Association of dopaminergic/GABAergic genes with attention deficit hyperactivity disorder in children

Wang, Guangxin; Ma, Yonggang; Wang, Shifu; Ren, Guang-Fang; Guo, Hui

doi:10.3892/mmr.2012.1028

Cited by 7 publications

(4 citation statements)

References 22 publications

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“…In the cortex, inhibitory GABAergic interneurons are modifying and directing neuronal activity, and interneuronal dysfunction is acknowledged to play an important role in the etiology of several psychiatric diseases, including ADHD (Wang et al, 2012) and ASD (Gao and Penzes, 2015;Hashemi et al, 2017). Oxidative stress can cause cellular damage of GABAergic interneurons, leading to decreased neuronal activity (Sakurai and Gamo, 2019).…”

Section: Discussionmentioning

confidence: 99%

Reduction of cortical parvalbumin-expressing GABAergic interneurons in a rodent hyperoxia model of preterm birth brain injury with deficits in social behavior and cognition

et al. 2021

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The inhibitory GABAergic system in the brain is involved in the etiology of various psychiatric problems, including autism spectrum disorders (ASD), attention deficit hyperactivity disorder (ADHD), and others. These disorders are influenced not only by genetic but also by environmental factors, such as preterm birth, although the mechanisms underlying are not known. In a translational hyperoxia model, exposing mice pups at age P5 to 80% oxygen for 48 hours to mimic a steep rise of oxygen exposure caused by preterm birth from in utero into room air, we documented a persistent reduction of cortical mature parvalbumin expressing interneurons until adulthood. Developmental delay of cortical myelin was observed together with decreased expression of oligodendroglial glial cell-derived neurotrophic factor (GDNF), a factor being involved in interneuronal development. Electrophysiological and morphological properties of remaining interneurons were unaffected. Behavioral deficits were observed for social interaction, learning, and attention. These results elucidate that neonatal oxidative stress can lead to decreased interneuron density and to psychiatric symptoms. The obtained cortical myelin deficit and decreased oligodendroglial GDNF expression indicate an impaired oligodendroglial-interneuronal interplay contributes to interneuronal damage.

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Section: Discussionmentioning

confidence: 99%

Reduction of cortical parvalbumin-expressing GABAergic interneurons in a rodent hyperoxia model of preterm birth brain injury with deficits in social behavior and cognition

et al. 2021

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“…For example, both ADHD and ASD involve synaptic mechanisms. Genes in dopaminergic [55], serotoninergic [53], glutamatergic [56,57] and GABAergic [58,59] systems have been implicated in both disorders. Variants in SHANK3-NLGN4-NRXN1 postsynaptic density genes were found in ASD [60].…”

Section: Biologicalmentioning

confidence: 99%

The comorbidity of ADHD and autism spectrum disorder

Antshel

Zhang-James

Faraone

2013

Expert Review of Neurotherapeutics

126

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ADHD and autism spectrum disorder are common psychiatric comorbidities to each another. In addition, there is behavioral, biological and neuropsychological overlap between the two disorders. There are also several important differences between autism spectrum disorder and ADHD. Treatment strategies for the comorbid condition will also be reviewed. Future areas of research and clinical need will be discussed.

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“…Although the etiology and pathophysiology of ADHD remain unclear, some data support the interaction between genetic and environmental factors ( Wang et al, 2012 ; Sun et al, 2018 ). In particular, Kwon and coauthors have shown an association between GABAB3 gene polymorphisms and ADHD in children ( Kwon et al, 2017 ).…”

Section: Gaba a Rs And Neuropsychiatric Disordersmentioning

confidence: 99%

Phenols and GABAA receptors: from structure and molecular mechanisms action to neuropsychiatric sequelae

Menzikov,

Zaichenko,

Moskovtsev

et al. 2024

Front. Pharmacol.

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γ-Aminobutyric acid type A receptors (GABAARs) are members of the pentameric ligand-gated ion channel (pLGIC) family, which are widespread throughout the invertebrate and vertebrate central nervous system. GABAARs are engaged in short-term changes of the neuronal concentrations of chloride (Cl−) and bicarbonate (HCO3−) ions by their passive permeability through the ion channel pore. GABAARs are regulated by various structurally diverse phenolic substances ranging from simple phenols to complex polyphenols. The wide chemical and structural variability of phenols suggest similar and different binding sites on GABAARs, allowing them to manifest themselves as activators, inhibitors, or allosteric ligands of GABAAR function. Interest in phenols is associated with their great potential for GABAAR modulation, but also with their subsequent negative or positive role in neurological and psychiatric disorders. This review focuses on the GABAergic deficit hypotheses during neurological and psychiatric disorders induced by various phenols. We summarize the structure–activity relationship of general phenol groups concerning their differential roles in the manifestation of neuropsychiatric symptoms. We describe and analyze the role of GABAAR subunits in manifesting various neuropathologies and the molecular mechanisms underlying their modulation by phenols. Finally, we discuss how phenol drugs can modulate GABAAR activity via desensitization and resensitization. We also demonstrate a novel pharmacological approach to treat neuropsychiatric disorders via regulation of receptor phosphorylation/dephosphorylation.

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Association of dopaminergic/GABAergic genes with attention deficit hyperactivity disorder in children

Cited by 7 publications

References 22 publications

Reduction of cortical parvalbumin-expressing GABAergic interneurons in a rodent hyperoxia model of preterm birth brain injury with deficits in social behavior and cognition

Reduction of cortical parvalbumin-expressing GABAergic interneurons in a rodent hyperoxia model of preterm birth brain injury with deficits in social behavior and cognition

The comorbidity of ADHD and autism spectrum disorder

Phenols and GABAA receptors: from structure and molecular mechanisms action to neuropsychiatric sequelae

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