Serotonin 5HT1A receptor availability and pathological crying after stroke

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Serotonin 5HT1A receptor availability and pathological crying after stroke. / Møller, Mette; Andersen, G; Gjedde, A.

In: Acta Neurologica Scandinavica, Vol. 116, No. 2, 2007, p. 83-90.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Møller, M, Andersen, G & Gjedde, A 2007, 'Serotonin 5HT1A receptor availability and pathological crying after stroke', Acta Neurologica Scandinavica, vol. 116, no. 2, pp. 83-90. https://doi.org/10.1111/j.1600-0404.2007.00869.x

APA

Møller, M., Andersen, G., & Gjedde, A. (2007). Serotonin 5HT1A receptor availability and pathological crying after stroke. Acta Neurologica Scandinavica, 116(2), 83-90. https://doi.org/10.1111/j.1600-0404.2007.00869.x

Vancouver

Møller M, Andersen G, Gjedde A. Serotonin 5HT1A receptor availability and pathological crying after stroke. Acta Neurologica Scandinavica. 2007;116(2):83-90. https://doi.org/10.1111/j.1600-0404.2007.00869.x

Author

Møller, Mette ; Andersen, G ; Gjedde, A. / Serotonin 5HT1A receptor availability and pathological crying after stroke. In: Acta Neurologica Scandinavica. 2007 ; Vol. 116, No. 2. pp. 83-90.

Bibtex

@article{929b489089cf11df928f000ea68e967b,
title = "Serotonin 5HT1A receptor availability and pathological crying after stroke",
abstract = "OBJECTIVES: Post-stroke depression and pathological crying (PC) implicate an imbalance of serotonergic neurotransmission. We claim that PC follows serotonin depletion that raises the binding potential (p(B)) of the 5-HT(1A) receptor antagonist [carbonyl-(11)C]WAY-100635, which is reversible by selective serotonin re-uptake inhibitor (SSRI) treatment. MATERIALS AND METHODS: We PET scanned patients with acute stroke and PC and age-matched control subjects. Maps of receptor availability were generated from the images of eight cortical regions and raphe nuclei. RESULTS: The maps showed highest binding in limbic areas and raphe nuclei, while binding in basal ganglia and cerebellum was negligible. Baseline binding potentials of patients were lower than that of control subjects (3.7 +/- 0.6 vs 4.2 +/- 0.2). Treatment with SSRI markedly reduced free receptor sites, whereas placebo administration led to a global increase. DISCUSSION: The study is the first suggestion of changes of serotonergic neurotransmission in the early phase of stroke and the modulation of these changes with SSRI treatment.",
author = "Mette M{\o}ller and G Andersen and A Gjedde",
note = "Keywords: Aged; Binding, Competitive; Brain; Citalopram; Crying; Depressive Disorder; Down-Regulation; Female; Humans; Limbic System; Male; Middle Aged; Pilot Projects; Positron-Emission Tomography; Presynaptic Terminals; Raphe Nuclei; Receptor, Serotonin, 5-HT1A; Serotonin; Serotonin Antagonists; Serotonin Uptake Inhibitors; Stroke; Synaptic Transmission",
year = "2007",
doi = "10.1111/j.1600-0404.2007.00869.x",
language = "English",
volume = "116",
pages = "83--90",
journal = "Acta Neurologica Scandinavica",
issn = "0001-6314",
publisher = "Wiley-Blackwell",
number = "2",

}

RIS

TY - JOUR

T1 - Serotonin 5HT1A receptor availability and pathological crying after stroke

AU - Møller, Mette

AU - Andersen, G

AU - Gjedde, A

N1 - Keywords: Aged; Binding, Competitive; Brain; Citalopram; Crying; Depressive Disorder; Down-Regulation; Female; Humans; Limbic System; Male; Middle Aged; Pilot Projects; Positron-Emission Tomography; Presynaptic Terminals; Raphe Nuclei; Receptor, Serotonin, 5-HT1A; Serotonin; Serotonin Antagonists; Serotonin Uptake Inhibitors; Stroke; Synaptic Transmission

PY - 2007

Y1 - 2007

N2 - OBJECTIVES: Post-stroke depression and pathological crying (PC) implicate an imbalance of serotonergic neurotransmission. We claim that PC follows serotonin depletion that raises the binding potential (p(B)) of the 5-HT(1A) receptor antagonist [carbonyl-(11)C]WAY-100635, which is reversible by selective serotonin re-uptake inhibitor (SSRI) treatment. MATERIALS AND METHODS: We PET scanned patients with acute stroke and PC and age-matched control subjects. Maps of receptor availability were generated from the images of eight cortical regions and raphe nuclei. RESULTS: The maps showed highest binding in limbic areas and raphe nuclei, while binding in basal ganglia and cerebellum was negligible. Baseline binding potentials of patients were lower than that of control subjects (3.7 +/- 0.6 vs 4.2 +/- 0.2). Treatment with SSRI markedly reduced free receptor sites, whereas placebo administration led to a global increase. DISCUSSION: The study is the first suggestion of changes of serotonergic neurotransmission in the early phase of stroke and the modulation of these changes with SSRI treatment.

AB - OBJECTIVES: Post-stroke depression and pathological crying (PC) implicate an imbalance of serotonergic neurotransmission. We claim that PC follows serotonin depletion that raises the binding potential (p(B)) of the 5-HT(1A) receptor antagonist [carbonyl-(11)C]WAY-100635, which is reversible by selective serotonin re-uptake inhibitor (SSRI) treatment. MATERIALS AND METHODS: We PET scanned patients with acute stroke and PC and age-matched control subjects. Maps of receptor availability were generated from the images of eight cortical regions and raphe nuclei. RESULTS: The maps showed highest binding in limbic areas and raphe nuclei, while binding in basal ganglia and cerebellum was negligible. Baseline binding potentials of patients were lower than that of control subjects (3.7 +/- 0.6 vs 4.2 +/- 0.2). Treatment with SSRI markedly reduced free receptor sites, whereas placebo administration led to a global increase. DISCUSSION: The study is the first suggestion of changes of serotonergic neurotransmission in the early phase of stroke and the modulation of these changes with SSRI treatment.

U2 - 10.1111/j.1600-0404.2007.00869.x

DO - 10.1111/j.1600-0404.2007.00869.x

M3 - Journal article

C2 - 17661792

VL - 116

SP - 83

EP - 90

JO - Acta Neurologica Scandinavica

JF - Acta Neurologica Scandinavica

SN - 0001-6314

IS - 2

ER -

ID: 20689145