Adenosine (A)2A receptor modulation of nicotine-induced locomotor sensitization. A pharmacological and transgenic approach

Jastrzębska, Joanna; Nowak, Ewa; Smaga, Irena; Bystrowska, Beata; Frankowska, Małgorzata; Bäder, Michael; Filip, Małgorzata; Fuxé, Kjell

doi:10.1016/j.neuropharm.2014.03.002

Cited by 17 publications

(16 citation statements)

References 34 publications

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“…It was found that spontaneous glutamate efflux was not different in the two genotypes, in agreement with a recent article which demonstrated that basal tissue glutamate levels were not different in the striatum of NSEA 2A animals with respect to control rats (Jastrzębska et al . ). On the contrary, K + ‐induced glutamate outflow was (i) significantly increased in NSEA 2A with respect to WT rats; (ii) increased by CGS 21680, with a significantly higher effect in NSEA 2A than in WT rats; (iii) reduced by ZM 241385 in NSEA 2A but not in WT rats; (iv) reduced by WIN, with a significantly lower effect in NSEA 2A than in WT.…”

Section: Discussionmentioning

confidence: 97%

Striatal adenosine–cannabinoid receptor interactions in rats over‐expressing adenosine A_2A receptors

Chiodi

Ferrante

Ferraro

et al. 2015

Journal of Neurochemistry

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Adenosine A 2A receptors (A 2A Rs) and cannabinoid CB 1 receptors (CB 1 Rs) are highly expressed in the striatum, where they functionally interact and form A 2A /CB 1 heteroreceptor complexes. We investigated the effects of CB 1 R stimulation in a transgenic rat strain over-expressing A 2A Rs under the control of the neural-specific enolase promoter (NSEA 2A rats) and in age-matched wild-type (WT) animals. The effects of the CB 1 R agonist WIN 55,212-2 (WIN) were significantly lower in NSEA 2A rats than in WT animals, as demonstrated by i) electrophysiological recordings of synaptic transmission in corticostriatal slices; ii) the measurement of glutamate outflow from striatal synaptosomes and iii) in vivo experiments on locomotor activity. Moreover, while the effects of WIN were modulated by both A 2A R agonist (CGS 21680) and antagonists (ZM 241385, KW-6002 and SCH-442416) in WT animals, the A 2A R antagonists failed to influence WIN-mediated effects in NSEA 2A rats. The present results demonstrate that in rats with genetic neuronal overexpression of A 2A Rs, the effects mediated by CB 1 R activation in the striatum are significantly reduced, suggesting a change in the stoichiometry of A 2A and CB 1 receptors and providing a strategy to dissect the involvement of A 2A R forming or not forming heteromers in the modulation of striatal functions. These findings add additional evidence for the existence of an interaction between striatal A 2A Rs and CB 1 Rs, playing a fundamental role in the regulation of striatal functions.

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Section: Discussionmentioning

confidence: 97%

Striatal adenosine–cannabinoid receptor interactions in rats over‐expressing adenosine A_2A receptors

Chiodi

Ferrante

Ferraro

et al. 2015

Journal of Neurochemistry

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“…Similarly, when cue-signaled reinforcement was predictable during the 5-CSRTT, ZM-241385 did not induce impulsive sign-tracking responses. It is possible that inhibition of the A 2A R, which includes the effects of caffeine, may mediate increases in locomotion, 40, 60, 61 which when in combination with reward/reinforcement unpredictability, leads to compounded exploratory activity and exacerbations in impulsive reward-seeking behavior. Therefore, we posit that dysfunctional adenosinergic regulation can exacerbate the inherent cognitive dissonance between the drive for reward gratification and a reward, which may or may not be available.…”

Section: Discussionmentioning

confidence: 99%

Adenosine A2A receptor and ERK-driven impulsivity potentiates hippocampal neuroblast proliferation

Oliveros

et al. 2017

Transl Psychiatry

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Dampened adenosine A2A receptor (A2AR) function has been implicated in addiction through enhancement of goal-directed behaviors. However, the contribution of the A2AR to the control of impulsive reward seeking remains unknown. Using mice that were exposed to differential reward of low rate (DRL) schedules during Pavlovian-conditioning, second-order schedule discrimination, and the 5-choice serial reaction time task (5-CSRTT), we demonstrate that deficits of A2AR function promote impulsive responses. Antagonism of the A2AR lowered ERK1 and ERK2 phosphorylation in the dorsal hippocampus (dHip) and potentiated impulsivity during Pavlovian-conditioning and the 5-CSRTT. Remarkably, inhibition of ERK1 and ERK2 phosphorylation by U0126 in the dHip prior to Pavlovian-conditioning exacerbated impulsive reward seeking. Moreover, we found decreased A2AR expression, and reduced ERK1 and ERK2 phosphorylation in the dHip of equilibrative nucleoside transporter type 1 (ENT1–/–) null mice, which displayed exacerbated impulsivity. To determine whether impulsive response behavior is associated with hippocampal neuroblast development, we investigated expression of BrdU+ and doublecortin (DCX+) following 5-CSRTT testing. These studies revealed that impulsive behavior driven by inhibition of the A2AR is accompanied by increased neuroblast proliferation in the hippocampus.

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“…A 2A R, belonging to Family A GPCRs, are widely expressed in the CNS including striatum, hippocampus, and cortex and play essential roles in the regulation of locomotion, sleep, anxiety, memory, and cognition [16, 17]. Recently, A 2A R has emerged as a non-dopaminergic target for the treatment of PD, owing to its physical and functional interaction with dopamine D 2 receptor in striato-pallidal GABA pathway [18].…”

Section: Introductionmentioning

confidence: 99%

An Anti-Parkinson’s Disease Drug via Targeting Adenosine A2A Receptor Enhances Amyloid-β Generation and γ-Secretase Activity

Lü

Cui

et al. 2016

PLoS ONE

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γ-secretase mediates the intramembranous proteolysis of amyloid precursor protein (APP) and determines the generation of Aβ which is associated with Alzheimer’s disease (AD). Here we identified that an anti-Parkinson’s disease drug, Istradefylline, could enhance Aβ generation in various cell lines and primary neuronal cells of APP/PS1 mouse. Moreover, the increased generation of Aβ42 was detected in the cortex of APP/PS1 mouse after chronic treatment with Istradefylline. Istradefylline promoted the activity of γ-secretase which could lead to increased Aβ production. These effects of Istradefylline were reduced by the knockdown of A2AR but independent of A2AR-mediated G protein- or β-arrestin-dependent signal pathway. We further observed that A2AR colocalized with γ-secretase in endosomes and physically interacted with the catalytic subunit presenilin-1 (PS1). Interestingly, Istradefylline attenuated the interaction in time- and dosage-dependent manners. Moreover the knockdown of A2AR which in theory would release PS1 potentiated both Aβ generation and γ-secretase activity. Thus, our study implies that the association of A2AR could modulate γ-secretase activity. Istradefylline enhance Aβ generation and γ-secretase activity possibly via modulating the interaction between A2AR and γ-secretase, which may bring some undesired effects in the central nervous system (CNS).

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Adenosine (A)2A receptor modulation of nicotine-induced locomotor sensitization. A pharmacological and transgenic approach

Cited by 17 publications

References 34 publications

Striatal adenosine–cannabinoid receptor interactions in rats over‐expressing adenosine A_2A receptors

Striatal adenosine–cannabinoid receptor interactions in rats over‐expressing adenosine A_2A receptors

Adenosine A2A receptor and ERK-driven impulsivity potentiates hippocampal neuroblast proliferation

An Anti-Parkinson’s Disease Drug via Targeting Adenosine A2A Receptor Enhances Amyloid-β Generation and γ-Secretase Activity

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Adenosine (A)2A receptor modulation of nicotine-induced locomotor sensitization. A pharmacological and transgenic approach

Cited by 17 publications

References 34 publications

Striatal adenosine–cannabinoid receptor interactions in rats over‐expressing adenosine A2A receptors

Striatal adenosine–cannabinoid receptor interactions in rats over‐expressing adenosine A2A receptors

Adenosine A2A receptor and ERK-driven impulsivity potentiates hippocampal neuroblast proliferation

An Anti-Parkinson’s Disease Drug via Targeting Adenosine A2A Receptor Enhances Amyloid-β Generation and γ-Secretase Activity

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Striatal adenosine–cannabinoid receptor interactions in rats over‐expressing adenosine A_2A receptors

Striatal adenosine–cannabinoid receptor interactions in rats over‐expressing adenosine A_2A receptors