antagonist seems to be associated with a preferential upregulation of this receptor on interneurons. Overall, these results are consistent with the hypothesis that the mechanism of action of atypical antipsychotic medications involves changes in D(1) receptor activity associated with local circuit neurons in rat mPFC.

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“…Researchers subsequently determined that it was a compensatory reaction to the medications. 21,22,23,24,25,26,27 The drug, they said, caused an "upregulation" of the receptors.…”

Section: A Paradox Explainedmentioning

confidence: 99%

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Nesset¹,

Teien²

2017

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[3H]SCH 23390 binding sites increase after chronic blockade of D-1 dopamine receptors

Cited by 98 publications

References 7 publications

Selective Alleviation of Compulsive Lever-Pressing in Rats by D1, but not D2, Blockade: Possible Implications for the Involvement of D1 Receptors in Obsessive–Compulsive Disorder

Selective Alleviation of Compulsive Lever-Pressing in Rats by D1, but not D2, Blockade: Possible Implications for the Involvement of D1 Receptors in Obsessive–Compulsive Disorder

Acute administration of SCH23390 increases D1 receptors on nonpyramidal neurons in rat mPFC

Reservasjonsrett i psykiatrien nå!

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