Chronic treatment with a dopamine uptake blocker changes dopamine and acetylcholine but not glutamate and GABA concentrations in prefrontal cortex, striatum and nucleus accumbens of the awake rat

Hernández, Luis Felipe Álvarez; Segovia, Gregorio; Mora, Francisco

doi:10.1016/j.neuint.2007.08.005

Cited by 16 publications

(13 citation statements)

References 64 publications

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“…We would like to state that while AcbC is a good target for sampling DA it might not be a good option for NE, EP, 5-HT or AD sampling. However, these neurochemicals have been collected and measured from AcbC as previously reported (Salem and Hope, 1999;Del Arco et al, 2008;Hernandez et al, 2008;Rada et al, 2010;Cannazza et al, 2012;Dobbs and Mark, 2012;Munari et al, 2013;Pajski and Venton, 2013;Dautan et al, 2014). Thus, these evidences indicate the trustworthy of our study.…”

Section: Discussionsupporting

confidence: 77%

Revealing the role of the endocannabinoid system modulators, SR141716A, URB597 and VDM-11, in sleep homeostasis

et al. 2016

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Abstract-The endocannabinoid system comprises receptors (CB 1 and CB 2 cannabinoid receptors), enzymes (Fatty Acid Amide Hydrolase [FAAH], which synthesizes the endocannabinoid anandamide), as well as the anandamide membrane transporter (AMT). Importantly, previous experiments have demonstrated that the endocannabinoid system modulates multiple neurobiological functions, including sleep. For instance, SR141716A (the CB 1 cannabinoid receptor antagonist) as well as URB597 (the FAAH inhibitor) increase waking in rats whereas VDM-11 (the blocker of the AMT) enhances sleep in rodents. However, no further evidence is available regarding the neurobiological role of the endocannabinoid system in the homeostatic control of sleep. Therefore, the aim of the current experiment was to test if SR141716A, URB597 or VDM-11 would modulate the sleep rebound after sleep deprivation. Thus, these compounds were systemically injected (5, 10, 20 mg/kg; ip; separately each one) into rats after prolonged waking. We found that SR141716A and URB597 blocked in dose-dependent fashion the sleep rebound whereas animals treated with VDM-11 displayed sleep rebound during the recovery period. Complementary, injection after sleep deprivation of either SR141716A or URB597 enhanced dose-dependently the extracellular levels of dopamine (DA), norepinephrine (NE), epinephrine (EP), serotonin (5-HT), as well as adenosine (AD) while VDM-11 caused a decline in contents of these molecules. These findings suggest that SR141716A or URB597 behave as a potent stimulants since they suppressed the sleep recovery period after prolonged waking. It can be concluded that elements of the endocannabinoid system, such as the CB 1 cannabinoid receptor, FAAH and AMT, modulate the sleep homeostasis after prolonged waking. Ó

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Section: Discussionsupporting

confidence: 77%

Revealing the role of the endocannabinoid system modulators, SR141716A, URB597 and VDM-11, in sleep homeostasis

et al. 2016

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“…In addition, chronic treatment with the DA reuptake inhibitor nomifensine (10 mg/kg, i.p. for 22 days) increased the basal extracellular DA levels in the prefrontal cortex (Hernández et al. 2008).…”

Section: Discussionmentioning

confidence: 99%

“…In view of the idea, it is also appears that methylphenidate increases the extracellular DA levels in the prefrontal cortex via an inhibition of the NA transporter besides the DA transporter. Furthermore, it is likely that methylphenidate‐induced increases in the prefrontal DA levels is mediated by an inhibition of the NA transporter rather than the DA transporter, as administration of the specific DA reuptake inhibitor nomifensine does not cause an increase in extracellular DA levels in the prefrontal cortex (Hernández et al. 2008).…”

Section: Discussionmentioning

confidence: 99%

Effects of acute and chronic administration of atomoxetine and methylphenidate on extracellular levels of noradrenaline, dopamine and serotonin in the prefrontal cortex and striatum of mice

Koda

Ago

Cong

et al. 2010

Journal of Neurochemistry

204

134

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K. K. and Y. A. contributed equally to this work.Abbreviations used: 5-HT, serotonin; ADHD, attention-deficit/hyperactivity disorder; AUC, area under the curve; DA, dopamine; i.p., intraperitoneally; NA, noradrenaline; PBS, phosphate buffered saline. AbstractAcute administration of atomoxetine and methylphenidate, attention-deficit/hyperactivity disorder (ADHD) drugs, activates catecholaminergic systems in rat brain, but the effects of their chronic administration are not known. This study examined the effects of acute and chronic administration of ADHD drugs on the extracellular levels of noradrenaline (NA), dopamine (DA) and serotonin (5-HT), and the expression of the neuronal activity marker c-Fos in the prefrontal cortex and striatum of mice. Acute ADHD drugs increased NA and DA, but not 5-HT, levels in the prefrontal cortex of mice. Maximal effects of atomoxetine and methylphenidate were observed at 1 mg/kg and 3 mg/kg, respectively. At these doses, both drugs did not affect the spontaneous locomotor activity of mice. Chronic administration of atomoxetine 1 mg/kg and methylphenidate 3 mg/kg for 21 days also increased NA and DA, but not 5-HT, levels in the prefrontal cortex. The increases in NA levels induced by atomoxetine, but not methylphenidate, were reduced by chronic treatment. In contrast, acute and chronic administration of atomoxetine 1 mg/kg and methylphenidate 3 mg/kg did not affect the monoamine levels in the striatum. Acute and chronic atomoxetine 1 mg/kg and methylphenidate 3 mg/kg increased the expression of c-Fos in the prefrontal cortex, but not in the striatum, to a similar extent. These results suggest that acute and chronic administration of the ADHD drugs selectively activate the prefrontal catecholamine systems in mice.

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“…We did not find any significant differences in resting levels of ACh among the mPFC subregions, and little variability existed within each subregion. Reported resting levels of ACh in the mPFC have widely varied from 0.58 ± 0.14 nM to 3.0 ± 0.3 μM in microdialysis studies (Arnold et al, 2001; Hernandez et al, 2008; Huang et al, 2008; Mork et al, 2009; Neigh-McCandless et al, 2002). Our ACh measurements of 0.59 – 0.96 μM fall into the higher end of the range of these previously reported microdialysis ACh concentrations.…”

Section: Discussionmentioning

confidence: 99%

Tonic and phasic release of glutamate and acetylcholine neurotransmission in sub-regions of the rat prefrontal cortex using enzyme-based microelectrode arrays

Mattinson

Burmeister

Quintero

et al. 2011

Journal of Neuroscience Methods

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Chronic treatment with a dopamine uptake blocker changes dopamine and acetylcholine but not glutamate and GABA concentrations in prefrontal cortex, striatum and nucleus accumbens of the awake rat

Cited by 16 publications

References 64 publications

Revealing the role of the endocannabinoid system modulators, SR141716A, URB597 and VDM-11, in sleep homeostasis

Revealing the role of the endocannabinoid system modulators, SR141716A, URB597 and VDM-11, in sleep homeostasis

Effects of acute and chronic administration of atomoxetine and methylphenidate on extracellular levels of noradrenaline, dopamine and serotonin in the prefrontal cortex and striatum of mice

Tonic and phasic release of glutamate and acetylcholine neurotransmission in sub-regions of the rat prefrontal cortex using enzyme-based microelectrode arrays

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