Decreased binding capacity (Bmax) of muscarinic acetylcholine receptors in fibroblasts from boys with attention-deficit/hyperactivity disorder (ADHD)Show others and affiliations
2013 (English)In: ADHD Attention Deficit and Hyperactivity Disorders, ISSN 1866-6116, E-ISSN 1866-6647, Vol. 5, no 3, p. 267-271Article in journal (Refereed) Published
Abstract [en]
Monoaminergic dysregulation is implicated in attention-deficit/hyperactivity disorder (ADHD), and methylphenidate and amphetamines are the most frequently prescribed pharmacological agents for treating ADHD. However, it has recently been proposed that the core symptoms of the disorder might be due to an imbalance between monoaminergic and cholinergic systems. In this study, we used fibroblast cell homogenates from boys with and without ADHD as an extraneural cell model to examine the cholinergic receptor density, that is, muscarinic acetylcholine receptors (mAChRs). We found that the binding capacity (Bmax) of [³H] Quinuclidinyl benzilate (³H-QNB) to mAChRs was decreased by almost 50 % in the children with ADHD (mean = 30.6 fmol/mg protein, SD = 25.6) in comparison with controls [mean = 63.1 fmol/mg protein, SD = 20.5, p ≤ 0.01 (Student's unpaired t test)]. The decreased Bmax indicates a reduced cholinergic receptor density, which might constitute a biomarker for ADHD. However, these preliminary findings need to be replicated in larger ADHD and comparison cohorts
Place, publisher, year, edition, pages
Berlin, Germany: Springer Berlin/Heidelberg, 2013. Vol. 5, no 3, p. 267-271
Keywords [en]
ADHD, Fibroblaster, Muscarinic acetylcholine receptor, Receptor binding assay, Biomarker
National Category
Medical and Health Sciences Psychiatry
Research subject
Psychiatry; Biomedicine
Identifiers
URN: urn:nbn:se:oru:diva-42579DOI: 10.1007/s12402-013-0103-0PubMedID: 23389940Scopus ID: 2-s2.0-84883061295OAI: oai:DiVA.org:oru-42579DiVA, id: diva2:787725
Funder
Östergötland County Council, FoUcenter Dr 91021Swedish Research Council, K2007-62X-08318-20-3The Karolinska Institutet's Research Foundation2015-02-112015-02-112018-05-26Bibliographically approved