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Mania, a psychological condition characterized by elevated mood, increased energy, and reduced sleep need, is part of the bipolar disorder cycle. The exact cause of mania isn't entirely known, but it is thought to be a combination of genetic, environmental, and neurological factors. Bipolar disorder involves alternating manic and depressive episodes. Mood stabilizers like lithium, antipsychotics, and anticonvulsants help manage these episodes. Lithium carbonate is particularly effective as...
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Functional Variation in RGS12 Should Not Preclude Methylphenidate Use in Bipolar Disorder with Established Mood

Percy S Agogo-Mawuli1, Joshua D Gross2, Vincent Setola3,4

  • 1Department of Pharmacology and Neuroscience, College of Biomedical & Translational Sciences, University of North Texas Health Science Center, Fort Worth, TX 76107, USA.

International Journal of Molecular Sciences
|December 30, 2025
PubMed
Summary
This summary is machine-generated.

Functional variation in the RGS12 gene does not affect methylphenidate response in mice. This suggests RGS12 gene variations should not contraindicate methylphenidate use for bipolar disorder (BD) and attention-deficit/hyperactivity disorder (ADHD) comorbidity.

Keywords:
attention-deficit/hyperactivity disorderbipolar disordermethylphenidatepsychostimulant-induced locomotionregulator of G protein signaling-12 (RGS12)

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Genetics

Background:

  • The use of psychostimulants for attention-deficit/hyperactivity disorder (ADHD) in patients with bipolar disorder (BD) is controversial due to potential mood destabilization.
  • RGS12, a regulator of dopamine transporter (DAT) function, is implicated in psychostimulant response, and a specific mutation is linked to familial BD.
  • RGS12's role in psychostimulant response and its association with BD warrant investigation into its functional variation's impact on treatment decisions.

Purpose of the Study:

  • To investigate whether functional variation in the human RGS12 gene influences behavioral responses to psychostimulants like methylphenidate.
  • To determine if genetic findings related to RGS12 should impact the clinical use of methylphenidate in BD patients with comorbid ADHD.

Main Methods:

  • Evaluation of RGS12-deficient mice for behavioral responses, specifically locomotor hyperactivity, to methylphenidate.
  • Comparison of these responses with those to other dopamine transporter-dependent stimulants, including amphetamine and methamphetamine.

Main Results:

  • RGS12 deficiency reduced hyperlocomotion in response to amphetamine and methamphetamine.
  • However, methylphenidate elicited normal hyperlocomotor responses in RGS12-deficient mice across all tested doses.
  • Methylphenidate responsiveness remained intact despite the absence of functional RGS12.

Conclusions:

  • The RGS12 gene's functional variation does not appear to contraindicate the use of methylphenidate in mood-stabilized patients with comorbid BD and ADHD.
  • These findings support the continued consideration of methylphenidate as a treatment option for ADHD in this patient population.
  • Further research into RGS12's specific role in dopaminergic pathways may refine understanding of psychostimulant response in psychiatric comorbidities.