Pharmacology of human experimental anxiety

Abstract

This review covers the effect of drugs affecting anxiety using four psychological procedures for inducing experimental anxiety applied to healthy volunteers and patients with anxiety disorders. The first is aversive conditioning of the skin conductance responses to tones. The second is simulated public speaking, which consists of speaking in front of a video camera, with anxiety being measured with psychometric scales. The third is the Stroop Color-Word test, in which words naming colors are painted in the same or in a different shade, the incongruence generating a cognitive conflict. The last test is a human version of a thoroughly studied animal model of anxiety, fear-potentiated startle, in which the eye-blink reflex to a loud noise is recorded. The evidence reviewed led to the conclusion that the aversive conditioning and potentiated startle tests are based on classical conditioning of anticipatory anxiety. Their sensitivity to benzodiazepine anxiolytics suggests that these models generate an emotional state related to generalized anxiety disorder. On the other hand, the increase in anxiety determined by simulated public speaking is resistant to benzodiazepines and sensitive to drugs affecting serotonergic neurotransmission. This pharmacological profile, together with epidemiological evidence indicating its widespread prevalence, suggests that the emotional state generated by public speaking represents a species-specific response that may be related to social phobia and panic disorder.

Neurotransmitter and Behaviour: Serotonin and Anxiety

“…To trigger anxiety, the subjects receive either fear-inducing agents (caffeine, pentylenetetrazol, lactate infusions or CO2 inhalation), or they undergo psychological tests in an aversive environment (Graeff et al 2003). If animals can experience fear (Tembrock 2000), it would be possible to observe behaviour and neurochemical changes similar to changes in humans.…”

The hypothalamic-pituitary-adrenal axis in anxiety and panic.

“…While the drug profile of the former is similar to that of GAD, SPS has a pharmacological profile that resembles PD and social anxiety disorder, and is believed to mobilize the same neural network that is involved in these disorders (for a review, see Graeff, Parente, Del-Ben, & Guimarães, 2003). As a consequence, two studies have been conducted by our research group to investigate whether SPS would affect HPA axis functioning.…”

Ansiedade, pânico e o eixo hipotálamo-pituitária-adrenal

“…SPS is believed to mobilize the same neurobiological mechanisms that are involved in SAD and PD and, indeed, the pharmacological profile of SPS is similar to that of these disorders. 17 In the mentioned study, 18 the participants were divided into three groups: 18 symptomatic panic patients, 16 nonsymptomatic, drug-treated panic patients, and 17 healthy controls. Throughout the experimental session, subjective anxiety -measured by the Visual Analog Mood Scale (VAMS) and by the total score of the Bodily Symptom Scale (BSS) -was higher in symptomatic patients than in controls, nonsymptomatic patients lying in between.…”