The autonomic stress-induced hyperthermia response is not enhanced by several anxiogenic drugs

While anxiety models are often based on locomotor activity responses, the stress-induced hyperthermia (SIH) paradigm uses the autonomic stress response by measuring body temperature. The effects of putative anxiogenic compounds in the SIH paradigm are inconclusive in mice and have not been examined in rats. Furthermore, it has been suggested that drug-induced effects on body temperature could be dependent on locomotor activity levels. Therefore, the effects of three anxiogenic substances, yohimbine (an α2 receptor antagonist), mCPP (a 5HT2C receptor agonist) and FG-7142 (a GABAA receptor inverse agonist acting at the benzodiazepine site) on the stress-induced body temperature and locomotor activity response were studied in rats using novel cage stress. All anxiogenic compounds resulted in hypothermia. In contrast, FG-7142 and yohimbine increased locomotor activity levels, whereas mCPP reduced locomotor activity levels. The lack of an increased body temperature response of anxiogenic compounds indicates that the anxiogenic capacity of a drug does not necessarily yield increased autonomic stress responsivity. Moreover, the present study shows that a drug-induced decreased body temperature can be accompanied by increased locomotor activity, suggesting that both parameters represent independent parameters of the stress response.

Research Highlights
► Anxiogenic drugs do not increase the stress-induced autonomic body temperature response
► Hypothermia due to anxiogenic drugs can be accompanied by increased locomotor activity
► Drugs that increase subjective stress do not necessarily enhance autonomic stress responsivity.