Neuroeconomics uses knowledge about brain mechanisms to inform economic analysis, and roots economics in biology. It opens up the "black box" of the brain, much as organizational economics adds detail to the theory of the firm. Neuroscientists use many tools— including brain imaging, behavior of patients with localized brain lesions, animal behavior, and recording single neuron activity. The key insight for economics is that the brain is composed of multiple systems which interact. Controlled systems ("executive function") interrupt automatic ones. Emotions and cognition both guide decisions. Just as prices and allocations emerge from the interaction of two processes—supply and demand— individual decisions can be modeled as the result of two (or more) processes interacting. Indeed, "dual-process" models of this sort are better rooted in neuroscientific fact, and more empirically accurate, than single-process models (such as utility-maximization). We discuss how brain evidence complicates standard assumptions about basic preference, to include homeostasis and other kinds of state-dependence. We also discuss applications to intertemporal choice, risk and decision making, and game theory. Intertemporal choice appears to be domain-specific and heavily influenced by emotion. The simplified s-d of quasi-hyperbolic discounting is supported by activation in distinct regions of limbic and cortical systems. In risky decision, imaging data tentatively support the idea that gains and losses are coded separately, and that ambiguity is distinct from risk, because it activates fear and discomfort regions. (Ironically, lesion patients who do not receive fear signals in prefrontal cortex are "rationally" neutral toward ambiguity.) Game theory studies show the effect of brain regions implicated in "theory of mind", correlates of strategic skill, and effects of hormones and other biological variables. Finally, economics can contribute to neuroscience because simple rational-choice models are useful for understanding highly-evolved behavior like motor actions that earn rewards, and Bayesian integration of sensorimotor information.

/pdf/neuroeconomics-how-neuroscience-can-inform-economics-39l750mxro.pdf

Neuroeconomics: How Neuroscience Can Inform Economics

We review recent developments in neuroeconomics and their implications for economics. The paper consists of six sections. Following the Introduction, the second section enumerates the different research methods that neuroscientists use evaluates their strengths and limitations for analyzing economic phenomena. The third section provides a review of basic findings in neuroscience that we deemed especially relevant to economics, and proposes a two-dimensional dichotomization of neural processes between automatic and controlled processes on the one hand, and cognitive and affective processes on the other. Section four reviews general implications of neuroscience for economics. Research in neuroscience, for example, raises questions about the usefulness of many economic constructs, such as 'time preference' and 'risk preference'. It also suggests that, contrary to the assumption that humans are likely to possess domain-specific intelligence - to be brilliant when it comes to problems that the brain is well evolved for performing and flat-footed for problems that lie outside of the brains existing specialized functions. Section 5 provides more detailed discussions of four specific applications: intertemporal choice, decision making under risk and uncertainty, game theory, and labor-market discrimination. Section 6 concludes by proposing a distinction between two general approaches in applying neuroscience to economics which we term 'incremental' and 'radical'. The former draws on neuroscience findings to refine existing economic models, while the latter poses more basic challenges to the standard economic understanding of human behavior.

Most common central nervous system disorders — such as depression, bipolar disorder and schizophrenia — seem to be polygenic in origin, and the most effective medications have exceedingly complex pharmacologies. Attempts to develop more effective treatments for diseases such as schizophrenia and depression by discovering drugs selective for single molecular targets (that is, 'magic bullets') have, not surprisingly, been largely unsuccessful. Here we propose that designing selectively non-selective drugs (that is, 'magic shotguns') that interact with several molecular targets will lead to new and more effective medications for a variety of central nervous system disorders.

/pdf/magic-shotguns-versus-magic-bullets-selectively-non-1kh3kg6v8w.pdf

Magic shotguns versus magic bullets: selectively non-selective drugs for mood disorders and schizophrenia

Assessing substrates underlying the behavioral effects of antidepressants using the modified rat forced swimming test.

http://public-files.prbb.org/publicacions/75091920-c384-012b-a7a7-000c293b26d5.pdf

Common Chronic Pain Conditions in Developed and Developing Countries: Gender and Age Differences and Comorbidity With Depression-Anxiety Disorders

Recent epidemiological surveys conducted in general populations have found that the lifetime prevalence of depression is in the range of 10% to 15%. Mood disorders, as defined by the World Mental Health and the Diagnostic and Statistical Manual of Mental Disorders, 4th edition, have a 12-month prevalence which varies from 3% in Japan to over 9% in the US. A recent American survey found the prevalence of current depression to be 9% and the rate of current major depression to be 3.4%. All studies of depressive disorders have stressed the importance of the mortality and morbidity associated with depression. The mortality risk for suicide in depressed patients is more than 20-fold greater than in the general population. Recent studies have also shown the importance of depression as a risk factor for cardiovascular death. The risk of cardiac mortality after an initial myocardial infarction is greater in patients with depression and related to the severity of the depressive episode. Greater severity of depressive symptoms has been found to be associated with significantly higher risk of all-cause mortality including cardiovascular death and stroke. In addition to mortality, functional impairment and disability associated with depression have been consistently reported. Depression increases the risk of decreased workplace productivity and absenteeism resulting in lowered income or unemployment. Absenteeism and presenteeism (being physically present at work but functioning suboptimally) have been estimated to result in a loss of $36.6 billion per year in the US. Worldwide projections by the World Health Organization for the year 2030 identify unipolar major depression as the leading cause of disease burden. This article is a brief overview of how depression affects the quality of life of the subject and is also a huge burden for both the family of the depressed patient and for society at large.

/pdf/the-increasing-burden-of-depression-5aqm8bsj61.pdf

The increasing burden of depression

The class of serotonin and norepinephrine reuptake inhibitors (SNRIs) now comprises three medications: venlafaxine, milnacipran, and duloxetine. These drugs block the reuptake of both serotonin (5-HT) and norepinephrine with differing selectivity. Whereas milnacipran blocks 5-HT and norepinephrine reuptake with equal affinity, duloxetine has a 10-fold selectivity for 5-HT and venlafaxine a 30-fold selectivity for 5-HT. All three SNRIs are efficacious in treating a variety of anxiety disorders. There is no evidence for major differences between SNRIs and SSRIs in their efficacy in treating anxiety disorders. In contrast to SSRIs, which are generally ineffective in treating chronic pain, all three SNRIs seem to be helpful in relieving chronic pain associated with and independent of depression. Tolerability of an SNRI at therapeutic doses varies within the class. Although no direct comparative data are available, venlafaxine seems to be the least well-tolerated, combining serotonergic adverse effects (nausea, sexual dysfunction, withdrawal problems) with a dose-dependent cardiovascular phenomenon, principally hypertension. Duloxetine and milnacipran appear better tolerated and essentially devoid of cardiovascular toxicity.

SNRIs: their pharmacology, clinical efficacy, and tolerability in comparison with other classes of antidepressants.

https://www.cell.com/trends/pharmacological-sciences/pdf/0165-6147(87)90101-5.pdf

Animal models of anxiety: the effect of compounds that modify 5-HT neurotransmission

Depression is one of the most common psychological diseases with significant potential morbidity and mortality. Although the underlying pathophysiology of depression has not been clearly defined, preclinical and clinical evidence suggest disturbances in serotonin (5-HT), norepinephrine (NE), and dopamine (DA) neurotransmission in the central nervous system. Virtually all currently available antidepressants act on one or more of the following mechanisms: inhibition of reuptake of 5-HT or NE (and DA), antagonism of inhibitory presynaptic 5-HT or NE receptors, or inhibition of monoamine oxidase. All of these mechanisms result in an enhanced neurotransmission of 5-HT and/or NE. Evidence for the involvement of NE in depression is abundant, and recent studies on neuronal pathways and symptoms highlight the specific role of NE in this disorder. NE plays a determinant role in executive functioning regulating cognition, motivation, and intellect, which are fundamental in social relationships. Social dysfunction is possibly one of the most important factors affecting the quality of life in depressed patients.

/pdf/the-importance-of-norepinephrine-in-depression-x6uo3udpoo.pdf

The importance of norepinephrine in depression.

Over 75% of depressed patients in primary care complain of painful physical symptoms such as headache, stomach pain, neck and back pain as well as non-specific generalized pain. The presence of such symptoms predicts a greater severity and a less favourable outcome of depression with a poorer health-related quality of life. World Health Organization data obtained in primary care centres worldwide show that 22% of all primary care patients suffer from persistent debilitating pain and that these patients are four times more likely to have co-morbid anxiety or depressive disorder than pain-free primary care patients. Not unexpectedly, the risk of depression is greater when the pain is more diffuse, as indicated by the number of painful sites, and has a greater effect on the quality of life. Certain depressive symptoms, such as low energy and sleep disturbances, are commonly found in patients with co-morbid pain, whereas the opposite is true for symptoms such as guilt and loneliness. Increasingly, major depression is seen as being composed of psychological, somatic and painful physical symptoms. In order to achieve full sustained remission it is necessary to treat symptoms in all three of these areas. The area of painful physical symptoms is unfortunately still poorly understood and clearly merits greater attention.

Mike Briley

Papers

The increasing burden of depression

SNRIs: their pharmacology, clinical efficacy, and tolerability in comparison with other classes of antidepressants.

Animal models of anxiety: the effect of compounds that modify 5-HT neurotransmission

The importance of norepinephrine in depression.

The epidemiology of pain in depression