Uridine decreases morphine-induced behavioral sensitization by decreasing dorsal striatal dopamine release possibly via agonistic effects at GABAA receptors

Liu, Ping; Wu, Chunfu; Wu, Song; Yu, Lisha; Yang, Xiaofeng; Xiang, Rongwu; Wang, Fang; Yang, Jingyu

doi:10.1016/j.euroneuro.2014.06.010

Cited by 7 publications

(1 citation statement)

References 37 publications

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“…Also, the ratio of glutamate to glutamine is known to decrease in the dorsolateral prefrontal cortex and basal ganglia of adult ADHD patients [ 45 ]. Beta-alanine is reported to possess attenuating effects on morphine-induced hyperactivity, which may be related to its property mimicking gamma-aminobutyric acid [ 47 ]. Phenylalanine is a well-known precursor of neurotransmitter, typically considered to play a role in neurological disorders.…”

Section: Discussionmentioning

confidence: 99%

GC-TOF-MS-Based Metabolomic Analysis and Evaluation of the Effects of HX106, a Nutraceutical, on ADHD-Like Symptoms in Prenatal Alcohol Exposed Mice

Lee

Jeon

et al. 2020

Nutrients

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Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder that occurs in children characterized by inattention and hyperactivity. Prenatal alcohol exposure (PAE) can disrupt fetal neuronal development and cause an ADHD-like hyperactive behavior in the offspring. In this study, we hypothesized that metabolic disturbance would involve in ADHD neuropathology and aimed to investigate the changes in metabolite profile in PAE-induced ADHD-like model and the effects of HX106, a nutraceutical, on ADHD-like pathophysiology and metabolite changes. To this end, we administered HX106 to the mouse offspring affected by PAE (OPAE) and assessed the hyperactivity using the open field test. We observed that HX106-treated OPAE showed less hyperactive behavior than vehicle-treated OPAE. The effects of HX106 were found to be related to the regulation of dopamine transporter and D2 dopamine receptor expression. Furthermore, using gas chromatography time-of-flight mass spectrometry-based metabolomics, we explored the metabolite changes among the experimental groups. The metabolite profile, particularly related with the amino acids, linoleic acid and amino sugar pathways, was altered by PAE and reversed by HX106 treatment partially similar to that observed in the control group. Overall, this study suggest that metabolite alteration would be involved in ADHD pathology and that HX106 can be an efficient supplement to overcome ADHD by regulating dopamine signaling-related protein expression and metabolite changes.

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Section: Discussionmentioning

confidence: 99%