Anti-manic effect of deep brain stimulation of the ventral tegmental area in an animal model of mania induced by methamphetamine.

bipolar disorder deep brain stimulation depression dopamine mania methamphetamine psychiatry

Journal

Bipolar disorders
ISSN: 1399-5618
Titre abrégé: Bipolar Disord
Pays: Denmark
ID NLM: 100883596

Informations de publication

Date de publication:
01 Apr 2024
Historique:
medline: 1 4 2024
pubmed: 1 4 2024
entrez: 1 4 2024
Statut: aheadofprint

Résumé

Treatment of refractory bipolar disorder (BD) is extremely challenging. Deep brain stimulation (DBS) holds promise as an effective treatment intervention. However, we still understand very little about the mechanisms of DBS and its application on BD. The present study aimed to investigate the behavioural and neurochemical effects of ventral tegmental area (VTA) DBS in an animal model of mania induced by methamphetamine (m-amph). Wistar rats were given 14 days of m-amph injections, and on the last day, animals were submitted to 20 min of VTA DBS in two different patterns: intermittent low-frequency stimulation (LFS) or continuous high-frequency stimulation (HFS). Immediately after DBS, manic-like behaviour and nucleus accumbens (NAc) phasic dopamine (DA) release were evaluated in different groups of animals through open-field tests and fast-scan cyclic voltammetry. Levels of NAc dopaminergic markers were evaluated by immunohistochemistry. M-amph induced hyperlocomotion in the animals and both DBS parameters reversed this alteration. M-amph increased DA reuptake time post-sham compared to baseline levels, and both LFS and HFS were able to block this alteration. LFS was also able to reduce phasic DA release when compared to baseline. LFS was able to increase dopamine transporter (DAT) expression in the NAc. These results demonstrate that both VTA LFS and HFS DBS exert anti-manic effects and modulation of DA dynamics in the NAc. More specifically the increase in DA reuptake driven by increased DAT expression may serve as a potential mechanism by which VTA DBS exerts its anti-manic effects.

Sections du résumé

BACKGROUND BACKGROUND
Treatment of refractory bipolar disorder (BD) is extremely challenging. Deep brain stimulation (DBS) holds promise as an effective treatment intervention. However, we still understand very little about the mechanisms of DBS and its application on BD.
AIM OBJECTIVE
The present study aimed to investigate the behavioural and neurochemical effects of ventral tegmental area (VTA) DBS in an animal model of mania induced by methamphetamine (m-amph).
METHODS METHODS
Wistar rats were given 14 days of m-amph injections, and on the last day, animals were submitted to 20 min of VTA DBS in two different patterns: intermittent low-frequency stimulation (LFS) or continuous high-frequency stimulation (HFS). Immediately after DBS, manic-like behaviour and nucleus accumbens (NAc) phasic dopamine (DA) release were evaluated in different groups of animals through open-field tests and fast-scan cyclic voltammetry. Levels of NAc dopaminergic markers were evaluated by immunohistochemistry.
RESULTS RESULTS
M-amph induced hyperlocomotion in the animals and both DBS parameters reversed this alteration. M-amph increased DA reuptake time post-sham compared to baseline levels, and both LFS and HFS were able to block this alteration. LFS was also able to reduce phasic DA release when compared to baseline. LFS was able to increase dopamine transporter (DAT) expression in the NAc.
CONCLUSION CONCLUSIONS
These results demonstrate that both VTA LFS and HFS DBS exert anti-manic effects and modulation of DA dynamics in the NAc. More specifically the increase in DA reuptake driven by increased DAT expression may serve as a potential mechanism by which VTA DBS exerts its anti-manic effects.

Identifiants

pubmed: 38558302
doi: 10.1111/bdi.13423
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
Organisme : National Health and Medical Research Council
ID : APP1160472
Organisme : National Health and Medical Research Council
ID : GNT1156072
Organisme : National Health and Medical Research Council
ID : 2017131
Organisme : The Centre of Research Excellence for the Development of Innovative Therapies for Psychiatric Disorders
ID : GNT1153607

Informations de copyright

© 2024 The Authors. Bipolar Disorders published by John Wiley & Sons Ltd.

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Auteurs

Roger B Varela (RB)

Functional Neuromodulation and Novel Therapeutics Laboratory, Asia Pacific Centre for Neuromodulation, Queensland Brain Institute, The University of Queensland, Brisbane, Queensland, Australia.

Suelen L Boschen (SL)

Department of Neurologic Surgery, Neural Engineering Laboratories, Mayo Clinic, Rochester, Minnesota, USA.
Department of Neurologic Surgery, Applied Computational Neurophysiology and Neuromodulation Laboratory, Mayo Clinic, Rochester, Minnesota, USA.

Nathanael Yates (N)

Functional Neuromodulation and Novel Therapeutics Laboratory, Asia Pacific Centre for Neuromodulation, Queensland Brain Institute, The University of Queensland, Brisbane, Queensland, Australia.

Tristan Houghton (T)

Functional Neuromodulation and Novel Therapeutics Laboratory, Asia Pacific Centre for Neuromodulation, Queensland Brain Institute, The University of Queensland, Brisbane, Queensland, Australia.

Charles D Blaha (CD)

Department of Neurologic Surgery, Neural Engineering Laboratories, Mayo Clinic, Rochester, Minnesota, USA.

Kendall H Lee (KH)

Department of Neurologic Surgery, Neural Engineering Laboratories, Mayo Clinic, Rochester, Minnesota, USA.

Kevin E Bennet (KE)

Department of Neurologic Surgery, Neural Engineering Laboratories, Mayo Clinic, Rochester, Minnesota, USA.
Division of Engineering, Mayo Clinic, Rochester, Minnesota, USA.

Abbas Z Kouzani (AZ)

School of Engineering, Deakin University, Geelong, Victoria, Australia.

Michael Berk (M)

School of Medicine, IMPACT-The Institute for Mental and Physical Health and Clinical Translation, Barwon Health, Deakin University, Geelong, Victoria, Australia.

João Quevedo (J)

Faillace Department of Psychiatry and Behavioral Sciences, Center for Interventional Psychiatry, McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth Houston), Houston, Texas, USA.
Faillace Department of Psychiatry and Behavioral Sciences, Center of Excellence on Mood Disorders, McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston, Texas, USA.
Faillace Department of Psychiatry and Behavioral Sciences, Translational Psychiatry Program, McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston, Texas, USA.
Translational Psychiatry Laboratory, Graduate Program in Health Sciences, University of Southern Santa Catarina (UNESC), Criciúma, Santa Catarina, Brazil.

Samira S Valvassori (SS)

Translational Psychiatry Laboratory, Graduate Program in Health Sciences, University of Southern Santa Catarina (UNESC), Criciúma, Santa Catarina, Brazil.

Susannah J Tye (SJ)

Functional Neuromodulation and Novel Therapeutics Laboratory, Asia Pacific Centre for Neuromodulation, Queensland Brain Institute, The University of Queensland, Brisbane, Queensland, Australia.
Department of Psychiatry and Psychology, Translational Neuroscience Laboratory, Mayo Clinic, Rochester, Minnesota, USA.
Department of Psychiatry, University of Minnesota, Minneapolis, Minnesota, USA.
Department of Psychiatry and Behavioral Sciences, Emory University, Atlanta, Georgia, USA.

Classifications MeSH