Motivational Quotes

In a prominent model of reward learning, Montague et al. (p. 1944, [304]) have argued that dopamine neurons deliver “information about prediction errors between the expected amount of reward and the actual reward”. Their computational model is based on data collected primarily by Schultz and colleagues in an important series of electro- physiological studies on the relationship between the discharge rate of presumed dopamine neurons and the presentation of food rewards, and conditioned stimuli predictive of food rewards [5,277,278,300,301,371,398,399,401- 403], Accordingly, Schultz himself concurs that dopamine neurons “signal deviations from the prediction of future appetitive events” .

The term ‘reinforcement’ can be used in a purely behaviorist sense   instead: to mean either strengthening a stimulus – response habit    Hull’s   sense of reinforcement or to increase the rate (probability) of   response emission    Skinner’s sense of reinforcement. Used in   those ways, it is purely descriptive    describing an environment-behavior   relation.. It applies only to responses that have actually been reinforced,   and is equivalent to the measured strength or rate of a behavioral   response. White has suggested a distinction between ‘reinforcement’      strengthening of stimulus–response tendencies, equivalent to the meaning   of non-Skinnerian behaviorists. and ‘reward’    confer-   ring ability to elicit approach, more similar to incentive motivation..   However, these meanings are often combined, and the term ‘reinforcement’   is typically used by behavioral neuroscientists in ways that   differ from the original behaviorist meaning of increased habit strength      quite reasonably, since the behaviorist meaning is inadequate to account   for many effects For example, place preference measures   are sometimes used to assess ‘reinforcement’ even when no response has   been ‘reinforced’    as when the animal is trained by putting it passively in   the ‘reinforced place’

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.   

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.

Stress generally is defined as any stimulus that challenges physiological homeostasis—that is, which alters the balance or equilibrium of the normal physiologicalstate of the organism. It is important to realize, however, that the term “stress” is rather nonspecific and should alwaysbe qualified. Although all forms ofstress alter homeostasis, they do not all do so in the same manner (i.e.,they have different physiological consequences). Different kinds of stress can stimulate different combinations of signaling molecules (i.e., molecules that aid in cell-to-cell communication, such as neurohormones), thereby producing unique effects on physiological processes.