Therapeutic effects of anodal transcranial direct current stimulation in a rat model of ADHD

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Abstract

Most therapeutic candidates for treating attention-deficit hyperactivity disorder (ADHD) have focused on modulating the dopaminergic neurotransmission system with neurotrophic factors. Regulation of this system by transcranial direct current stimulation (tDCS) could contribute to the recovery of cognitive symptoms observed in patients with ADHD. Here, male spontaneously hypertensive rats (SHR) were subjected to consecutive high-definition tDCS (HD-tDCS) (20 min, 50 μA, current density 63.7 A/m ², charge density 76.4 kC/m ²) over the prefrontal cortex. This treatment alleviated cognitive deficits, with an increase in tyrosine hydroxylase and vesicular monoamine transporter two and significantly decreased plasma membrane reuptake transporter (DAT). HD-tDCS application increased the expression of several neurotrophic factors, particularly brain-derived neurotrophic factor (BDNF), and activated hippocampal neurogenesis. Our results suggest that anodal HD-tDCS over the prefrontal cortex may ameliorate cognitive dysfunction via regulation of DAT and BDNF in the mesocorticolimbic dopaminergic pathways, and therefore represents a potential adjuvant therapy for ADHD.

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Essential role of BDNF in the mesolimbic dopamine pathway in social defeat stress.

Olivier Berton, Colleen A. McClung, Ralph J Dileone … (2006)

Mice experiencing repeated aggression develop a long-lasting aversion to social contact, which can be normalized by chronic, but not acute, administration of antidepressant. Using viral-mediated, mesolimbic dopamine pathway-specific knockdown of brain-derived neurotrophic factor (BDNF), we showed that BDNF is required for the development of this experience-dependent social aversion. Gene profiling in the nucleus accumbens indicates that local knockdown of BDNF obliterates most of the effects of repeated aggression on gene expression within this circuit, with similar effects being produced by chronic treatment with antidepressant. These results establish an essential role for BDNF in mediating long-term neural and behavioral plasticity in response to aversive social experiences.

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Dopamine neuronal loss contributes to memory and reward dysfunction in a model of Alzheimer's disease

Annalisa Nobili, Emanuele Latagliata, Maria Teresa Viscomi … (2017)

Alterations of the dopaminergic (DAergic) system are frequently reported in Alzheimer's disease (AD) patients and are commonly linked to cognitive and non-cognitive symptoms. However, the cause of DAergic system dysfunction in AD remains to be elucidated. We investigated alterations of the midbrain DAergic system in the Tg2576 mouse model of AD, overexpressing a mutated human amyloid precursor protein (APPswe). Here, we found an age-dependent DAergic neuron loss in the ventral tegmental area (VTA) at pre-plaque stages, although substantia nigra pars compacta (SNpc) DAergic neurons were intact. The selective VTA DAergic neuron degeneration results in lower DA outflow in the hippocampus and nucleus accumbens (NAc) shell. The progression of DAergic cell death correlates with impairments in CA1 synaptic plasticity, memory performance and food reward processing. We conclude that in this mouse model of AD, degeneration of VTA DAergic neurons at pre-plaque stages contributes to memory deficits and dysfunction of reward processing.

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BDNF regulates eating behavior and locomotor activity in mice.

S G Kernie, D J Liebl, L Parada (2000)

Brain-derived neurotrophic factor (BDNF) was studied initially for its role in sensory neuron development. Ablation of this gene in mice leads to death shortly after birth, and abnormalities have been found in both the peripheral and central nervous systems. BDNF and its tyrosine kinase receptor, TrkB, are expressed in hypothalamic nuclei associated with satiety and locomotor activity. In heterozygous mice, BDNF gene expression is reduced and we find that all heterozygous mice exhibit abnormalities in eating behavior or locomotor activity. We also observe this phenotype in independently derived inbred and hybrid BDNF mutant strains. Infusion with BDNF or NT4/5 can transiently reverse the eating behavior and obesity. Thus, we identify a novel non-neurotrophic function for neurotrophins and indicate a role in behavior that is remarkably sensitive to alterations in BDNF activity.

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Author and article information

Contributors

Byung Tae Choi:

ORCID: https://orcid.org/0000-0002-5965-4346

Richard B Ivry: Role: Senior Editor

Marom Bikson: Role: Reviewing Editor

Journal

Journal ID (nlm-ta): eLife

Journal ID (iso-abbrev): Elife

Journal ID (publisher-id): eLife

Title: eLife

Publisher: eLife Sciences Publications, Ltd

ISSN (Electronic): 2050-084X

Publication date (Electronic, pub): 21 September 2020

Publication date Collection: 2020

Volume: 9

Electronic Location Identifier: e56359

Affiliations

[1 ]Department of Korean Medical Science, School of Korean Medicine, Pusan National University YangsanRepublic of Korea

[2 ]Graduate Training Program of Korean Medicine for Healthy Aging, Pusan National University YangsanRepublic of Korea

[3 ]Korean Medical Science Research Center for Healthy Aging, Pusan National University YangsanRepublic of Korea

[4 ]Department of Radiological Science, Health Science Division, Dongseo University BusanRepublic of Korea

[5 ]Department of Korean Pediatrics, School of Korean Medicine, Pusan National University YangsanRepublic of Korea

[6 ]Department of Rehabilitation Medicine, School of Medicine, Pusan National University YangsanRepublic of Korea

University of California, Berkeley United States

The City College of New York of the City University of New York, Department of Biomedical Engineering United States

Author information

Ki Bong Kim https://orcid.org/0000-0001-5724-4653

Byung Tae Choi https://orcid.org/0000-0002-5965-4346

Article

Publisher ID: 56359

DOI: 10.7554/eLife.56359

PMC ID: 7535928

PubMed ID: 32955434

SO-VID: b094a84a-08d8-43ee-bcc7-eada5606a230

License:

This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.

History

Date received : 25 February 2020

Date accepted : 19 September 2020

Funding

Funded by: FundRef http://dx.doi.org/10.13039/501100003725, National Research Foundation of Korea;

Award ID: 2018R1A2A2A05018926

Award Recipient : Byung Tae Choi

Funded by: FundRef http://dx.doi.org/10.13039/501100003725, National Research Foundation of Korea;

Award ID: 2014R1A5A2009936

Award Recipient : Byung Tae Choi

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

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Author impact statement High-definition anodal transcranial stimulation alleviated cognitive deficits, affected dopaminergic neurotransmission factors, increased expression of several neurotrophic factors involving brain-derived neurotrophic factor (BDNF), and activated hippocampal neurogenesis.

ScienceOpen disciplines: Life sciences

Keywords: anodal transcranial direct current stimulation,attention deficit hyperactivity disorder,dopaminergic neurotransmission factor,brain-derived neurotrophic factor,rat

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ScienceOpen disciplines: Life sciences

Keywords: anodal transcranial direct current stimulation, attention deficit hyperactivity disorder, dopaminergic neurotransmission factor, brain-derived neurotrophic factor, rat

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Therapeutic effects of anodal transcranial direct current stimulation in a rat model of ADHD

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Animal models of intrauterine growth restriction (IUGR)

Most cited references 39

Essential role of BDNF in the mesolimbic dopamine pathway in social defeat stress.

Dopamine neuronal loss contributes to memory and reward dysfunction in a model of Alzheimer's disease

BDNF regulates eating behavior and locomotor activity in mice.

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Cited by 10

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