Pharmacology Unit, University of Bristol
Oxfordshire and Buckinghamshire Mental Health NHS Foundation Trust
Medical Research Council Cyclotron Unit, Hammersmith Hospital, London
Pharmacology Unit, University of Bristol
Medical Research Council Cyclotron Unit, Hammersmith Hospital, London
Pharmacology Unit, University of Bristol, UK
Correspondence: Professor David Nutt, Psychopharmacology Unit, University of Bristol, Dorothy Hodgkins Building, Whitson Street, Bristol BS1 3NY, UK. Email: David.J.Nutt{at}bristol.ac.uk
Pump priming for the study was provided by a small grant from SmithKline Beecham (now GlaxoSmithKline). Funding detailed in Acknowledgements.
* These authors contributed equally to the work.
Background
The importance of the neurotransmitter serotonin (5-HT) in the pathophysiology of anxiety is well known. A key role for postsynaptic 5-HT1A receptors has recently been suggested in studies of genetic knockout mice.
Aims
To measure 5-HT1A receptor binding in patients with panic disorder in the untreated state and after recovery on treatment with selective serotonin reuptake inhibitors (SSRIs).
Method
Nine symptomatic untreated patients with panic disorder, seven patients recovered on SSRI medication and nineteen healthy volunteers underwent a single positron emission tomography (PET) scan using the 5-HT1A tracer [11C]WAY-100635.
Results
In comparison with controls, both presynaptic and postsynaptic 5-HT1A receptor binding was reduced in untreated patients, with the most significant reductions being in the raphe, orbitofrontal cortex, temporal cortex and amygdala. In recovered patients presynaptic binding was reduced, but there was no significant reduction in postsynaptic binding.
Conclusions
Panic disorder is associated with reduced 5-HT1A receptor availability, which is also known to have a key role in depression.
Related articles in BJP: