Sensitized nucleus accumbens dopamine terminal responses to methylphenidate and dopamine transporter releasers after intermittent-access self-administration

Calipari, Erin S.

doi:10.1016/j.neuropharm.2014.02.021

Cited by 23 publications

(18 citation statements)

References 61 publications

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“…Increased D 2 sensitivity in our limited access mice was observed 24hrs following removal of the HF diet, so it is possible that enhanced D 2 sensitivity may be related to acute withdrawal from HF. AMPH exposure, however, reduced autoreceptor function in the limited access group, in line with the classical development of behavioral sensitization, and other reports showing that repeated psychostimulant exposure is associated with reduced D 2 autoreceptor function (Calipari and Jones, 2014; Mateo et al, 2005). The reduced ability of quinpirole to regulate presynaptic dopamine release suggests that decreased D 2 function after repeated AMPH likely drove the enhanced behavioral sensitization we observed in mice with limited access to HF.…”

Section: Discussionsupporting

confidence: 85%

High fat diet augments amphetamine sensitization in mice: Role of feeding pattern, obesity, and dopamine terminal changes

Fordahl

Locke

2016

Neuropharmacology

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High fat (HF) diet-induced obesity has been shown to augment behavioral responses to psychostimulants that target the dopamine system. The purpose of this study was to characterize dopamine terminal changes induced by a HF diet that correspond with enhanced locomotor sensitization to amphetamine. C57BL/6J mice had limited (2hr 3d/week) or extended (24h 7d/week) access to a HF diet or standard chow for six weeks. Mice were then repeatedly exposed to amphetamine (AMPH), and their locomotor responses to an amphetamine challenge were measured. Fast scan cyclic voltammetry was used to identify changes in dopamine terminal function after AMPH exposure. Exposure to a HF diet reduced dopamine uptake and increased locomotor responses to acute, high-dose AMPH administration compared to chow fed mice. Microdialysis showed elevated extracellular dopamine in the nucleus accumbens (NAc) coincided with enhanced locomotion after acute AMPH in HF-fed mice. All mice exhibited locomotor sensitization to amphetamine, but both extended and limited access to a HF diet augmented this response. Neither HF-fed group showed the robust amphetamine sensitization-induced increases in dopamine release, reuptake, and amphetamine potency observed in chow fed animals. However, the potency of amphetamine as an uptake inhibitor was significantly elevated after sensitization in mice with extended (but not limited) access to HF. Conversely, after amphetamine sensitization, mice with limited (but not extended) access to HF displayed reduced autoreceptor sensitivity to the D2/D3 agonist quinpirole. Additionally, we observed reduced membrane dopamine transporter (DAT) levels after HF, and a shift in DAT localization to the cytosol was detected with limited access to HF. This study showed that different patterns of HF exposure produced distinct dopamine terminal adaptations to repeated AMPH, which differed from chow fed mice, and enhanced sensitization to AMPH. Locomotor sensitization in chow fed mice coincided with elevated DAT function and increased AMPH potency; however, the enhanced behavioral response to AMPH after HF exposure was unique in that it coincided with reduced DAT function and diet pattern-specific adaptations.

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Section: Discussionsupporting

confidence: 85%

High fat diet augments amphetamine sensitization in mice: Role of feeding pattern, obesity, and dopamine terminal changes

Fordahl

Locke

2016

Neuropharmacology

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“…MPH exhibits an inverted "U"-shaped profile that is indicative of a dopamine transporter blocker ( Fig. 4A; Ferris et al, 2012;Calipari et al, 2014b). ANOVA revealed a main effect of MPH on dopamine release (F 3,80 5 11.89, P , 0.05).…”

Section: Resultsmentioning

confidence: 93%

“…Previously published work from our laboratory has shown that, although MPH is a DAT blocker, it is affected by changes at the DAT that alter releaser potency, possibly due to the amphetamine-like structure of the compound (Calipari et al, , 2014bFerris et al, 2012). DAT binding is highly dependent on structural components; accordingly, work has shown that MPH binds to the DAT in a fashion that is similar to amphetamine (Wayment et al, 1999;Dar et al, 2005).…”

Section: Introductionmentioning

confidence: 98%

Intermittent Cocaine Self-Administration Produces Sensitization of Stimulant Effects at the Dopamine Transporter

Calipari

Ferris

Siciliano

et al. 2014

J Pharmacol Exp Ther

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Previous literature investigating neurobiological adaptations following cocaine self-administration has shown that high, continuous levels of cocaine intake (long access; LgA) results in reduced potency of cocaine at the dopamine transporter (DAT), whereas an intermittent pattern of cocaine administration (intermittent access; IntA) results in sensitization of cocaine potency at the DAT. Here, we aimed to determine whether these changes are specific to cocaine or translate to other psychostimulants. Psychostimulant potency was assessed by fast-scan cyclic voltammetry in brain slices containing the nucleus accumbens following IntA, short access, and LgA cocaine self-administration, as well as in brain slices from naive animals. We assessed the potency of amphetamine (a releaser), and methylphenidate (a DAT blocker, MPH). MPH was selected because it is functionally similar to cocaine and structurally related to amphetamine. We found that MPH and amphetamine potencies were increased following IntA, whereas neither was changed following LgA or short access cocaine self-administration. Therefore, whereas LgA-induced tolerance at the DAT is specific to cocaine as shown in previous work, the sensitizing effects of IntA apply to cocaine, MPH, and amphetamine. This demonstrates that the pattern with which cocaine is administered is important in determining the neurochemical consequences of not only cocaine effects but potential cross-sensitization/cross-tolerance effects of other psychostimulants as well.

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“…Because the striatal DA system is an important site of action for many drugs of abuse (Calipari and Jones, 2014; Calipari et al, 2014), including ethanol (Yim et al, 1998), we examined changes in presynaptic DA kinetics in a mouse model of dependence (Becker and Hale, 1993). In summary, our data show that CIE produces a pattern of presynaptic DA signaling changes, including decreased DA release, increased DA uptake, and D2 autoreceptor supersensitivity, resulting in functional hypodopaminergia during withdrawal.…”

Section: 4 Conclusionmentioning

confidence: 99%

Chronic intermittent ethanol exposure reduces presynaptic dopamine neurotransmission in the mouse nucleus accumbens

Karkhanis¹,

Rose²,

Huggins³

et al. 2015

Drug and Alcohol Dependence

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BACKGROUND Increasing evidence suggests that chronic ethanol exposure decreases dopamine (DA) neurotransmission in the nucleus accumbens (NAc), contributing to a hypodopaminergic state during withdrawal. However, few studies have investigated adaptations in presynaptic DA terminals after chronic intermittent ethanol (CIE) exposure. In monkeys and rats, chronic ethanol exposure paradigms have been shown to increase DA uptake and D2 autoreceptor sensitivity. METHODS The current study examined the effects of ethanol on DA terminals in CIE exposed mice during two time-points after the cessation of CIE exposure. DA release and uptake were measured using fast scan cyclic voltammetry in NAc core slices from C57BL/6J mice, 0 and 72 hours following three weekly cycles (4 days of 16 hrs ethanol vapor/8 hrs room air/day + 3 days withdrawal) of CIE vapor exposure. RESULTS Current results showed that DA release was reduced, uptake rates were increased, and inhibitory D2-type autoreceptor activity was augmented following CIE exposure in mice. CONCLUSIONS Overall, these CIE-induced adaptations in the accumbal DA system reduce DA signaling and therefore reveal several potential mechanisms contributing to a functional hypodopaminergic state during alcohol withdrawal.

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Sensitized nucleus accumbens dopamine terminal responses to methylphenidate and dopamine transporter releasers after intermittent-access self-administration

Cited by 23 publications

References 61 publications

High fat diet augments amphetamine sensitization in mice: Role of feeding pattern, obesity, and dopamine terminal changes

High fat diet augments amphetamine sensitization in mice: Role of feeding pattern, obesity, and dopamine terminal changes

Intermittent Cocaine Self-Administration Produces Sensitization of Stimulant Effects at the Dopamine Transporter

Chronic intermittent ethanol exposure reduces presynaptic dopamine neurotransmission in the mouse nucleus accumbens

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