December 2016

Studies of the neurobiology of reward are important to    advance affective neuroscience, and they provide insights    into a variety of psychopathologies, including drug addiction,    eating disorders, obsession and depression. Progress    has been helped by the ability of neuroscientists to manipulate    an ever-expanding number of brain components.    Future studies will be most useful for elucidating the roles    of brain components if they can similarly parse behavioral    reward into its actual psychological components.   

Hochschild, Arlie R. 2003. The managed heart: Commercialization of human feeling. The book is a bona fide analysis of what its author calls selling emotions. According to this book we can imaging most internal traits of a human mind, such as joy or pleasure, under control of the narrative ego and even certain outside (hereby management) needs. Check your smile motto isn’t just for supermarket workers. It’s for nearly every sphere of public life. Resorting to what Karl Marx once said, we have to objectify our thoughts constantly (Verdinglichung, eng. Reification). It means turn some of our mental vibes to things (material and ideal).

However, the present results suggest   that drug-induced mood-elevating effects are more closely related   to neurotransmitters other than DA [3,37,62–69], perhaps   serotonin, norepinephrine, glutamate, GABA, endocannabinoids   and endogenous opioids [2,70–75].  If DA’s influence on reward seeking behaviors is not accounted   for by enhanced pleasure, this raises the question of why it has   these effects. Perhaps the best-supported alternative interpretation   from the animal literature proposes that DA enhances the   incentive salience of reward related cues, increasing their ability   to elicit focused interest and sustain effortful seeking [2,43,76].   This conclusion is largely based on extensive evidence that   decrements in DA neurotransmission reduce the willingness to   work for rewards [37,76] without changing responses in an index   of feeding related pleasure [2,43]. Accumulating work in humans   supports this interpretation also ([62],

However, the present results suggest   that drug-induced mood-elevating effects are more closely related   to neurotransmitters other than DA [3,37,62–69], perhaps   serotonin, norepinephrine, glutamate, GABA, endocannabinoids   and endogenous opioids [2,70–75].  If DA’s influence on reward seeking behaviors is not accounted   for by enhanced pleasure, this raises the question of why it has   these effects. Perhaps the best-supported alternative interpretation   from the animal literature proposes that DA enhances the   incentive salience of reward related cues, increasing their ability   to elicit focused interest and sustain effortful seeking [2,43,76].   This conclusion is largely based on extensive evidence that   decrements in DA neurotransmission reduce the willingness to   work for rewards [37,76] without changing responses in an index   of feeding related pleasure [2,43]. Accumulating work in humans   supports this interpretation also ([62], Table 2). For example, in a   series of studies conducted here, decreasing DA neurotransmission   disrupted the tendency of subjects to respond preferentially to   reward-related cues [55] and decreased the willingness to work for   abused drugs [53,58] and monetary reward [Cawley et al,   unpublished observations] on progressive ratio breakpoint schedules;   each of these effects was produced without reductions in   pleasure. Indeed, the majority of studies in humans have failed to   replicate an ability of various DA lowering manipulations to   diminish drug-induced pleasure [45–58].   The present results should be considered in light of the   following. First, there was no direct measure of the ability of LDOPA   to increase DA, leaving open the possibility that mood   changes were not detected because L-DOPA failed to increase DA   levels. However, this seems unlikely since similar doses of L-DOPA   given to healthy human volunteers induce behavioural effects [77–   79] and increase striatal DA synthesis [80]. Pre-clinical studies   confirm that L-DOPA increases DA levels in the intact brains of   healthy animals, albeit to a lesser extent than in animal models of   Parkinson’s disease [81]. Although, to our knowledge, there are no   reports of L-DOPA induced DA release in healthy humans, the   administration of 250 mg more than doubles ventricular CSF   levels of the DA metabolite, DOPAC [82]. Moreover, robust LDOPA   induced DA responses have been seen in patients with   Parkinson’s disease [83]; intriguingly, these effects are largest in   those who have developed pathological gambling and the ‘‘DA   dysregulation syndrome’’ [84,85]. Moreover, in these patients,   larger L-DOPA-induced DA responses are associated with higher   novelty- and fun-seeking personality traits, greater L-DOPA induced   psychomotor activation, and greater drug ‘‘wanting’’ but   not drug ‘‘liking’’ [84].

References

Liggins, John, Robert O. Pihl, Chawki Benkelfat, and Marco Leyton. 2012. “The dopamine augmenter L-DOPA does not affect positive mood in healthy human volunteers.” PloS one 7 (1): e28370. doi:10.1371/journal.pone.0028370.

À la guerre comme à la guerre ( at war as at war). Let’s try to use it as an epigraph to our further discourse. Indeed, the conditions of a certain society or community give an answer to the possible borders of the narrative ego control over the whole human mind structure. Extremal conditions and strict system of social control practiced at war makes a person endure hardships and obey every clear order from others. The picture of a war, which is well understood due to the cinema, is a good example of the idea of the narrative ego’s total and absolute control of the whole mental structure. The parallel shows some other things too.