Role of the blood-brain barrier in differential response to opioid peptides and morphine in mouse lines divergently bred for high and low swim stress-induced analgesia.

Stress-induced analgesia is suppression of pain sensitivity upon exposure to a stressful stimulus. This behavioural phenomenon has been known for over 30 years in experimental animals (Akil et al. 1976) as well as in humans (Carr et al 1981). Over 20 years ago, a group headed by Sadowski separated two strains of mice, one with high sensitivity (HA) and the other with low (LA) sensitivity to stress-induced analgesia initiated by swim stressor (SSIA), followed by measurement of analgesia with the tail-flick test (Panocka et al. 1986a,b). Following this study, both strains were extensively screened for biochemical differences. Although these studies identified some phenotypic differences (Panocka et al. 1991, Marek et al. 1993, Sadowski and Panocka 1993, Sadowski and Konarzewski 1999, Kest et al. 1999, Sacharczuk et al. 2010a) none of them fully explained the differences in stress-induced analgesia. Just recently, electron microscopy structural analysis (Gajkowska et al. 2011) proposed that increased leakage of the blood-brain barrier (BBB) in the HA line created the differences between the HA and LA lines in response to SSIA. The microvascular structure of the LA line is similar to the healthy, control group of Swiss-Webster mice, whereas the HA line is characterised by a leaky capillary wall. The BBB ultrastrucRole of the blood-brain barrier in differential response to opioid peptides and morphine in mouse lines divergently bred for high and low swim stress-induced analgesia