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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.
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).
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.
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.
Panic disorder is associated with reduced 5-HT1A receptor availability, which is also known to have a key role in depression.
Specific psychotropic drugs and disorders
Smita A. Pandit, Psychopharmacology Unit, School of Medical Sciences, Bristol, UK,
Spilios V. Argyropoulos, Psychopharmacology Unit, School of Medical Sciences, Bristol, UK,
Patrick G. Kehoe, Psychopharmacology Unit, School of Medical Sciences, Bristol, UK,
David J. Nutt, Psychopharmacology Unit, School of Medical Sciences, Bristol, UK
Bernard Lerer, Hadassah-Hebrew Medical Center, Jerusalem
The benzodiazepines (BDZ) have proven to be both effective and controversial in the treatment of anxiety. New insights into the genetics of the BD2 receptor system may lead to the development of new drugs that act on the γ-aminobutyric acid (GABA) receptor complex and are devoid of the problems associated with the classical BDZs. This pharmacotherapeutic approach has gathered impetus following the discovery of the various subunits of the GABA receptor, which play an important role in the regulation of anxiety and the actions of anxiolytics, and which demonstrate differential brain expression. This chapter discusses the above with reference to recent evidence from animal and human studies, as well as the implications for future anxiolytic treatment strategies. It focuses on the development of the GABA-BDZ receptor field of research. Unlike the BDZ site, the modulation of the GABA receptor by neurosteroids requires the presence of a β-subunit.
Sleep effects of antidepressants are important clinically and for elucidating mechanism of action: selective serotonin reuptake inhibitors disturb sleep and 5-HT2 receptor-blocking compounds may enhance sleep quality.
To compare the objective and subjective effects on sleep of paroxetine and nefazodone in patients with moderate to severe depression.
Forty patients with depression were randomised to take paroxetine 20-40 mg/day or nefazodone 400–600 mg/day for 8 weeks. Objective and subjective quality of sleep and depression measures were assessed throughout.
Nefazodone significantly increased objective sleep efficiency and total sleep time, and improved subjective sleep on days 3 and 10. Paroxetine decreased sleep efficiency early in treatment and some sleep disruption remained at week 8. Paroxetine but not nefazodone produced marked suppression of rapid eye movement (REM) sleep.
Nefazodone improves sleep in early treatment compared with paroxetine in patients with moderate to severe depression. These effects are seen within the first 2 weeks of treatment and diminish thereafter.
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