Effects of haloperidol on rat behavior and density of dopaminergic D2-like receptors

Vasconcelos, Silvânia Maria Mendes; Nascimento, Viviane S.; Nogueira, Carlos Renato Alves; Vieira, Carlos M.A.G.; Sousa, F.C.F.; Fonteles, M.M.F.; Viana, Glauce Socorro Barros

doi:10.1016/s0376-6357(03)00028-7

Cited by 31 publications

(24 citation statements)

References 28 publications

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“…In consistent with the results of the previous studies (Burt et al, 1977;Ginovart et al, 2009;Laruelle et al, 1992;Vasconcelos et al, 2003;Watanabe et al, 1993), HAL treatment for 3 and 6 weeks increased levels of D 2 receptor in CP in the present study ( Fig. 4A and C).…”

Section: Discussionsupporting

confidence: 94%

“…While some early studies showed downregulations (Ritter and Meador-Woodruff, 1997;Watanabe et al, 1993), a recent study reported an up-regulation of D 2 receptors in the hippocampus by HAL (Vasconcelos et al, 2003). In the present study, HAL treatment for 6 weeks, but not for 3 weeks, increased levels of hippocampal D 2 receptors in mice ( Fig.…”

Section: Discussionsupporting

confidence: 44%

“…5C and D). These different results may be related to the influence of dose, age, and time of drug withdrawal as suggested by Vasconcelos et al (2003). Again, we considered the up-regulation of hippocampal D 2 receptors, the compensatory effect of subjects in response to the chronic blockade of the receptors by HAL.…”

Section: Discussionmentioning

confidence: 99%

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Chronic haloperidol-induced spatial memory deficits accompany the upregulation of D1 and D2 receptors in the caudate putamen of C57BL/6 mouse

Yang

Rose

2012

Life Sciences

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Section: Discussionsupporting

confidence: 94%

Section: Discussionsupporting

confidence: 44%

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Chronic haloperidol-induced spatial memory deficits accompany the upregulation of D1 and D2 receptors in the caudate putamen of C57BL/6 mouse

Yang

Rose

2012

Life Sciences

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“…However, in mature animals (Tarazi et al, 2001; Vasconcelos et al, 2003; Samaha et al, 2007; Ginovart et al, 2009) and human patients (Silvestri et al, 2000; Remington and Kapur, 2010), chronic treatment with typical and atypical APDs (including Ola) over a protracted period can upregulate D 2 binding, depending on the duration and percentage of D 2 receptor blockade. This causes a loss of therapeutic efficacy in patients (Silvestri et al, 2000; Remington and Kapur, 2010).…”

Section: Discussionmentioning

confidence: 99%

Olanzapine treatment of adolescent rats alters adult reward behaviour and nucleus accumbens function

Vinish

Elnabawi

Milstein

et al. 2013

International Journal of Neuropsychopharmacology

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Antipsychotic drugs are increasingly used in children and adolescents to treat a variety of psychiatric disorders. However, little is known about the long-term effects of early life antipsychotic drug (APD) treatment. Most APDs are potent antagonists or partial agonists of dopamine (DA) D2 receptors ; atypical APDs also have multiple serotonergic activities. DA and serotonin regulate many neurodevelopmental processes. Thus, early life APD treatment can, potentially, perturb these processes, causing long-term behavioural and neurobiological sequelae. We treated adolescent, male rats with olanzapine (Ola) on post-natal days 28–49, under dosing conditions that approximate those employed therapeutically in humans. As adults, they exhibited enhanced conditioned place preference for amphetamine, as compared to vehicle-treated rats. In the nucleus accumbens core, DA D1 receptor binding was reduced, D2 binding was increased and DA release evoked by electrical stimulation of the ventral tegmental area was reduced. Thus, adolescent Ola treatment enduringly alters a key behavioural response to rewarding stimuli and modifies DAergic neurotransmission in the nucleus accumbens. The persistence of these changes suggests that even limited periods of early life Ola treatment may induce enduring changes in other reward-related behaviours and in behavioural and neurobiological responses to therapeutic and illicit psychotropic drugs. These results underscore the importance of improved understanding of the enduring sequelae of paediatric APD treatment as a basis for weighing the benefits and risks of adolescent APD therapy, especially prophylactic treatment in high-risk, asymptomatic patients.

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“…Haloperidol at the higher dose and risperidone at the lower dose increased the time of animal permanence in the bar, reflecting improvement in the motor coordination, however not sufficient to reduce the ketamine-increased number of falls. These data led us to suggest that such effect could be the result of an acute blockade of dopamine D 2 receptors in the striatum [45,46]. The time of permanence on the bar of the groups treated exclusively with neuroleptics was not different from the controls, suggesting that the sedative effect of these drugs could contribute to the increased number of falls particularly at the higher doses, thus not being able to reverse the ketamine-increased number of falls in this test.…”

Section: Discussionmentioning

confidence: 89%

Activities of the Antipsychotic Drugs Haloperidol and Risperidone on Behavioural Effects Induced by Ketamine in Mice

Arruda

2008

Sci. Pharm.

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This study presents the actions of risperidone (Risp) and haloperidol (Hal) on the behavioral effects elicited by ketamine (Ket) on open-field (OF), rota rod (RR) and tail suspension (TS) tests in mice. Male Swiss albino mice (25-30g) were used. Antipsychotics were administered alone (Risp: 0.1 or 0.2 mg/kg, ip; Hal: 0.1 and 0.2 mg/kg, ip) or thirty minutes before Ket (10 mg/Kg, ip). Ket increased (Ket: 63.3 ± 4.2) the locomotor activity compared to control, while neuroleptics decreased it (25.5 ± 4.2). Pretreatment with neuroleptics, in both doses, blocked hyperlocomotion caused by Ket. In RR, Ket decreased (Ket: 15 ± 4.1) the permanence time of the animals compared to control (Control: 59 ± 0.6), but this effect was not observed when neuroleptics were administered alone. Pretreatment with neuroleptics reverted the effect of Ket only in the RR. While Ket (17.3 ± 5.6) decreased the time of immobility in the tail suspension test compared to the control (80.2 ± 10.2), the pretreatment with neuroleptics reverted this mobility. The action of neuroleptics in this model made possible the blockade of the effects caused by acute administration of Ket. Thus, the mechanism of action of ketamine may involve the dopaminergic system.

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Effects of haloperidol on rat behavior and density of dopaminergic D2-like receptors

Cited by 31 publications

References 28 publications

Chronic haloperidol-induced spatial memory deficits accompany the upregulation of D1 and D2 receptors in the caudate putamen of C57BL/6 mouse

Chronic haloperidol-induced spatial memory deficits accompany the upregulation of D1 and D2 receptors in the caudate putamen of C57BL/6 mouse

Olanzapine treatment of adolescent rats alters adult reward behaviour and nucleus accumbens function

Activities of the Antipsychotic Drugs Haloperidol and Risperidone on Behavioural Effects Induced by Ketamine in Mice

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