Biphasic Mechanisms of Amphetamine Action at the Dopamine Terminal

Siciliano, Cody A.; Calipari, Erin S.; Ferris, Mark J.

doi:10.1523/jneurosci.4050-13.2014

Cited by 52 publications

(71 citation statements)

References 29 publications

(1 reference statement)

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“…In contrast, the authors also showed that higher concentrations of only 10 μM amphetamine induced dopamine release via a DATindependent mechanism. These data further support the idea that low doses of amphetamines are insufficient to disrupt vesicular sequestration and act solely as inhibitors of DAT (Siciliano et al, 2014).…”

Section: Dose Dependent Effects Of Amphetamine and Methamphetaminesupporting

confidence: 78%

“…However, it has been suggested that high concentrations of amphetamine (N100 μM) would be required to accomplish this effect (Schwartz et al, 2006). More recently Siciliano et al (2014) demonstrated that low concentrations (10 nM) of amphetamine cause DAT-dependent dopamine release. In contrast, the authors also showed that higher concentrations of only 10 μM amphetamine induced dopamine release via a DATindependent mechanism.…”

Section: Dose Dependent Effects Of Amphetamine and Methamphetaminementioning

confidence: 99%

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The neuroprotective potential of low-dose methamphetamine in preclinical models of stroke and traumatic brain injury

Rau

Ziemniak

Poulsen

2016

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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Methamphetamine is a psychostimulant that was initially synthesized in 1920. Since then it has been used to treat attention deficit hyperactive disorder (ADHD), obesity and narcolepsy. However, methamphetamine has also become a major drug of abuse worldwide. Under conditions of abuse, which involve the administration of high repetitive doses, methamphetamine can produce considerable neurotoxic effects. However, recent evidence from our laboratory indicates that low doses of methamphetamine can produce robust neuroprotection when administered within 12h after severe traumatic brain injury (TBI) in rodents. Thus, it appears that methamphetamine under certain circumstances and correct dosing can produce a neuroprotective effect. This review addresses the neuroprotective potential of methamphetamine and focuses on the potential beneficial application for TBI.

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Section: Dose Dependent Effects Of Amphetamine and Methamphetaminesupporting

confidence: 78%

Section: Dose Dependent Effects Of Amphetamine and Methamphetaminementioning

confidence: 99%

The neuroprotective potential of low-dose methamphetamine in preclinical models of stroke and traumatic brain injury

Rau

Ziemniak

Poulsen

2016

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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“…Specifically, this potentiation was found with the lower NOC-12 concentrations (300 and 400 lM), after 15, 30, and 45 min (data not shown) of incubation with Amph, but not at the higher ones. DA release induced by Amph has been shown to be DAT dependent at low concentrations, such as 10 or 100 nM, whereas at high concentrations, such as 10 lM, the same used here, it involves vesicular depletion (Siciliano et al 2014). Our results suggest that Amph 10 lM added to NOC-12 at 400 lM may have reached a ceiling effect on DA release.…”

Section: Neurotox Resmentioning

confidence: 50%

“…Statistical analysis was performed by one-way ANOVA followed by Duncan post hoc, P \ 0.05 and, together with the toxic effects of DA and Amph (described bellow) on DA neurons, are decreasing DA (Trabace and Kendrick 2000). It also should be taken into account that Amph-induced DA release is dependent on DAT, especially under low doses of Amph (Siciliano et al 2014) and levels of DAT may influence the effects of DA releasers and vary across brain regions (Calipari et al 2015). Therefore, the present results should be interpreted considering the limitations of experiments made with primary mesencephalic cell culture, which cannot reproduce such regional variation in DAT and the influence of other brain regions on these cells.…”

Section: Neurotox Resmentioning

confidence: 99%

Signaling Mechanisms in the Nitric Oxide Donor- and Amphetamine-Induced Dopamine Release in Mesencephalic Primary Cultured Neurons

et al. 2015

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Previous research has shown that nitric oxide (NO) synthase inhibitors prevent rodents' sensorimotor gating impairments induced by dopamine releasing drugs, such as amphetamine (Amph) and methylphenidate. The mechanisms of this effect have not been entirely understood. In the present work, we investigated some possible mechanisms by which the NO donor, NOC-12 (3-ethyl-3-(ethylaminoethyl)-1-hydroxy-2-oxo-1-triazene), influence spontaneous and Amph-induced dopamine release, using rat mesencephalic primary cultured neurons preparations. Our results showed that NOC-12 increased dopamine release in a concentration-dependent manner and potentiated the Amph-induced one. Dopamine release induced by NOC-12 was disrupted by N-acetyl-L-cystein (NAC-a free radical scavenger) and MK-801, a NMDA (N-methyl-D-aspartate) non-competitive antagonist, and was concentration dependently affected by oxadiazolo[4,3]quinoxalin-1-one, an inhibitor of the soluble guanylate cyclase (sGC). In contrast, dopamine released by Amph was facilitated by NAC and by MK-801 and not affected by nifedipine (a L-type-Ca(+2) channel blocker), which enhanced NOC-12-induced dopamine release. The present work demonstrates that DA release induced by NOC-12 is partially dependent on sGC and on NMDA activation, and is modulated by L-type Ca(+2) channel and the antioxidant NAC. This mechanism differs from the Amph-induced one, which appears not to depend on L-type Ca(+2) channel and seems to be facilitated by NMDA channel blocking and by NAC. These results suggest that Amph and NOC-12 induce dopamine release through complementary pathways, which may explain the potentiation of Amph-induced dopamine release by NOC-12. These findings contribute to understand the involvement of NO in dopamine-related neuropsychiatric and neurodegenerative diseases.

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“…Given the role of DAT in removing DA after release, it is plausible that lower levels of DAT in MA vs cocaine addiction may lead to greater amphetamine-induced DA occupancies (recorded with PET) in MA users, ie, an apparent lack of 'blunting'. Indeed, a recent study suggests that in MA users lower DAT levels are associated with increased methylphenidate-induced DA signal (Volkow et al, 2015); heterozygote DAT KO mice (+/ − ), unlike homozygotes (− / − ) (Jones et al, 1998), had increased amphetamine-induced DA response in the striatum compared wth the wild type (+/+) (Ji and Dluzen, 2008); low dose of amphetamine as used in our human neuroimaging studies might depend more on DAT blocking (vs vesicular depletion) to increase extracellular DA (Siciliano et al, 2014).…”

Section: Pet [ 11 C]-(+)-phno Bp Ndmentioning

confidence: 81%

Heightened Dopaminergic Response to Amphetamine at the D3 Dopamine Receptor in Methamphetamine Users

Boileau

Payer

Rusjan

et al. 2016

Neuropsychopharmacol

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Neuroimaging studies in stimulant use (eg, cocaine, methamphetamine) disorders show that diminished dopamine release by dopamineelevating drugs is a potential marker of relapse and suggest that increasing dopamine at the D 2/3 receptors may be therapeutically beneficial. In contrast, recent investigations indicate heightened D 3 receptor levels in stimulant users prompting the view that D 3 antagonism may help prevent relapse. Here we tested whether a 'blunted' response to amphetamine in methamphetamine (MA) users extends to D 3 -rich brain areas. Fourteen MA users and 15 healthy controls completed two positron emission tomographic scans with a D 3 -preferring probe [11 C]-(+)-PHNO at baseline and after amphetamine (0.4 mg/kg). Relative to healthy controls, MA users had greater decreases in [11 C]-(+)-PHNO binding (increased dopamine release) after amphetamine in D 3 -rich substantia nigra (36 vs 20%, p = 0.03) and globus pallidus (30 vs 17%, p = 0.06), which correlated with self-reported 'drug wanting'. We did not observe a 'blunted' dopamine response to amphetamine in D 2 -rich striatum; however, drug use severity was negatively associated with amphetamine-induced striatal changes in [ 11 C]-(+)-PHNO binding. Our study provides evidence that dopamine transmission in extrastriatal 'D 3 -areas' is not blunted but rather increased in MA users. Together with our previous finding of elevated D 3 receptor level in MA users, the current observation suggests that greater dopaminergic transmission at the D 3 dopamine receptor may contribute to motivation to use drugs and argues in favor of D 3 antagonism as a possible therapeutic tool to reduce craving and relapse in MA addiction.

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Biphasic Mechanisms of Amphetamine Action at the Dopamine Terminal

Abstract: In light of recent studies suggesting that amphetamine (AMPH) increases electrically evoked dopamine release ([DA]

Cited by 52 publications

References 29 publications

The neuroprotective potential of low-dose methamphetamine in preclinical models of stroke and traumatic brain injury

The neuroprotective potential of low-dose methamphetamine in preclinical models of stroke and traumatic brain injury

Signaling Mechanisms in the Nitric Oxide Donor- and Amphetamine-Induced Dopamine Release in Mesencephalic Primary Cultured Neurons

Heightened Dopaminergic Response to Amphetamine at the D3 Dopamine Receptor in Methamphetamine Users

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