https://focus.psychiatryonline.org/doi/pdf/10.1176/foc.9.3.foc311

The Neurocircuitry of Fear, Stress, and Anxiety Disorders

1. Clarification: The 2013 Guidelines make a distinction between euthanasia, humane killing, and slaughter, and state that neither slaughter nor humane killing is covered in the document P.68, S6.1.1. Not included among the definitions of these terms are ending the lives of healthy animals or scientific collection of animals. For clarification, whatever the term used, classification of the method, or reason given for killing animals: euthanasia, humane killing, slaughter, harvest, depopulation, scientific collection, or research-related, the Council on Accreditation’s foremost concern, in all situations, is with humane technique. The goal of humane technique is to minimize pain, distress, and the negative effect to the animal. The technique employed should result in rapid loss of consciousness followed by cardiac or respiratory arrest and, ultimately, a loss of brain function. Although complete absence of pain and distress is preferred, it is understood that it cannot always be achieved P7.13.2.

https://works.bepress.com/cheryl_greenacre/14/download/

AVMA Guidelines for the Euthanasia of Animals: 2013 Edition

The effects of sex and hormonal status on the physiological response to acute psychosocial stress.

Social anxiety disorder.

Links between sleep and depression are strong. About three quarters of depressed patients have insomnia symptoms, and hypersomnia is present in about 40% of young depressed adults and 10% of older patients, with a preponderance in females. The symptoms cause huge distress, have a major impact on quality of life, and are a strong risk factor for suicide. As well as the subjective experience of sleep symptoms, there are well-documented changes in objective sleep architecture in depression. Mechanisms of sleep regulation and how they might be disturbed in depression are discussed. The sleep symptoms are often unresolved by treatment, and confer a greater risk of relapse and recurrence. Epidemiological studies have pointed out that insomnia in nondepressed subjects is a risk factor for later development of depression. There is therefore a need for more successful management of sleep disturbance in depression, in order to improve quality of life in these patients and reduce an important factor in depressive relapse and recurrence.

Sleep disorders as core symptoms of depression

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

/pdf/serotonin-5-ht1a-receptor-binding-in-people-with-panic-f66wixmzbr.pdf

Serotonin 5-HT1A receptor binding in people with panic disorder: positron emission tomography study

Mechanisms of action of selective serotonin reuptake inhibitors in the treatment of psychiatric disorders

Studies of the correlation of subjective and objective sleep measures in depressed patients have produced mixed results so far. Further, they were carried out in sleep laboratories and tended to obtain one-off assessments, thus not taking into account the effect of treatment. We investigated forty (40) patients over the course of 8-week treatment of depression with either paroxetine or nefazodone. We used home polysomnography at baseline, nights 3 and 10, and week 8 of treatment, with extensive assessments of subjective sleep, the morning after each sleep recording. The patients were able to judge accurately their total sleep time and sleep onset latency, both before and during treatment. However, they were inaccurate in estimating the number of times they woke up during the night. Sleep satisfaction correlated negatively with Stage 1 sleep at baseline. Sleep quality was represented by a combination of subjective parameters measuring the ease of initiation and maintenance of sleep, and it appeared to derive from slow wave sleep and sleep continuity as seen in polysomnography. The partial discrepancy between subjective and objective measures suggests that a cognitive element is combined with the biological element to produce the sleep problems reported by depressed patients.

Correlation of subjective and objective sleep measurements at different stages of the treatment of depression

There have been numerous studies on the effects of caffeine on behaviour and cardiovascular function. It is now important to clarify the mechanisms that underlie such effects, and the main objective of the present study was to investigate whether changes in central noradrenaline underlie some of the behavioural and cardiovascular effects of caffeine. This was examined using a clonidine challenge paradigm. Twenty-four healthy volunteers were assigned to one of four conditions: (i) clonidine/caffeine; (ii) clonidine/placebo; (iii) placebo/caffeine: (iv) placebo/placebo. Baseline measurements of mood, cognitive performance, saccadic eye movements and cardiovascular function were recorded. Subsequently, volunteers were given either clonidine (200 microg) or placebo and consumed coffee containing caffeine (1.5 mg/kg) or placebo. The test battery was then repeated 30 min, 150 min and 270 min later. A second cup of coffee (with the same amount of caffeine as the first) was consumed 120 min after the first cup. The results showed that clonidine reduced alertness, impaired many aspects of performance and slowed saccadic eye movements; caffeine removed many of these impairments. Both clonidine and caffeine influenced blood pressure (clonidine reduced it, caffeine raised it) but the effects appeared to be independent, suggesting that separate mechanisms were involved. In addition, there were some behavioural effects of caffeine that were independent of the clonidine effect (e.g. effects on speed of encoding of new information) and these may reflect other neurotransmitter systems (e.g cholinergic effects). Overall, the results suggest that caffeine counteracts reductions in the turnover of central noradrenaline. This mechanism may underlie the beneficial effects of caffeine seen in low alertness states.

https://journals.sagepub.com/doi/pdf/10.1177/02698811030173010

Jon Nash

Papers

Serotonin 5-HT1A receptor binding in people with panic disorder: positron emission tomography study

Mechanisms of action of selective serotonin reuptake inhibitors in the treatment of psychiatric disorders

Correlation of subjective and objective sleep measurements at different stages of the treatment of depression

Caffeine and central noradrenaline: effects on mood, cognitive performance, eye movements and cardiovascular function

Inhalation of 35% CO2 results in activation of the HPA axis in healthy volunteers