Serotonin 5HT1A receptor availability and pathological crying after stroke.
OBJECTIVE
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.


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.


CONCLUSIONS
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.
Møller
M
M
Center of Functionally Integrative Neuroscience, Aarhus University, Denmark. moller@pet.auh.dk
Andersen
G
G
Gjedde
A
A
D000368:Aged; D001667:Binding, Competitive / Q000187:drug effects / Q000502:physiology; D001921:Brain / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000503:physiopathology; D015283:Citalopram / Q000494:pharmacology; D003448:Crying / Q000502:physiology; D003866:Depressive Disorder / Q000188:drug therapy / Q000209:etiology* / Q000378:metabolism*; D015536:Down-Regulation / Q000502:physiology; D005260:Female; D006801:Humans; D008032:Limbic System / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D010865:Pilot Projects; D049268:Positron-Emission Tomography; D017729:Presynaptic Terminals / Q000187:drug effects / Q000378:metabolism; D011903:Raphe Nuclei / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D044282:Receptor, Serotonin, 5-HT1A / Q000378:metabolism*; D012701:Serotonin / Q000172:deficiency; D012702:Serotonin Antagonists / Q000378:metabolism; D017367:Selective Serotonin Reuptake Inhibitors / Q000494:pharmacology; D020521:Stroke / Q000150:complications* / Q000378:metabolism* / Q000503:physiopathology; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology
D015283:Citalopram; D044282:Receptor, Serotonin, 5-HT1A; D012701:Serotonin; D012702:Serotonin Antagonists; D017367:Selective Serotonin Reuptake Inhibitors