Acute amphetamine and/or phencyclidine effects on the dopamine receptor specific binding in the rat brain

Tomić, Miloš; Vukosavic, Slobodanka; Joksimović, J.

doi:10.1016/s0924-977x(97)00398-2

Cited by 16 publications

(11 citation statements)

References 22 publications

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“…Our results are in agreement with a previous study conducted in male rats in which D1R and D2R levels were examined in the 2 hour period after exposure to PCP 17). Tomić et al17) reported decreases following PCP treatment in [ 3 H] SCH 23390 binding of 25% and 33% in the striatum and nucleus accumbens.…”

Section: Discussionsupporting

confidence: 93%

“…In addition, PCP induced behaviours can be attenuated or blocked by a range of D1 and D2 dopamine receptor antagonists 10,14-16). Few studies however have examined short term changes that occur in dopamine receptor systems following PCP exposure particularly in the female rat brain17) despite reported sexual dimorphism in some metabolic and behavioural responses to PCP treatment 18-20)…”

Section: Introductionmentioning

confidence: 99%

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Rapid Changes in D1 and D2 Dopamine Receptor Binding in Striatal Subregions after a Single Dose of Phencyclidine

Dalton

Zavitsanou

2011

Clin Psychopharmacol Neurosci

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ObjectiveIn humans, a single exposure to phencyclidine (PCP) can induce a schizophrenia-like psychosis which can persist for up to two weeks. In rats, an acute dose of PCP increases dopaminergic activity and causes changes in dopamine related behaviours some of which are sexually dimorphic. To better understand the effects of PCP on dopamine receptor adaptations in the short term we examined dopamine D1-like receptors (D1R) and D2-like receptors (D2R) in the mesolimbic and nigrostriatal dopamine pathways, 4 hours after exposure to PCP in female rats.MethodsAnimals received a single dose of 40 mg/kg PCP and were sacrificed 4 hours later. In vitro autoradiography was carried out using [3H] SCH 23390 and [3H] raclopride that target D1R and D2R respectively, in cryostat brain sections.ResultsTwo way analysis of variance (ANOVA), revealed an overall effect of PCP treatment (F [1,63]=9.065; p=0.004) on D1R binding with an 18% decrease (p<0.01) in binding in the medial caudate putamen. PCP treatment also had an overall effect on D2R binding (F [1,47]=5.450; p=0.024) and a trend for an increase in D2R binding across all the brain regions examined.ConclusionThese results suggest opposing D1R and D2R adaptations in striatal subregions of female rats following acute exposure to PCP that may occur through indirect mechanisms.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Rapid Changes in D1 and D2 Dopamine Receptor Binding in Striatal Subregions after a Single Dose of Phencyclidine

Dalton

Zavitsanou

2011

Clin Psychopharmacol Neurosci

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“…In more recent animal studies using relatively selective dopamine D1 receptor radioligands, striatal dopamine D1 receptor number has been reported to be unchanged [36][37][38][39][40][41] or reduced. 42,43 Decreased striatal dopamine D1 receptor levels have been observed in rodents who had received a high dose of methamphetamine sufficient to cause damage to dopamine nerve terminals. 44,45 Similarly, in a preliminary study, we found a statistically non-significant trend for lower dopamine D1 receptor concentration in striatum (the rodent counterpart of the human caudate and putamen; −15%) and nucleus accumbens (−31%) of rats killed 3 h after the last of 10 daily injections of methamphetamine (20 mg kg…”

Section: Dopamine Receptors In Brain Of Drug Usersmentioning

confidence: 99%

Dopamine D1 receptor protein is elevated in nucleus accumbens of human, chronic methamphetamine users

et al. 2000

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Animal data have long suggested that an adaptive upregulation of nucleus accumbens dopamine D1 receptor function might underlie part of the dependency on drugs of abuse. We measured by quantitative immunoblotting protein levels of dopamine D1 and, for comparison, D2 receptors in brain of chronic users of methamphetamine, cocaine, and heroin. As compared with the controls, brain dopamine D1 receptor concentrations were selectively increased (by 44%) in the nucleus accumbens of the methamphetamine users, whereas a trend was observed in this brain area for reduced protein levels of the dopamine D2 receptor in all three drug groups (؊25 to ؊37%; P < 0.05 for heroin group only). Our data support the hypothesis that aspects of the drug-dependent state in human methamphetamine users might be related to increased dopamine D1 receptor function in limbic brain. Molecular Psychiatry (2000) 5, 664-672.

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“…Therefore the aforementioned independent analysis of each variable was justified. Tomic et al, 1997), the stimulatory effects of C T are not reversed by feedback mechanisms (Gill and Meren, 1978;Landis et al, 1989;Burton et al, 1991Burton et al, , 1998Spiegel, 1996;Z eiger et al, 1997). Because C T and elevated cAM P levels permanently potentiate neuron excitability (Geller et al, 1993;Hernandez-L opez et al, 1997) and induce excitation-associated neurological and behavioral changes (Cunningham and Kelley, 1993;Burton et al, 1998), similar excitatory signaling changes should be induced within the CT-expressing neurons of D1C T-7 mice.…”

Section: Efficacy Of the D1ct Transgenementioning

confidence: 99%

OCD-Like Behaviors Caused by a Neuropotentiating Transgene Targeted to Cortical and Limbic D1+ Neurons

et al. 1999

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To study the behavioral role of neurons containing the D1 dopamine receptor (D1ϩ), we have used a genetic neurostimulatory approach. We generated transgenic mice that express an intracellular form of cholera toxin (CT), a neuropotentiating enzyme that chronically activates stimulatory G-protein (G s ) signal transduction and cAMP synthesis, under the control of the D1 promoter. Because the D1 promoter, like other CNSexpressed promoters, confers transgene expression that is regionally restricted to different D1ϩ CNS subsets in different transgenic lines, we observed distinct but related psychomotor disorders in different D1CT-expressing founders. In a D1CT line in which transgene expression was restricted to the following D1ϩ CNS regions-the piriform cortex layer II, layers II-III of somatosensory cortical areas, and the intercalated nucleus of the amygdala-D1CT mice showed normal CNS and D1ϩ neural architecture but increased cAMP content in whole extracts of the piriform and somatosensory cortex. These mice also exhibited a constellation of compulsive behavioral abnormalities that strongly resembled human cortical-limbic-induced compulsive disorders such as obsessive-compulsive disorder (OCD). These compulsive behaviors included episodes of perseverance or repetition of any and all normal behaviors, repetitive nonaggressive biting of siblings during grooming, and repetitive leaping. These results suggest that chronic potentiation of cortical and limbic D1ϩ neurons thought to induce glutamatergic output to the striatum causes behaviors reminiscent of those in human cortical-limbic-induced compulsive disorders.

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Acute amphetamine and/or phencyclidine effects on the dopamine receptor specific binding in the rat brain

Cited by 16 publications

References 22 publications

Rapid Changes in D1 and D2 Dopamine Receptor Binding in Striatal Subregions after a Single Dose of Phencyclidine

Rapid Changes in D1 and D2 Dopamine Receptor Binding in Striatal Subregions after a Single Dose of Phencyclidine

Dopamine D1 receptor protein is elevated in nucleus accumbens of human, chronic methamphetamine users

OCD-Like Behaviors Caused by a Neuropotentiating Transgene Targeted to Cortical and Limbic D1+ Neurons

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