Wake-Promoting Actions of Dopamine D1 and D2 Receptor Stimulation

Isaac, S O; Berridge, Craig W.

doi:10.1124/jpet.103.053918

Cited by 108 publications

(58 citation statements)

References 40 publications

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“…the absence of locomotor activation (Figure 4; Isaac and Berridge, 2003). Given stimulants enhance DA efflux widely throughout the brain; these and other observations (Nishino et al, 1998;Wisor et al, 2001) suggest a prominent role of DA in the wake-promoting actions of these drugs.…”

Section: Wake-promoting Actions Of Dasupporting

confidence: 51%

“…At modestly higher doses associated with moderate increases in time spent awake, more prominent increases in NE and DA efflux were observed outside the PFC. Combined, these observations suggest that (1) low-dose stimulants can preferentially target NE/DA neurotransmission within the PFC, and (2) Po0.05 compared with the low dose of the respective drug (see Isaac and Berridge, 2003).…”

Section: Amph-induced Increases In Arousal and Ne And Da Release Are mentioning

confidence: 91%

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Neural Substrates of Psychostimulant-Induced Arousal

Berridge

2006

Neuropsychopharmacol

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Extensive research has provided substantial insight into the neurobiological mechanisms underlying the reinforcing, locomotor-activating and stereotypy-inducing actions of psychostimulants. The diverse behavioral effects of these drugs are superimposed on potent arousalenhancing actions. Psychostimulant-induced arousal is a prominent contributing factor to the widespread use and abuse of these drugs. Moreover, enhanced arousal may be a critical component of the reinforcing and other behavioral actions of these drugs. Although long overlooked, recent work begins to identify the neural mechanisms involved in psychostimulant-induced arousal. For example, microdialysis studies demonstrate a close relationship between amphetamine-induced waking/arousal and amphetamine-induced increases in norepinephrine and dopamine efflux. Additionally, it is now clear that both norepinephrine and dopamine exert robust wakepromoting actions. The wake-promoting effects of norepinephrine involve synergistic actions of a 1 -and b-receptors, whereas dopamineinduced waking involves both D1 and D2 receptors. Finally, additional studies have identified subcortical regions involved in the wakepromoting actions of both norepinephrine and amphetamine. These regions include, but may not be limited to, the medial septal area, the medial preoptic area, and the lateral hypothalamus. Combined, these and other observations indicate a prominent involvement of both norepinephrine and dopamine in stimulant-induced arousal via actions within a network of subcortical regions. Although it is clear that both norepinephrine and dopamine contribute to psychostimulant-induced arousal, the degree to which each transmitter system is necessary for the expression of stimulant-induced arousal remains to be fully elucidated.

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Section: Wake-promoting Actions Of Dasupporting

confidence: 51%

Section: Amph-induced Increases In Arousal and Ne And Da Release Are mentioning

confidence: 91%

Neural Substrates of Psychostimulant-Induced Arousal

Berridge

2006

Neuropsychopharmacol

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“…These include basal forebrain (España et al, 2001;Thakkar et al, 2001) and brainstem structures such as the locus coeruleus (Hagan et al, 1999;Horvath et al, 1999;Bourgin et al, 2000), the dorsal raphe (Liu et al, 2002;Kohlmeier et al, 2004), the lateral dorsal tegmental nucleus (Burlet et al, 2002;Kohlmeier et al, 2004) and the tuberomammillary nucleus (Eriksson et al, 2001). DA systems have also been implicated in the modulation of behavioral state and state-dependent processes, particularly under high arousal appetitive and aversive conditions (Trulson, 1985;Smith et al, 1992;Arnsten et al, 1994;Isaac and Berridge, 2003). Thus, it is of interest that VTA and substantia nigra neurons express HCRT receptor mRNA (Marcus et al, 2001) and that HCRT activates VTA (though not substantia nigra) DA neurons in vitro (Uramura et al, 2001;Korotkova et al, 2002Korotkova et al, , 2003.…”

Section: Discussionmentioning

confidence: 99%

“…Combined, these observations suggest a pivotal role for the HCRT system in the regulation of behavioral state and state-dependent processes associated with alert, active waking. Dopaminergic systems also modulate behavioral state and state-dependent processes, particularly under high-arousal appetitive and aversive conditions (Trulson, 1985;Smith et al, 1992;Arnsten et al, 1994;Isaac and Berridge, 2003). Acting within the prefrontal cortex (PFC) and nucleus accumbens (Acc), dopamine (DA) exerts prominent modulatory actions on a variety of higher-level cognitive and affective processes (Ikemoto and Panksepp, 1999;SmithRoe and Kelley, 2000;Baldwin et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Hypocretin/Orexin Selectively Increases Dopamine Efflux within the Prefrontal Cortex: Involvement of the Ventral Tegmental Area

Vittoz

Berridge

2005

Neuropsychopharmacol

172

114

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Hypocretins (HCRTs) modulate a variety of behavioral and physiological processes, in part via interactions with multiple ascending modulatory systems. Further, HCRT efferents from the lateral hypothalamus innervate midbrain dopamine (DA) nuclei, and DA cell bodies express HCRT receptors. Combined, these observations suggest that HCRT may influence behavioral state and/or statedependent processes via modulation of DA neurotransmission. The current studies used in vivo microdialysis in the unanesthetized rat to first characterize the effect of intracerebroventricular infusion of HCRT-1 (0.07, 0.7 nmol) on extracellular levels of DA within the prefrontal cortex (PFC) and nucleus accumbens (Acc). Electroencephalographic/electromyographic measures of sleep-wake state were collected along with select behavioral measures (eg locomotor activity, grooming). HCRT-1 dose-dependently increased PFC dialysate DA levels, and these increases were closely correlated with increases in time spent awake. In contrast, Acc DA levels were unaffected. Additional studies examined whether HCRT-1 acts directly within the ventral tegmental area (VTA) to selectively increase PFC DA efflux and modulate behavioral state. Unilateral infusion of HCRT-1 (0.1, 1.0 nmol) within the VTA increased PFC, but not Acc, DA levels. Importantly, intra-VTA infusion of HCRT-1 increased the time spent awake and grooming. Moreover, HCRT-induced increases in both time spent awake and time spent grooming were significantly correlated with post-infusion PFC DA levels. The current observations predict a prominent modulatory influence of HCRT on PFC-dependent cognitive and affective processes that results, in part, from actions within the VTA. Additionally, these observations suggest that the activation of VTA DA neurons contributes to the behavioral state-modulatory actions of HCRT.

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“…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).…”

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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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Wake-Promoting Actions of Dopamine D1 and D2 Receptor Stimulation

Cited by 108 publications

References 40 publications

Neural Substrates of Psychostimulant-Induced Arousal

Neural Substrates of Psychostimulant-Induced Arousal

Hypocretin/Orexin Selectively Increases Dopamine Efflux within the Prefrontal Cortex: Involvement of the Ventral Tegmental Area

Drosophila D1 dopamine receptor mediates caffeine-induced arousal

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