Co-administration of either a selective D1 or D2 dopamine antagonist with methamphetamine prevents methamphetamine-induced behavioral sensitization and neurochemical change, studied by in vivo intracerebral dialysis

Hamamura, Takashi; Akiyama, Kazufumi; Akimoto, Kiyoshi; Kashihara, Kenichi; Okumura, Kazuya; Ujike, Hiroshi; Otsuki, Saburo

doi:10.1016/0006-8993(91)91156-u

Cited by 103 publications

(60 citation statements)

References 37 publications

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“…In addition, the blockade of dopamine D 1 and D 2 receptors by their respective antagonists, SCH23390 and sulpiride, significantly attenuated place preference induced by cocaine. Similar inhibitory roles of both dopamine D 1 and D 2 receptors in the development of the place preference of cocaine have been also reported (33,34). These data therefore suggest a possibility that there may be a functional and/or regulatory pathway between the expression of RyRs involved in place preference of cocaine and dopamine receptors.…”

Section: Sal Cocasupporting

confidence: 82%

“…Although both types of dopamine receptors have the potential to produce the cocaine-induced rewarding effect (33,34) as well as to mediate reinforcing signals of abuse (36), opposing effects of dopamine D 1 and D 2 receptor activation on cAMP-dependent signaling have been reported in many studies (37). That is, dopamine D 1 receptors activate adenylate cyclase through stimulatory Gαs protein, and dopamine D 2 receptors inhibit adenylate cyclase via inhibitory Gαi/o protein.…”

Section: Sal Cocamentioning

confidence: 99%

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Dopamine D1 Receptors Participate in Cocaine-Induced Place Preference via Regulation of Ryanodine Receptor Expression

et al. 2011

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Abstract. Ryanodine receptors (RyRs) with three different isoforms in the brain play a role to facilitate Ca 2+ release from the intracellular Ca 2+ pool. Although cocaine is a strongly addictive psychostimulant that dramatically affects the central nervous system function, the role of RyRs and regulation of their expression by cocaine-induced place preference have not yet been defined well. The present study investigated the regulation of RyR expression in mice under intermittent cocaine treatment using the place preference procedure. The cocaine-induced place preference was inhibited by intracerebroventricular pretreatment with dantrolene, a RyRs antagonist, in a dosedependent manner. The levels of RyR-1 and -2 in the limbic forebrain and frontal cortex significantly increased in the cocaine-conditioned mice, whereas that of RyR-3 in these two brain regions showed no changes. Although the up-regulation of RyRs was not affected by blockade of L-type voltage-gated calcium channels, the increase of RyR-1 and -2 in the limbic forebrain and frontal cortex was completely abolished by SCH23390, a selective antagonist of dopamine D 1 receptors, but not by sulpiride, a selective antagonist of dopamine D 2 receptors. These findings indicate that RyRs play a critical role in the development of cocaine-induced place preference and that the upregulation of RyRs in the brain of a mouse showing cocaine-induced place preference is regulated by dopamine D 1 receptors.

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Section: Sal Cocasupporting

confidence: 82%

Section: Sal Cocamentioning

confidence: 99%

Dopamine D1 Receptors Participate in Cocaine-Induced Place Preference via Regulation of Ryanodine Receptor Expression

et al. 2011

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“…Furthermore, the seizure-induced elevation of DA release could be enhanced if seizures were induced repeatedly (Strecker and Moneta, 1994;Dazzi et al, 1997;Becker et al, 2000). This phenomenon is comparable to the process of 'behavioral sensitization', in which repeated administration of DA agonists augment abnormal behaviors with the concominant enhancement of DA release (Kazahaya et al, 1989;Hamamura et al, 1991; also see review of Kalivas and Stewart, 1991). In our study, the prolonged seizure activity associated with limbic status epilepticus might produce excessive DA release and have such sensitization-like effects on DA systems.…”

Section: Seizure-induced Pathological Sensitization Of the Da Systemsupporting

confidence: 64%

Enhancement of Central Dopaminergic Activity in the Kainate Model of Temporal Lobe Epilepsy: Implication for the Mechanism of Epileptic Psychosis

Ando

Morimoto

Watanabe

et al. 2004

Neuropsychopharmacol

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There is an increased incidence of schizophrenia-like psychosis in temporal lobe epilepsy (TLE), and several risk factors have been implicated, including the duration of epilepsy and temporal lobe neuropathology. To investigate the biological mechanism of epileptic psychosis, we examined alterations of central dopaminergic systems in the kainate model of TLE. In adult rats, kainate was microinjected into the left amygdala to induce status epilepticus. An indirect dopamine agonist methamphetamine (MAP, 2 mg/kg, i.p.) was administered before and 1 month after the kainate treatment. MAP-induced locomotor activity was significantly enhanced in the kainate group compared with the baseline (pre-kainate) level, which was antagonized by pretreatment with haloperidol. The enhancement of locomotor activity in the kainate group was significantly correlated with the density of hippocampal CA1 neurons. Although the basal extracellular dopamine concentration was significantly lower in the striatum in the kainate group than in the control group (5.5 vs 39.2 fmol/20-min sample), the maximal concentration following MAP administration did not differ between the two groups. These results clearly demonstrate that hypersensitivity of the dopamine systems develops in the chronic phase of the kainate-induced TLE model, which may be responsible for the mechanism of epileptic psychosis.

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“…Similarly, in an effort to unravel the mechanism of this uncoupling, the effect of exposure to GBR 12783, a specific DA reuptake inhibitor was tested. Finally, because the stimulation of D1 receptors was often shown to be critical in the effects of drugs of abuse (Vezina and Stewart, 1989;Hamamura et al, 1991;Jeziorski and White, 1995), we have analyzed the effects of SCH23390, the D1 receptor antagonist generally used in these experiments, to explore its role on noradrenergic and serotonergic transmissions.…”

Section: Introductionmentioning

confidence: 99%

Drugs of Abuse Specifically Sensitize Noradrenergic and Serotonergic Neurons Via a Non-Dopaminergic Mechanism

Lanteri

Salomon

Torrens

et al. 2007

Neuropsychopharmacol

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A challenge in drug dependence is to delineate long-term neurochemical modifications induced by drugs of abuse. Repeated damphetamine was recently shown to disrupt a mutual regulatory link between noradrenergic and serotonergic neurons, thus inducing long-term increased responses to d-amphetamine and para-chloroamphetamine, respectively. We show here that such a sensitization of noradrenergic and serotonergic neurons also occurs following repeated treatment with cocaine, morphine, or alcohol, three compounds belonging to main groups of addictive substances. In all cases, this sensitization is prevented by a1b-adrenergic and 5-HT 2A receptors blockade, indicating the critical role of these receptors on long-term effects of drugs of abuse. However, repeated treatments with two non-addictive antidepressants, venlafaxine, and clorimipramine, which nevertheless inhibit noradrenergic and serotonergic reuptake, do not induce noradrenergic and serotonergic neurons sensitization. Similarly, this sensitization does not occur following repeated treatments with a specific inhibitor of dopamine (DA) reuptake, GBR12783. Moreover, we show that the effects of SCH23390, a D1 receptor antagonist known to inhibit development of d-amphetamine behavioral sensitization, are due to its 5-HT 2C receptor agonist property. SCH23390 blocks amphetamine-induced release of norepinephrine and RS102221, a 5-HT 2C antagonist, can reverse this inhibition as well as inhibition of noradrenergic sensitization and development of behavioral sensitization induced by repeated damphetamine. We propose that noradrenergic/serotonergic uncoupling is a common neurochemical consequence of repeated consumption of drugs of abuse, unrelated with DA release. Our data also suggest that compounds able to restore the link between noradrenergic and serotonergic modulatory systems could represent important therapeutic targets for investigation.

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Co-administration of either a selective D1 or D2 dopamine antagonist with methamphetamine prevents methamphetamine-induced behavioral sensitization and neurochemical change, studied by in vivo intracerebral dialysis

Cited by 103 publications

References 37 publications

Dopamine D1 Receptors Participate in Cocaine-Induced Place Preference via Regulation of Ryanodine Receptor Expression

Dopamine D1 Receptors Participate in Cocaine-Induced Place Preference via Regulation of Ryanodine Receptor Expression

Enhancement of Central Dopaminergic Activity in the Kainate Model of Temporal Lobe Epilepsy: Implication for the Mechanism of Epileptic Psychosis

Drugs of Abuse Specifically Sensitize Noradrenergic and Serotonergic Neurons Via a Non-Dopaminergic Mechanism

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