The Social Motivation Hypothesis for Prosocial Behavior

Existing economic models of prosociality have been rather silent in terms of proximate psychological mechanisms. We nevertheless identify the psychologically most informed accounts and offer a critical discussion of their hypotheses for the proximate psychological explanations. Based on convergent evidence from several fields of research, we argue that there nevertheless is a more plausible alternative proximate account available: the social motivation hypothesis. The hypothesis represents a more basic explanation of the appeal of prosocial behavior, which is in terms of anticipated social rewards. We also argue in favor of our own social motivation hypothesis over Robert Sugden’s fellow-feeling account (due originally to Adam Smith). We suggest that the social motivation not only stands as a proximate account in its own right but also provides a plausible scaffold for other more sophisticated motivations (e.g., fellow-feelings). We conclude by discussing some possible implications of the social motivation hypothesis on existing modeling practice.Peer reviewe

The Social Motivation Hypothesis for Prosocial Behavior

Existing economic models of prosociality have been rather silent in terms of proximate psychological mechanisms. We nevertheless identify the psychologically most informed accounts and offer a critical discussion of their hypotheses for the proximate psychological explanations. Based on convergent evidence from several fields of research, we argue that there nevertheless is a more plausible alternative proximate account available: the social motivation hypothesis. The hypothesis represents a more basic explanation of the appeal of prosocial behavior, which is in terms of anticipated social rewards. We also argue in favor of our own social motivation hypothesis over Robert Sugden’s fellow-feeling account (due originally to Adam Smith). We suggest that the social motivation not only stands as a proximate account in its own right but also provides a plausible scaffold for other more sophisticated motivations (e.g., fellow-feelings). We conclude by discussing some possible implications of the social motivation hypothesis on existing modeling practice.Peer reviewe

The Social Motivation Hypothesis for Prosocial Behavior

Existing economic models of prosociality have been rather silent in terms of proximate psychological mechanisms. We nevertheless identify the psychologically most informed accounts and offer a critical discussion of their hypotheses for the proximate psychological explanations. Based on convergent evidence from several fields of research, we argue that there nevertheless is a more plausible alternative proximate account available: the social motivation hypothesis. The hypothesis represents a more basic explanation of the appeal of prosocial behavior, which is in terms of anticipated social rewards. We also argue in favor of our own social motivation hypothesis over Robert Sugden’s fellow-feeling account (due originally to Adam Smith). We suggest that the social motivation not only stands as a proximate account in its own right but also provides a plausible scaffold for other more sophisticated motivations (e.g., fellow-feelings). We conclude by discussing some possible implications of the social motivation hypothesis on existing modeling practice.Peer reviewe

When is Green Nudging Ethically Permissible?

This review article provides a new perspective on the ethics of green nudging. We advance a new model for assessing the ethical permissibility of green nudges (GNs). On this model, which provides normative guidance for policymakers, a GN is ethically permissible when the intervention is (1) efficacious, (2) cost-effective, and (3) the advantages of the GN (i.e. reducing the environmental harm) are not outweighed by countervailing costs/harms (i.e. for nudgees). While traditional ethical objections to nudges (paternalism, etc.) remain potential normative costs associated with GNs, any such costs must be weighed against the injunction to reduce environmental harm to third parties

Sodium Phenylbutyrate Controls Neuroinflammatory and Antioxidant Activities and Protects Dopaminergic Neurons in Mouse Models of Parkinson’s Disease

Neuroinflammation and oxidative stress underlie the pathogenesis of various neurodegenerative disorders. Here we demonstrate that sodium phenylbutyrate (NaPB), an FDA-approved therapy for reducing plasma ammonia and glutamine in urea cycle disorders, can suppress both proinflammatory molecules and reactive oxygen species (ROS) in activated glial cells. Interestingly, NaPB also decreased the level of cholesterol but involved only intermediates, not the end product of cholesterol biosynthesis pathway for these functions. While inhibitors of both geranylgeranyl transferase (GGTI) and farnesyl transferase (FTI) inhibited the activation of NF-κB, inhibitor of GGTI, but not FTI, suppressed the production of ROS. Accordingly, a dominant-negative mutant of p21rac, but not p21ras, attenuated the production of ROS from activated microglia. Inhibition of both p21ras and p21rac activation by NaPB in microglial cells suggests that NaPB exerts anti-inflammatory and antioxidative effects via inhibition of these small G proteins. Consistently, we found activation of both p21ras and p21rac in vivo in the substantia nigra of acute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson’s disease. Oral administration of NaPB reduced nigral activation of p21ras and p21rac, protected nigral reduced glutathione, attenuated nigral activation of NF-κB, inhibited nigral expression of proinflammatory molecules, and suppressed nigral activation of glial cells. These findings paralleled dopaminergic neuronal protection, normalized striatal neurotransmitters, and improved motor functions in MPTP-intoxicated mice. Consistently, FTI and GGTI also protected nigrostriata in MPTP-intoxicated mice. Furthermore, NaPB also halted the disease progression in a chronic MPTP mouse model. These results identify novel mode of action of NaPB and suggest that NaPB may be of therapeutic benefit for neurodegenerative disorders