Amphetamine: Effects on Catecholamine Systems and Behavior

Seiden, Lewis S.; Sabol, Karen E.; Ricaurte, George A.

doi:10.1146/annurev.pa.33.040193.003231

Cited by 703 publications

(206 citation statements)

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“…These data are also consistent with results from studies documenting differences between the effects of dopamine receptor knockouts on psychostimulant-induced locomotion and reward (41), and with the differences in dose-response relationships for amphetamine-induced locomotion and reward (42). These data, taken together, also fail to support substantial roles for other lower potency amphetamine actions, such as blockade of the inactivating ͞degrading enzyme monoamine oxidase (7), in the differences observed in the current studies.…”

Section: Generation Of the Vmat2 Knockoutcontrasting

confidence: 84%

“…Amphetamines dissipate proton gradients across the membranes of synaptic vesicles, disrupt VMAT2 function, enhance cytoplasmic monoamine concentrations, and cause calcium-independent, nonvesicular monoamine release into synapses (7)(8)(9). They also act like cocaine in blocking the plasma membrane neurotransmitter transporters that use transmembrane sodium and chloride gradients to pump dopamine, norepinephrine, and serotonin from extracellular spaces into presynaptic neurons (7,(10)(11)(12). There is currently little evidence to document which amphetamine action provides which contribution to amphetamine-induced locomotion or behavioral reward.…”

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confidence: 99%

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VMAT2 knockout mice: Heterozygotes display reduced amphetamine-conditioned reward, enhanced amphetamine locomotion, and enhanced MPTP toxicity

Takahashi

Miner

Sora

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

379

312

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The brain vesicular monoamine transporter (VMAT2) pumps monoamine neurotransmitters and Parkinsonism-inducing dopamine neurotoxins such as 1-methyl-4-phenyl-phenypyridinium (MPP ؉ ) from neuronal cytoplasm into synaptic vesicles, from which amphetamines cause their release. Amphetamines and MPP ؉ each also act at nonvesicular sites, providing current uncertainties about the contributions of vesicular actions to their in vivo effects. To assess vesicular contributions to amphetamine-induced locomotion, amphetamine-induced reward, and sequestration and resistance to dopaminergic neurotoxins, we have constructed transgenic VMAT2 knockout mice. Heterozygous VMAT2 knockouts are viable into adult life and display VMAT2 levels one-half that of wild-type values, accompanied by smaller changes in monoaminergic markers, heart rate, and blood pressure. Weight gain, fertility, habituation, passive avoidance, and locomotor activities are similar to wild-type littermates. In these heterozygotes, amphetamine produces enhanced locomotion but diminished behavioral reward, as measured by conditioned place preference. Administration of the MPP ؉ precursor N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine to heterozygotes produces more than twice the dopamine cell losses found in wild-type mice. These mice provide novel information about the contributions of synaptic vesicular actions of monoaminergic drugs and neurotoxins and suggest that intact synaptic vesicle function may contribute more to amphetamine-conditioned reward than to amphetamine-induced locomotion.

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Section: Generation Of the Vmat2 Knockoutcontrasting

confidence: 84%

mentioning

confidence: 99%

VMAT2 knockout mice: Heterozygotes display reduced amphetamine-conditioned reward, enhanced amphetamine locomotion, and enhanced MPTP toxicity

Takahashi

Miner

Sora

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

379

312

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“…Glucocorticoids share the neurochemical actions of psychostimulants in that they both increase extracellular concentrations of dopamine (this paper) and both seem to exert this effect through inhibition of dopamine reuptake and inhibition of monoamino oxidase activity (23)(24)(25)(26)(27)(28)(29). At the behavioral level, corticosterone induces self-administration (19) and dopamine-dependent locomotor activity as do psychostimulants (30).…”

Section: Discussionmentioning

confidence: 86%

Glucocorticoids have state-dependent stimulant effects on the mesencephalic dopaminergic transmission.

Piazza

Rougé‐Pont

Deroche

et al. 1996

Proc. Natl. Acad. Sci. U.S.A.

306

185

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An increase in the activity of mesencephalic dopaminergic neurons has been implicated in the appearance of pathological behaviors such as psychosis and drug abuse. Several observations suggest that glucocorticoids might contribute to such an increase in dopaminergic activity. The present experiments therefore analyzed the effects of corticosterone, the major glucocorticoid in the rat, both on dopamine release in the nucleus accumbens of freely moving animals by means of microdialysis, and on locomotor activity, a behavior dependent on accumbens dopamine. Given that glucocorticoids have certain state-dependent neuronal effects, their action on dopamine was studied in situations differing in dopaminergic tonus, including during the light and dark phases of the circadian cycle, during eating, and in groups of animals differing in their locomotor reactivity to novelty. Dopaminergic activity is increased in the dark period, further increased during food-intake, and is higher in rats defined as high responders to novelty than in low responders. Corticosterone, peripherally administered in a dose that approximates stress-induced plasma concentrations, increased extracellular concentrations of dopamine, and this increase was augmented in the dark phase, during eating, and in high responder rats. Corticosterone had little or no effects in the light phase and in low responder rats. Corticosterone also stimulated locomotor activity, an effect that paralleled the release of dopamine and was abolished by neurochemical (6-hydroxydopamine) depletion of accumbens dopamine. In conclusion, glucocorticoids have state-dependent stimulant effects on mesencephalic dopaminergic transmission, and an interaction between these two factors might be involved in the appearance of behavioral disturbances.It is generally admitted that an increase in the activity of the mesencephalic dopaminergic (DA) neurons is related to the appearance of pathological behaviors. The major antipsychotic drugs are antagonists of DA receptors (1) and prolonged use of psychotropic compounds known to increase DA activity can induce psychotic symptoms (2). Furthermore, an enhanced DA activity in the nucleus accumbens is associated with an increased vulnerability to develop drug self-administration in laboratory rats (3).Indirect observations suggest that glucocorticoids, the final product of the activation of the hypothalamus-pituitaryadrenal axis by stress, might be one factor capable of increasing the activity of mesencephalic DA neurons. DA neurons express corticosteroid receptors (4) and dopamine-mediated behaviors are profoundly facilitated by glucocorticoids (5). Furthermore, increased glucocorticoid levels can induce behavioral changes similar to those attributed to enhanced DA activity. In humans, high levels of glucocorticoids can induce mood changes ranging from euphoria to psychosis (6, 7). In animals, glucocorticoids, within the range of stressor-induced plasma concentrations, increase the propensity to develop self-administration of drugs of a...

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“…On the other hand, it is well known that methamphetamine-induced hyperlocomotion is mediated by the dopaminergic system. 20,21) The psychostimulatory effects of methamphetamine are associated with an increase in extracellular DA levels in the brain, by facilitating the release of DA from presynaptic nerve terminals and inhibiting reuptake. Thus the underlying mechanism of MK-801-induced hyperlocomotion is different from that of methamphetamineinduced hyperlocomotion.…”

Section: Discussionmentioning

confidence: 99%

Yokukansan Inhibits Social Isolation-Induced Aggression and Methamphetamine-Induced Hyperlocomotion in Rodents

Uchida

Egashira

Iwasaki

et al. 2009

Biological & Pharmaceutical Bulletin

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The majority of patients with Alzheimer's disease (AD) and other forms of senile dementia display various psychiatric symptoms, such as aggression, agitation, irritability, and hallucinations at some point during the course of their illness. These are collectively known as the behavioral and psychological symptoms of dementia (BPSD). The BPSD are a major cause of distress to family members and caregivers. 1) Furthermore, the presence of BPSD may have a negative impact on the course of the disease.2,3) Atypical antipsychotics are often chosen to treat BPSD, such as psychosis, aggression, and agitation, in patients with dementia. 4) However, effective drug therapy for BPSD has not been established. Recently, the traditional Japanese medicine Yokukansan (YKS, Yi-gan san in Chinese) has been demonstrated to improve BPSD, such as aggression, agitation, irritability, and hallucinations, in a randomized, single-blind, placebo-controlled study.5) However, the psychopharmacologic effects of YKS remain unexplored.The aggressive behavior of animals can be influenced by stress such as social isolation. For example, mouse-killing behavior (muricide) is induced in male Wistar rats by chronic isolation.6) The social isolation also induces aggression in male mice. 7,8) Moreover, supine restraint stress induces aggression, which is expressed as biting a wooden stick. 9)N-Methyl-D-aspartate (NMDA) receptor antagonists, such as phencyclidine (PCP) and MK-801, have been used as pharmacologic models of schizophrenia. NMDA receptor antagonists produce positive, negative and disorganization symptoms of schizophrenia in healthy individuals.10) In rodents, NMDA receptor blockers induce hyperlocomotion. 11)On the other hand, methamphetamine-induced hyperlocomotion has been used as a classic dopaminergic model for the identification of antipsychotics.In the present study, we investigated the effect of YKS on social isolation-induced aggressive behavior and methamphetamine-or MK-801-induced hyperlocomotion in rodents. MATERIALS AND METHODSAnimals Naïve 7-week-old male Wistar rats and 5-week-old male ddY mice were obtained from Kyudo, Saga, Japan. Animals were housed either in social isolation (1 rat per cage) or in social groups (5 rats per cage) for 11-13 weeks prior to rat behavioral testing, and in groups of 5 per cage for 1-2 weeks for mice, under standardized lighting conditions (lights on 07:00-19:00) at a constant temperature (23Ϯ2°C) with food and water available ad libitum. All procedures regarding animal care and use were performed in compliance with the regulations established by the Experimental Animal Care and Use Committee of Fukuoka University.Drugs YKS (Tsumura & Co., Tokyo, Japan) was dissolved in distilled water. Quetiapine (AstraZeneca, Wilmington, DE, U.S.A.) was suspended in 0.5% CMC-Na. Methamphetamine (Dainippon Pharmaceutical Co., Ltd., Osaka, Japan), MK-801 (Research Biochemicals Inc., Natick, MA, U.S.A.), and risperidone (Janssen Research Foundation, Beerse, Belgium) were dissolved in saline. YKS, quetiapine, and ...

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Amphetamine: Effects on Catecholamine Systems and Behavior

Cited by 703 publications

References 62 publications

VMAT2 knockout mice: Heterozygotes display reduced amphetamine-conditioned reward, enhanced amphetamine locomotion, and enhanced MPTP toxicity

VMAT2 knockout mice: Heterozygotes display reduced amphetamine-conditioned reward, enhanced amphetamine locomotion, and enhanced MPTP toxicity

Glucocorticoids have state-dependent stimulant effects on the mesencephalic dopaminergic transmission.

Yokukansan Inhibits Social Isolation-Induced Aggression and Methamphetamine-Induced Hyperlocomotion in Rodents

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