Stress, savouring, and coping: The role of savouring in psychological adjustment following a stressful life event.

There is increasing research on the role of savouring positive emotional experience in the context of stress. As such, we need a better understanding of how savouring and coping relate to each other and to psychological adjustment outcomes following a stressful life event. In particular, this study seeks to understand whether savouring is better conceptualized as a coping resource or a coping response. Three hundred people who experienced a highly stressful event in the past year completed measures of impact of event, savouring, coping, positive emotions, depression, anxiety, and life satisfaction. Results of bivariate correlations showed that savouring is positively correlated with positive coping (i.e., mastery and meaning-based coping) and socially-supported coping (i.e., using emotional and instrumental support) and negatively correlated with negative coping (i.e., self-judgement and avoidance coping). The results of path analyses support a model that positions savouring as a coping response that relates to other coping responses and indirectly relates to better psychological adjustment through positive emotions (when psychological adjustment is conceptualized as depression or life satisfaction but not anxiety). Findings provide preliminary support for conceptualizing savouring as a coping response; future research should consider measuring savouring as a coping response to further our understanding of savouring following a stressful life event.

Verapamil protects dopaminergic neuron damage through a novel anti-inflammatory mechanism by inhibition of microglial activation.

Verapamil has been shown to be neuroprotective in several acute neurotoxicity models due to blockade of calcium entry into neurons. However, the potential use of verapamil to treat chronic neurodegenerative diseases has not been reported. Using rat primary mesencephalic neuron/glia cultures, we report that verapamil significantly inhibited LPS-induced dopaminergic neurotoxicity in both pre- and post-treatment experiments. Reconstituted culture studies revealed that the presence of microglia was essential in verapamil-elicited neuroprotection. Mechanistic studies showed that decreased production of inflammatory mediators from LPS-stimulated microglia underlay neuroprotective property of verapamil. Further studies demonstrated that microglial NADPH oxidase (PHOX), the key superoxide-producing enzyme, but not calcium channel in neurons, is the site of action for the neuroprotective effect of verapamil. This conclusion was supported by the following two observations: 1) Verapamil failed to show protective effect on LPS-induced dopaminergic neurotoxicity in PHOX-deficient (deficient in the catalytic subunit of gp91(phox)) neuron/glia cultures; 2) Ligand binding studies showed that the binding of [(3)H]Verapamil onto gp91(phox) transfected COS7 cell membranes was higher than the non-transfected control. The calcium channel-independent neuroprotective property of verapamil was further supported by the finding that R(+)-verapamil, a less active form in blocking calcium channel, showed the same potency in neuroprotection, inhibition of pro-inflammatory factors production and binding capacity to gp91(phox) membranes as R(-)-verapamil, the active isomer of calcium channel blocker. In conclusion, our results demonstrate a new indication of verapamil-mediated neuroprotection through a calcium channel-independent pathway and provide a valuable avenue for the development of therapy for inflammation-related neurodegenerative diseases.