Duodenal pain and spinal morphine induce conditioned taste aversion in rats.

Conditioned taste aversion (CTA) is a behavioural response essential to the survival of an individual. The combination of taste and odour of most foods provides a strong conditioned stimulus (CS) for an animal to respond in an appropriate way to any harmful unconditioned stimuli (US) that follow. The most widely used conditioned stimuli are drinkable sweet solutions, such as saccharin and sucrose. CTA-like responses are also found for environmental unconditioned stimuli, but these usually take longer training. In the present study, the aversive nature of a duodenal distention with an implanted balloon catheter was studied in freely moving rats using either CTA against a sucrose solution, or a light-dark passive avoidance (PA) paradigm. In addition, the effect of spinal morphine on CTA and the cardiovascular response to duodenal distention were studied. CTA could be induced by a single, but long-lasting 20-minute duodenal distention, which did not induce PA behaviour in a light-dark box. Spinal infusion of morphine alone induced CTA, suggesting that the model is unsuitable to investigate spinal pharmacological modulation of visceral pain. Spinal morphine did reduce the cardiovascular response to duodenal distention, strengthening its validity as a visceral pain model. Since CTA is a complicating factor in the field of chemotherapy in cancer patients and spinal morphine causes nausea and vomiting in humans, CTA may also complicate spinal drug treatment or anaesthesia.

Individual reactivity to the open-field predicts the expression of cardiovascular and behavioural sensitisation to novel stress.

Posttraumatic stress disorder (PTSD) is the fourth most common psychiatric disorder. It is associated with cardiovascular disorders and irritable bowel syndrome (IBS). Besides stressful life-events, a prior history of gastrointestinal infection is a predisposing factor for the development of IBS. Only a proportion of persons exposed to traumatic events develop PTSD. Several factors, like genetic predisposition, stressor intensity, cognitive appraisal mechanisms and coping processes influence the likelihood of developing PTSD after exposure to a trauma. We used a single session of footshocks in rats, an animal model with a high degree of validity for PTSD, to study whether transient colonic inflammation alters local and distal visceral sensitivity, and whether reactivity to the open-field (low (LA) or high (HA) active) predicts long-term stress-induced behavioural and cardiovascular sensitisation and altered visceral pain sensitivity. A distention series and noise challenge were given 2 weeks after foot-shocks, followed by a transient colonic inflammation period and a second distention series and noise challenge 4 weeks after foot-shocks. During exposure to noise, both before and after inflammation, footshocked rats showed increased immobility compared to controls, which was significantly greater in LA rats than in HA rats. LA preshocked rats also showed a greater blood pressure response to the noise test, but this only became evident in the second noise-test. Neither footshocks nor colonic inflammation affected duodenal pain sensitivity. The results provide additional evidence for long-lasting cardiovascular hyperresponsivity after a stressful event and indicate that its degree is predicted by personality traits or coping style.

Individual reactivity to the open-field predicts the expression of stress-induced behavioural and somatic pain sensitisation.

Posttraumatic stress disorder (PTSD) is the fourth most common psychiatric disorder. It is associated with somatic complaints like pain problems. Only a proportion of persons exposed to traumatic events develop PTSD. Several factors, like genetic predisposition, stressor intensity, cognitive appraisal mechanisms and coping processes influence the likelihood of developing PTSD after exposure to a trauma. We used a single session of footshocks in rats, an animal model with a high degree of validity for PTSD, to study whether individual behavioural traits predict long-term stress-induced sensitisation of behavioural responsivity and somatic pain sensitivity and therefore can act as a vulnerability factor. Rats were selected for low (LA) and high (HA) open-field locomotor reactivity and then underwent a single session of footshocks. Two to 5 weeks after footshocks, behavioural sensitisation was investigated using a noise challenge, an electrified prod challenge and a forced swim test. Somatic pain sensitivity was measured using a tail-immersion test. During exposure to noise in a novel cage, footshocked rats showed increased immobility compared to controls, which was significantly greater in LA than in HA rats. Footshocked rats showed increased burying in the electrified prod challenge and no effect was found in the forced swim test. Footshocks caused hyperalgesia in LA rats, but hypoalgesia in HA rats. We conclude that low open-field locomotor reactivity predicts the degree of stress-induced behavioural sensitisation and the direction of altered somatic pain sensitivity, suggesting that an anxiety-prone personality or passive coping style may increase the risk of developing stress-related psychosomatic disorders.