Neural responses clarify how ecolabels promote sustainable purchases.

While behavioral and policy interventions such as ecolabels (e.g., the Energy Star label) promote sustainable purchases, the reason for their influence remains unclear. We combined incentive-compatible purchasing experiments, neuroimaging assessments, and a national stated choice survey to examine how the Energy Star label might influence choices of light bulbs within individuals, across individuals (n = 36), and out-of-sample in a national survey (n = 1550). Presence of the Energy Star label increased activity in neural regions associated with positive affective responses that predicted purchasing (e.g., the Nucleus Accumbens or NAcc), particularly in more impulsive individuals. Group-averaged NAcc activity could also account for consumer demand for similar sustainable product combinations in a national survey. These findings suggest that ecolabels may leverage affective responses in individuals as well as markets to promote sustainable purchases, which might inform the promotion of sustainable products.

Neural valuation of environmental resources.

How do people value environmental resources? To estimate public valuation of natural resources, researchers often conduct surveys that ask people how much they would be willing to pay to preserve or restore threatened natural resources. However, these survey responses often elicit complex affective responses, including negative reactions toward proposed destructive land uses of those resources. To better characterize processes that underlie the valuation of environmental resources, we conducted behavioral and neuroimaging experiments in which subjects chose whether or not to donate money to protect natural park lands (iconic versus non-iconic) from proposed land uses (destructive versus non-destructive). In both studies, land use destructiveness motivated subjects' donations more powerfully than did the iconic qualities of the parks themselves. Consistent with an anticipatory affect account, nucleus accumbens (NAcc) activity increased in response to more iconic parks, while anterior insula activity increased in response to more destructive uses, and the interaction of these considerations altered activity in the medial prefrontal cortex (MPFC). Further, anterior insula activity predicted increased donations to preserve parks threatened by destructive uses, but MPFC activity predicted reduced donations. Finally, individuals with stronger pro-environmental attitudes showed greater anterior insula activity in response to proposed destructive uses. These results imply that negative responses to destructive land uses may play a prominent role in environmental valuation, potentially overshadowing positive responses to the environmental resources themselves. The findings also suggest that neuroimaging methods might eventually complement traditional survey methods by allowing researchers to disentangle distinct affective responses that influence environmental valuation.

Dual roles of the MAPK/ERK1/2 cell signaling pathway after stroke.

Extracellular signal-regulated kinase 1/2 (ERK1/2), one of the best-characterized members of the mitogen-activated protein kinase (MAPK) family, mediates a range of activity from metabolism, motility, and inflammation to cell death and survival. It is phosphorylated and activated through a three-tiered MEK mode via cell surface receptors stimulated by growth factors or cytokines. The phosphorylated ERK1/2 level is usually increased after cerebral ischemia/reperfusion, but whether an increase in ERK1/2 phosphorylation is protective or detrimental is highly debatable. Much of the support for ERK1/2's role as a neuroprotectant against stroke stems from its apparent involvement in the beneficial effects of growth factors, estrogen, preconditioning, and hypothermia on the ischemic brain. Conversely, evidence supporting the detrimental effects of ERK1/2 activity is derived from its activation promoting inflammation and oxidative stress and its inhibition reducing ischemic damage. The dual potential of ERK1/2 actions in the ischemic brain is likely related to its responses to a diverse array of agonists and cell surface receptors. Plausibly, the ERK1/2 activity generated by cytokines and free radicals or other inflammatory factors after stroke may worsen ischemic damage, whereas the ERK1/2 activity produced by exogenous growth factors, estrogen, and preconditioning favors neuroprotection. Future experiments should be conducted to optimize the protective effect of ERK1/2 while blocking its detrimental actions.