Декабрь 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.  

Эта книга считается классическим анализом процесса, который сам автор называет продажей эмоций. Следуя канве этой книги, можно представить, как самые интимные черты человеческой психики, например, такие, как проявление радости или удовольствия, можно поставить под контроль не только нарративному Я, но и неким внешним (в данном случае управленческим) запросам.

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 (на войне, как на войне, at war as at war).  Попробуем использовать эту фразу как эпиграф к последующим рассуждениям. Действительно, состояние, в котором иногда пребывает то или иное общество, дает нам ответ о возможных границах контроля нарративного Я над всей структурой человеческой психики. Экстремальные условия, а так же жесткая система общественного регулирования, которую практикует общество в условиях войны, не только заставляет человека терпеть лишения, но и выполнять все внешние указания, осуществляющиеся в форме недвусмысленного приказа. Образ войны, который благодаря тому же кинематографу хорошо воспринимается в качестве художественного образца, дает хоть не точный, но наглядный  пример для тезиса о том, что нарративное Я не только в состоянии осуществить полный контроль внутри нашей ментальной структуры, но и быть тотальным хозяином или начальником ее.