Neural Substrates of Psychostimulant-Induced Arousal

Berridge, Craig W.

doi:10.1038/sj.npp.1301159

Cited by 80 publications

(71 citation statements)

References 67 publications

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“…Conversely, the fact that clinically relevant doses of psychostimulants exert only a modest impact on circuitry associated with psychostimulant-induced arousal (eg, MSA NE; Berridge, 2006) and motor activation (eg, NAc; Kelley et al, 1989) is consistent with their minimal arousal-promoting and motor-activating effects. Moreover, the fact that clinically relevant doses of psychostimulants exert a modest impact on DA levels in the NAc, a key region involved in the reinforcing effects of psychostimulants, is also consistent with evidence indicating that the clinical use of psychostimulants does not increase, and may reduce, the liability for drug abuse in ADHD populations (Biederman, 2003).…”

Section: The Pharmacology Of Adhd: Preferential Targeting Of the Pfcmentioning

confidence: 89%

Neurocircuitry Underlying the Preferential Sensitivity of Prefrontal Catecholamines to Low-Dose Psychostimulants

Schmeichel

Berridge

2013

Neuropsychopharmacol

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Low doses of psychostimulants, including methylphenidate (MPH), are highly effective in the treatment of attention-deficit/hyperactivity disorder (ADHD). At these doses, psychostimulants improve prefrontal cortex (PFC)-dependent function. Recent evidence indicates that low and clinically relevant doses of psychostimulants target norepinephrine (NE) and dopamine (DA) signaling preferentially in the PFC. To better understand the neural mechanisms responsible for the regional selectivity of low-dose psychostimulant action, it is important to first identify the underlying neurocircuitry. The current study used reverse microdialysis to test the hypothesis that the preferential targeting of PFC catecholamines by low-dose psychostimulants involves direct action within the PFC, reflecting an intrinsic property of this region. For these studies, the effects of varying concentrations of MPH (0.25, 1.0, and 4.0 mM) on NE and DA efflux were examined within the PFC and select subcortical fields in unanesthetized rats. Low concentrations of MPH elicited significantly larger increases in extracellular levels of NE and DA in the PFC than in subcortical regions linked to motor-activating and arousal-promoting actions of psychostimulants (nucleus accumbens and medial septal area, respectively). The differential action of MPH across regions disappeared at higher concentrations. The enhanced sensitivity of PFC catecholamines to low and clinically relevant doses of psychostimulants, at least in part, reflects a unique sensitivity of this region to NE/DA transporter blockade. Available evidence suggests that the increased sensitivity of PFC catecholamines likely involves DA clearance through the NE transporter within the PFC.

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Section: The Pharmacology Of Adhd: Preferential Targeting Of the Pfcmentioning

confidence: 89%

Neurocircuitry Underlying the Preferential Sensitivity of Prefrontal Catecholamines to Low-Dose Psychostimulants

Schmeichel

Berridge

2013

Neuropsychopharmacol

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“…These short term effects and the mechanisms that mediate them have been extensively studied. Amphetamine and related compounds are used recreationally in part because of such effects (reviewed in Berridge, 2006;Robinson and Berridge, 1993;Segal and Kuczenski, 1994).…”

Section: Introductionmentioning

confidence: 99%

Time-dependent effects of amphetamine on feeding in rats

2007

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Following administration of a moderate dose of amphetamine, rats appear to pass through a sequence of physiological/ psychological states, including stimulant and depressant states. The present research evaluated whether these states could be inferred from time-dependent changes in feeding-related measures. Male rats were housed in individual stations (light-dark 12-12 hr, free access to water) where, at three hour intervals, they could respond for food for one hour. The work requirement was fixed ratio 1, and each lever press produced 6 94-mg food pellets. When the pattern of responding for food stabilized across the light-dark cycle, a series of 6 or 7 tests was run. During each test, rats received a saline treatment (1.0 ml/ kg, subcutaneously) followed by a 48-hour monitoring period, and then they received an amphetamine treatment (2.0 mg/ kg, subcutaneously) followed by a 72-hour monitoring period. Different groups were treated at either light onset or light offset. Lever presses and head-in-feeding-bin responses were monitored throughout these tests. Administration of amphetamine at light onset and at light offset produced cumulative food intake functions having four regions: post-treatment hours 1-6 (hypophagia), 7-12 (normal intake), 13-27 (hypophagia), and 28 and beyond (normal intake). The sequence, duration, and quality of the amphetamine-induced changes in food intake resembled those formerly seen in cue state and activity, and provided further evidence of a transient withdrawal state 20-24 hr post-amphetamine treatment.

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“…Acute METH exposure in mammals induces wakefulness attributable, in part, to increased dopaminergic signaling (8,18). We have shown previously that METH-induced arousal correlates with increased dopaminergic signaling in Drosophila (12).…”

Section: Meth-induced Wakefulness Does Not Involve Modulation Of Dda1mentioning

confidence: 99%

“…D1-like receptors in mammals mediate the wake-promoting and motor-activating properties of psychostimulants such as cocaine and amphetamines (8,(16)(17)(18). CAFF leads to increased dopaminergic transmission by antagonizing A1 receptors on presynaptic dopaminergic neurons (19).…”

Section: Adenosinergic and Dopaminergic Systems Mediate Wake-promotingmentioning

confidence: 99%

Drosophila D1 dopamine receptor mediates caffeine-induced arousal

Andretic

Kim

Jones

et al. 2008

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

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The arousing and motor-activating effects of psychostimulants are mediated by multiple systems. In Drosophila, dopaminergic transmission is involved in mediating the arousing effects of methamphetamine, although the neuronal mechanisms of caffeine (CAFF)-induced wakefulness remain unexplored. Here, we show that in Drosophila, as in mammals, the wake-promoting effect of CAFF involves both the adenosinergic and dopaminergic systems. By measuring behavioral responses in mutant and transgenic flies exposed to different drug-feeding regimens, we show that CAFFinduced wakefulness requires the Drosophila D1 dopamine receptor (dDA1) in the mushroom bodies. In WT flies, CAFF exposure leads to downregulation of dDA1 expression, whereas the transgenic overexpression of dDA1 leads to CAFF resistance. The wakepromoting effects of methamphetamine require a functional dopamine transporter as well as the dDA1, and they engage brain areas in addition to the mushroom bodies.ptimal behavioral performance in humans and animals depends on an adequate arousal level, which often involves diffuse afferent inputs from the dopaminergic system. Caffeine (CAFF) displays strong arousing properties and is the most consumed psychoactive drug in the world. CAFF competitively inhibits adenosine A1 and A2 receptors, antagonizing the effects of the sleep-promoting neuromodulator adenosine that accumulates during waking (1). CAFF also leads to increased dopaminergic and glutamatergic transmission in different striatal subcompartments, which has been linked to its activating and reinforcing effects (2-4).Although CAFF-induced wakefulness has been related to modulation of cholinergic and histaminergic arousal systems (5, 6), CAFF's induction of increased dopaminergic transmission and its effect on wakefulness have not been adequately examined. Animals with increased dopaminergic transmission, such as dopamine transporter (DAT) mutant mice, have decreased non-rapid eye movement sleep and increased sensitivity to the wake-promoting action of CAFF (7). Dopaminergic action on both the D1 and D2 receptors contributes to the alert waking state, based on the action of centrally administered D1 and D2 agonists in rodents (8). Molecularly, CAFF modulates D2 transcription in vitro and in vivo (9). Motor-activating effects of CAFF are diminished in D2R mutant mice (10, 11); however, the role of D2R in the arousing effect of CAFF remains unknown, and functional tests of the brain regions mediating these effects are lacking in mammals.We have shown previously that the wake-promoting effects of methamphetamine (METH) in Drosophila are mediated through dopaminergic transmission, indicating some evolutionary conservation in the behavioral and neurochemical effects of psychostimulants (12).Treatment of flies with CAFF induces wakefulness; however, the mechanism underlying this activity is currently unknown (13,14). In the present study, we investigate the role of dopamine signaling in the wake-inducing properties of CAFF and METH, with emphasis on the role of the Dr...

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Neural Substrates of Psychostimulant-Induced Arousal

Cited by 80 publications

References 67 publications

Neurocircuitry Underlying the Preferential Sensitivity of Prefrontal Catecholamines to Low-Dose Psychostimulants

Neurocircuitry Underlying the Preferential Sensitivity of Prefrontal Catecholamines to Low-Dose Psychostimulants

Time-dependent effects of amphetamine on feeding in rats

Drosophila D1 dopamine receptor mediates caffeine-induced arousal

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