Developmental striatal critical period of activity-dependent plasticity is also a window of susceptibility for haloperidol induced adult motor alterations

Soiza-Reilly, Mariano; Azcurra, Julio M.

doi:10.1016/j.ntt.2009.03.001

Cited by 13 publications

(19 citation statements)

References 49 publications

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“…Second, activity measures were recorded during the animals’ light cycle for twenty minutes in a darkened room with no habituation to the testing room. This approach is consistent with much previous work on APD administration and locomotor activity, with the length of testing slightly longer than that reported in some papers (Shalaby & Spear, 1980; Soiza-Reilly & Azcurra, 2009; Wiley, 2008; Wiley & Evans, 2008; 2009; Zuo et al, 2008), and shorter than reported in others (Cuomo et al, 1981; Samaha et al, 2008). Locomotor activity is influenced by multiple parameters that are too numerous to discuss here.…”

Section: Discussionsupporting

confidence: 91%

“…For example, rats exposed to the typical APD, haloperidol, in utero or during the first three weeks of life, were found to exhibit hyperactivity, impaired impulse control, and greater behavioral sensitivity to dopamine agonists and antagonists during adulthood (Cuomo et al, 1981: Scalzo & Spear, 1985; Shalaby & Spear, 1980; although see Rosengarten & Friedhoff, 1979 for contrasting outcomes of prenatal versus postnatal APD treatment). More recently, Soiza-Reilly and Azcurra (2009) administered haloperidol to rats during later stages of development that are more akin to those when human children receive APD treatment. This study uncovered a potential critical period - rats treated with haloperidol during postnatal days 30 – 37 were hyperactive as adults, but those treated during postnatal days 20 – 27 or 40 – 47 were not.…”

Section: Discussionmentioning

confidence: 99%

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Adult rats treated with risperidone during development are hyperactive.

Bardgett¹,

Franks-Henry²,

Colemire³

et al. 2013

Experimental and Clinical Psychopharmacology

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Risperidone is an antipsychotic drug approved for use in children, but little is known about the long-term effects of early-life risperidone treatment. In animals, prolonged risperidone administration during development increases forebrain dopamine receptor expression immediately upon the cessation of treatment. A series of experiments was performed to ascertain whether early-life risperidone administration altered locomotor activity, a behavior sensitive to dopamine receptor function, in adult rats. One additional behavior modulated by forebrain dopamine function, spatial reversal learning, was also measured during adulthood. In each study, Long-Evans rats received daily subcutaneous injections of vehicle or one of two doses of risperidone (1.0 and 3.0 mg/kg per day) from postnatal days 14 – 42. Weight gain during development was slightly yet significantly reduced in risperidone-treated rats. In the first two experiments, early-life risperidone administration was associated with increased locomotor activity at one week post-administration through approximately nine months of age, independent of changes in weight gain. In a separate experiment, it was found that the enhancing effect of early-life risperidone on locomotor activity occurred in males and female rats. A final experiment indicated that spatial reversal learning was unaffected in adult rats administered risperidone early in life. These results indicate that locomotor activity during adulthood is permanently modified by early-life risperidone treatment. The findings suggest that chronic antipsychotic drug use in pediatric populations (e.g., treatment for the symptoms of autism) could modify brain development and alter neural set-points for specific behaviors during adulthood.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Adult rats treated with risperidone during development are hyperactive.

Bardgett¹,

Franks-Henry²,

Colemire³

et al. 2013

Experimental and Clinical Psychopharmacology

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“…Others have reported that spontaneous locomotor activity during adulthood is not modified in rats that received the atypical antipsychotic drugs, clozapine, during the first three weeks of life (Cuomo et al, 1983a) or olanzapine from postnatal day 28–49 (Milstein et al, 2013). Consistent with the effects reported by Soiza-Reilly and Azcurra (2009), but contrary to the others, daily risperidone administration between postnatal days 14–42 elicited higher levels of locomotor activity during early adulthood. Specifically, when tested four days after the cessation of daily injections, rats that received risperidone during development were more active on the first day of testing.…”

Section: Discussionsupporting

confidence: 89%

“…Daily haloperidol injections across the first three weeks of development do not alter spontaneous activity in adulthood (Cuomo et al, 1981), whereas daily injections of somewhat larger doses of haloperidol between postnatal days 30 – 37 have been associated with higher activity levels (Soiza-Reilly and Azcurra, 2009). Others have reported that spontaneous locomotor activity during adulthood is not modified in rats that received the atypical antipsychotic drugs, clozapine, during the first three weeks of life (Cuomo et al, 1983a) or olanzapine from postnatal day 28–49 (Milstein et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

Early-life risperidone enhances locomotor responses to amphetamine during adulthood

Stubbeman

Brown

Yates

et al. 2017

European Journal of Pharmacology

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Antipsychotic drug prescriptions for pediatric populations have increased over the past 20 years, particularly the use of atypical antipsychotic drugs such as risperidone. Most antipsychotic drugs target forebrain dopamine systems, and early-life antipsychotic drug exposure could conceivably reset forebrain neurotransmitter function in a permanent manner that persists into adulthood. This study determined whether chronic risperidone administration during development modified locomotor responses to the dopamine/norepinephrine agonist, D-amphetamine, in adult rats. Thirty-five male Long-Evans rats received an injection of one of four doses of risperidone (vehicle, 0.3, 1.0, 3.0 mg/kg) each day from postnatal day 14 through 42. Locomotor activity was measured for 1 h on postnatal days 46 and 47, and then for 24 h once a week over the next two weeks. Beginning on postnatal day 75, rats received one of four doses of amphetamine (saline, 0.3, 1.0, 3.0 mg/kg) once a week for four weeks. Locomotor activity was measured for 27 h after amphetamine injection. Rats administered risperidone early in life demonstrated increased activity during the 1 and 24 h test sessions conducted prior to postnatal day 75. Taking into account baseline group differences, these same rats exhibited significantly more locomotor activity in response to the moderate dose of amphetamine relative to controls. These results suggest that early-life treatment with atypical antipsychotic drugs, like risperidone, permanently alters forebrain catecholamine function and increases sensitivity to drugs that target such function.

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“…Of these striatal receptors, the D 2 Rs are particularly important because of their involvement in impulsivity (Besson et al 2010; Lee et al 2009) and in the beneficial and adverse motor side effects produced by classic antipsychotic drugs, all of which are D 2 R blockers (Artigas 2010; Schlagenhauf et al 2008; Soiza-Reilly and Azcurra 2009). …”

Section: Introductionmentioning

confidence: 99%

Quinpirole elicits differential in vivo changes in the pre- and postsynaptic distributions of dopamine D2 receptors in mouse striatum: relation to cannabinoid-1 (CB1) receptor targeting

et al. 2011

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RationaleThe nucleus accumbens (Acb) shell and caudate-putamen nucleus (CPu) are respectively implicated in the motivational and motor effects of dopamine, which are mediated in part through dopamine D2-like receptors (D2Rs) and modulated by activation of the cannabinoid-1 receptor (CB1R). The dopamine D2/D3 receptor agonist, quinpirole elicits internalization of D2Rs in isolated cells; however, dendritic and axonal targeting of D2Rs may be highly influenced by circuit-dependent changes in vivo and potentially influenced by endogenous CB1R activation.ObjectiveWe sought to determine whether quinpirole alters the surface/cytoplasmic partitioning of D2Rs in striatal neurons in vivo.MethodsTo address this question, we examined the electron microscopic immunolabeling of D2 and CB1 receptors in the Acb shell and CPu of male mice at 1 h following a single subcutaneous injection of quinpirole (0.5 mg/kg) or saline, a time point when quinpirole reduced locomotor activity.ResultsMany neuronal profiles throughout the striatum of both treatment groups expressed the D2R and/or CB1R. As compared with saline, quinpirole-injected mice showed a significant region-specific decrease in the plasmalemmal and increase in the cytoplasmic density of D2R-immunogold particles in postsynaptic dendrites without CB1R-immunolabeling in the Acb shell. However, quinpirole produced a significant increase in the plasmalemmal density of D2R immunogold in CB1R negative axons in both the Acb shell and CPu.ConclusionsOur results provide in vivo evidence for agonist-induced D2R trafficking that is inversely related to CB1R distribution in postsynaptic neurons of Acb shell and in presynaptic axons in this region and in the CPu.

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Developmental striatal critical period of activity-dependent plasticity is also a window of susceptibility for haloperidol induced adult motor alterations

Cited by 13 publications

References 49 publications

Adult rats treated with risperidone during development are hyperactive.

Adult rats treated with risperidone during development are hyperactive.

Early-life risperidone enhances locomotor responses to amphetamine during adulthood

Quinpirole elicits differential in vivo changes in the pre- and postsynaptic distributions of dopamine D2 receptors in mouse striatum: relation to cannabinoid-1 (CB1) receptor targeting

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