Inducing Anxiety In Humans

One advantage of studying humans is that it is possible to confirm that a given experimental intervention does actually induce anxiety in the subject. A disadvantage is that any research into the neurobiological changes that underlie the subjects' psychological status is limited to the analysis of accessible tissue samples, such as plasma or urine. Such measurements will, at best, be indirect indications of what is happening in the brain. As a result, research of anxiety in humans has concentrated on drugs with a known pharmacological target (usually a neurotransmitter receptor) and has compared their effects in anxious patients and normal subjects. Some treatments that induce or

Brain Stress Medicine

Figure 19.2 (a) Average curves of punished and unpunished responses of rats, never previously treated with a benzodiazepine (BDZ), during several days of administration of a test BDZ. The apparent delay in the increase in punished responses is due to the reduction in all responses (including unpunished ones) at the start of drug administration. The progressive recovery of unpunished responses reflects the development of tolerance to the sedative effects of the test compound. (b) Average curves of punished and unpunished responses of rats, previously treated with a BDZ, during administration of a test BDZ. Note the immediate increase in punished responses and the lack of a decline in unpunished responses, indicating pre-existing tolerance to the sedative effects of the test compound. (Based on Margules and Stein 1968)

Figure 19.2 (a) Average curves of punished and unpunished responses of rats, never previously treated with a benzodiazepine (BDZ), during several days of administration of a test BDZ. The apparent delay in the increase in punished responses is due to the reduction in all responses (including unpunished ones) at the start of drug administration. The progressive recovery of unpunished responses reflects the development of tolerance to the sedative effects of the test compound. (b) Average curves of punished and unpunished responses of rats, previously treated with a BDZ, during administration of a test BDZ. Note the immediate increase in punished responses and the lack of a decline in unpunished responses, indicating pre-existing tolerance to the sedative effects of the test compound. (Based on Margules and Stein 1968)

Table 19.3 Substances that induce panic attacks in humans

Sodium lactate (mechanism unresolved) C02 (inhalation) (mechanism unresolved) Caffeine (adenosine, A2 receptor antagonism?) Yohimbine (a2-adrenoceptor antagonism?)

m-Chlorophenylpiperazine (mCPP, 5-HT2A/2C receptor agonism?)

CCK-4 (CCKb receptor agonism?)

FG7142 (benzodiazepine receptor inverse agonism?)

exacerbate anxiety in humans are listed in Table 19.3 and their presumed neuro-biological targets have formed the bases of theories to explain the cause(s) of this disorder. A full appraisal of this topic is beyond the scope of this chapter but the links between drugs that affect central monoamine transmission and anxiety are discussed in later sections. Details of findings from research in humans can be found in Ballenger (1990) and Coupland, Glue and Nutt (1992).

Continue reading here: Drug Treatments For Anxiety

Was this article helpful?

0 0