What is the difference between motivation and emotion

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What is difference between motivation and mobilization? What do motivation and emotion have in common? What does the Latin root word for 'motivation' mean? What is the difference between the Enlightenment and great awakening? People also asked. View results. Study Guides. Trending Questions.

Still have questions? Find more answers. Previously Viewed. Unanswered Questions. Do you have to place in all round to be eligible to compete on individual events? Get the Answers App. All Rights Reserved. The material on this site can not be reproduced, distributed, transmitted, cached or otherwise used, except with prior written permission of Answers. Thus, a range of views that differ in the various principles of self-regulation were appeared.

A first common feature is to expound self-regulation as a dynamic motivational system of setting goals, developing and performing strategies to achieve those goals, appraising progress, and revising goals and strategies accordingly.

Motivation is the common desire and willingness a person possesses to effectuate a behavior. As the demand for both physical and psychological knowledge, competence, and energy is needed to ensue behavior, the emotional aspect of motivation also plays a major role. Interpersonal relationships represent one of the fields of action most studied today, since from the psychological perspective, there are diverse behaviors that must be understood for an effective stimulation of relationships between human beings.

In this sense, there are different theories such as the one presented by Cialdini , points out that within interpersonal relationships, there must be a motivational component that allows ideas to be better communicated between two or more people.

In the same way, satisfy the set of intrinsic needs that go hand in hand with the reasons why they establish such communications between people. In this sense, in the present work paper, the main characteristics of the motivation in interpersonal relationships. It is interesting to explore the avenues down which the two go hand in hand, as there are many aspects of human behaviour which could be as a result of self-esteem.

It is something that determines the quality of life for human-beings. Open Document. Essay Sample Check Writing Quality. Motivation and emotion are usually viewed as two psychological features that seemingly share cause-and-effect relationship.

We often see motivation as something that stimulates a person to act and behave to achieve a desired goal, while emotion is the feelings that emerge from the motive or drive itself, from the actions caused by the motive and from the achievement or failure of the desired goal.

Motivation has been defined in different ways over the years, but a common component of the different definitions is that motivation is a force that energizes, activates and directs behaviour. Motivation has been defined in various ways …show more content… Second, emotions often go together with motives.

And third, it is typical for basic emotions to possess motivational properties of their own. For example, happiness motivates a person to achieve better performance. To go on to claim that emotion as a psychological process is exclusively a conscious feeling is to make an empirical claim about psychological fact.

This claim requires actual evidence, which must be looked for in psychological studies. No one can define facts in advance. Second, what is the evidence? Quite a lot of evidence exists, and in my view it does not support the idea that emotions are necessarily conscious, nor that verbal reports are the best way to assess emotion. Considerable experimental evidence indicates that some features of human emotion and motivation cannot actually be accessed well via introspection or described in subjective reports Nisbett and Wilson, ; Wilson and Schooler, ; Schwarz, ; Dijksterhuis et al.

In some cases, asking people to describe their emotional reasons for making a choice may lead them to construct false explanations of their own behavior. It can lead them astray from their immediate gut reactions that would be more emotionally authentic. Thinking too much and trying to verbally report feelings can distort emotional reactions. Indeed, bringing introspective attention to pleasure feelings may actually dissipate those hedonic feelings: less introspective attention can mean more emotion, as well as more accuracy about the underlying emotional reaction, in some cases Wilson and Schooler, ; Dijksterhuis et al.

Studies of implicit prejudice similarly suggest that introspective verbal reports may miss some important emotional reactions Greenwald and Banaji, Implicit prejudices can only be revealed by objective measures, such as the emotional Stroop test of reaction time to affective mismatch, sometimes to the surprise and dismay of the person who is subjectively unprejudiced. What is subjectively reported may only be a constructed explanation of what we think we should feel or would like to feel, rather than an accurate readout of underlying emotional reactions.

For example, cocaine addicts under some conditions will objectively work to take cocaine infusions, and choose them over saline infusions, even when the cocaine dose is too low to produce any subjective drug feelings of pleasure or arousal Fischman and Foltin, Further, in ordinary adults under certain circumstances, subliminally brief visual flashes of happy or angry facial expressions can elicit unconscious affective reactions, either positive or negative, which produced no change in subjective mood reports but nonetheless controlled motivated behavior some minutes afterward Winkielman et al.

In that study, before and after seeing subliminal faces, participants rated their emotional feelings. Their subjective ratings of mood or emotion were not changed at all by exposures to subliminal and backward-masked emotional faces, whether happy or angry Winkielman et al. Yet subliminal exposure to happy faces elicited a positive affective reaction that remained unconscious, but which could be revealed by presenting thirsty participants with a relevant incentive: a pitcher of fruit beverage.

Those happy-exposed participants poured more drink, drank more of what they poured, and were willing to pay a much higher monetary price for the drink offered than after viewing emotionally-neutral faces.

It might be objected that subliminally viewing a happy facial expression merely increased unvalenced arousal, which increased drink motivation, and was not truly affective. However, the test of true affect is whether it is valenced positive versus negative. Valence was evident in that subliminal viewing of angry faces had an opposite negative-valenced impact on the same thirsty participants: they poured less, drank less, and were willing to pay less than after seeing only neutral facial expressions — again without any intervening change in their subjective ratings of emotional mood Berridge and Winkielman, ; Winkielman et al.

In passing, it is important that these unconscious affects were evident only if participants were already thirsty Winkielman et al. Thirst is a physiological state that should specifically amplify brain mesolimbic reactivity to perception of a drink, amplifying its incentive salience, and providing a higher brain motivation signal for unconscious emotional reactions to modulate.

This interaction between percept and state in controlling motivational value follows what I call Bindra-Toates rules of incentive salience, which will be described below. Of course, subliminally seeing emotional facial expressions is not equivalent to inducing the corresponding full emotion Adolphs et al. But subliminal expressions do induce a valenced affective reaction in human viewers: positive to smiling faces and negative to angry faces Zajonc, For now, my main point is simply that these results demonstrate that bivalent affective reactions can be subjectively unconscious even in adult humans, and even when detected objectively in behavior.

Defining affect or emotion solely as subjective feelings misses something important. Finally, regarding language as a gold standard for emotion, talking about feelings evoked by sunsets is not proof even of the emotions that are declared.

Linguistic computer programs may soon pass an emotional Turing test by talking compellingly about enjoyment of sunsets, so that a listener thinks the computer has emotional feelings. Even in the s some people poured out their own feelings to ELIZA, a linguistic computer program with scripted responses that simulated the responsive questions of a Rogerian psychoanalyst via text messages, and seemed to human interlocutors to convey great emotional sensitivity e.

I am unhappy. Weizenbaum, In humans too, as already mentioned talking about emotions may cognitively distort underlying processes based on what people think their emotions should be, rather than accurately report emotional content Wilson and Schooler, ; Dijksterhuis et al.

This aims for a schematic understanding of other minds, rather than an introspective mirroring of phenomenal experience. Schematic understanding is the way we study perception, learning, memory and cognition in animals. What is a schematic understanding of emotion?

Schemas are hypothetical information-processing units, closely linked to observed behaviors. Similarly, the psychologists of emotion Nico Frijda and W. Other psychologists and neuroscientists have expressed similar views about fundamental affective reactions in animals and human infants Darwin, ; Berridge, ; Keltner and Ekman, ; Steiner et al. Of course, one goal of animal studies is to gain insights that have application to understanding human emotions and motivations.

For that, we need to posit continuity between those affective mechanisms in animals and humans. Otherwise, it would be impossible to make the jump from discoveries about animal affective processes, to human affective processes or to human clinical disorders of addiction, depression, schizophrenia, etc.

This jump is not always easy. Indeed another reason LeDoux gives for denying that animals are capable of fear is because animal fear conditioning studies failed to provide new effective medications for human anxiety or panic disorders. However, this lack of therapeutic development could just as well mean that Pavlovian fear learning e. It is an unfounded leap to conclude instead it means that rats are incapable of fear.

Other animal tests of fear or anxiety using different reactions and situations might be more successful. And there are many other cases where animal studies of emotion have produced results with successful implications for understanding human psychology and disorders.

We had believed until the late s that the two concepts necessarily went together, as two semantic sides of the same psychological coin. Evidence from our studies of brain mechanisms for food reward in rats forced us to change our minds. But for the first decade of this hypothesis, the schematic understanding from animal evidence was all we had, based on objective affective reactions, which stood alone and pointed the way.

Our initial discovery came from studies of the role of brain mesolimbic dopamine systems in reward. Conversely, Wise suggested an opposite anhedonia hypothesis for the psychological effect of drugs that blocked dopamine receptors often called neuroleptic drugs or dopamine antagonist drugs , which posited those drugs to cause tasty foods and all other reward to lose their pleasure or hedonic impact.

To give credit where due, some other neuroscientists, such as John Salamone and Jaak Panksepp had also expressed early doubts about the dopamine-as-pleasure hypothesis. In human infants, sweet tastes typically elicit relaxed and rhythmic mouth and tongue movements, and licking of the lips. Some of these affective facial expressions to taste are shared by apes and other primates, and even by rats and other non-primates Grill and Norgren, ; Berridge, But only animal evidence existed for these hypotheses until nearly That made ours a lonely position, because most affective neuroscientists still wrote of dopamine as a pleasure mechanism throughout the s and often into the s.

Similarly, it is now increasingly clear that increases of human dopamine do not reliably cause enhancement of subjective ratings of pleasure although many rewards do induce dopamine release as a consequence and correlate, but not the cause, of pleasure Leyton et al.

For example, giving ordinary people the medication L-DOPA, which produces surges in brain dopamine levels, does not increase their subjective ratings of pleasure feelings Liggins et al. Dopamine surges in nucleus accumbens evoked by addictive amphetamine or by L-DOPA correlate poorly with human subjective liking ratings of the drug - but do control their subjective wanting ratings to take more of that drug Leyton et al. Was our animal-based conclusion about human liking and wanting simply a lucky guess?

Instead it was a schematic inference about hedonic and motivation mechanisms of reward gained from animals, with direct applications to human psychology and clinical affective disorders.

Sensitized mesolimbic dopamine neurons release more dopamine when a drug is taken, their dopamine-receiving target neurons become more receptive to excitatory glutamate signals, etc.

This neural sensitization creates dopamine hyper-reactivity to drugs and their cues in sensitized individuals. Neural sensitization can happen in many of the same brain dopamine-related neurons that undergo drug tolerance because the two changes proceed through parallel chains of molecular events inside neurons, almost like ships passing in the night. In the short run, tolerance and withdrawal often win and mask sensitization — as long as drugs continue to be taken. Then sensitization wins.

Originally we applied this incentive-sensitization theory only to drug addiction, because only drugs were then known to induce mesolimbic neural sensitization.

However, it has subsequently become clear that it is also possible to induce mesolimbic sensitization without drugs in susceptible individuals, such as by exposures to traumatic stresses, exposures to strong specific appetites, etc.

There are strong individual differences in sensitization vulnerability, due to genes, hormones, previous experiences, etc. Presumably those who develop behavioral addictions are the most vulnerable individuals, able to develop mesolimbic sensitization via endogenous mechanisms, without need of drugs. Evidence that sensitization happens in behavioral addictions is that fMRI studies have reported individuals with gambling addiction, shopping addiction, internet addiction or sex addiction, to exhibit brain signatures of mesolimbic sensitization to appropriate stimuli: that is, neural hyper-reactivity to their own addictive cues, higher than non-addicted people show to the same reward, and higher than the same addicted individuals show to cues for other non-addicted rewards Davis and Carter, ; Gearhardt et al.

Those addictive urges would be further amplified when the cues were encountered during stress, emotional excitement, intoxication or other states that prime the reactivity of mesolimbic systems.

New dopamine-stimulating medications have produced addictive-like motivations in people who were previously least likely to ever become addicts. Receptor-stimulated DDS patients can become sensitized, and are reported to compulsively pursue incentive activities in an addictive-like fashion: gambling, shopping, sex, internet, hobbies, taking drugs or even over-consuming their medications in much higher quantities than intended by their physicians Ondo and Lai, ; Callesen et al.

Patients who show DDS compulsions have been suggested to also have neural features of incentive-sensitization, for example releasing more dopamine in nucleus accumbens than other patients when stimulated with L-Dopa.

These conditions have traditionally have been described as involving anhedonia or incapacity to experience pleasure similar to the original Wise hypothesis that dopamine blockade reduced pleasure. Now we will shift gears, and turn to a very different question. Namely, the nature of motivation processes themselves, and how motivations actually control behavior. Motivation concepts have changed a lot over the last few decades. For example, from to the s, much of the thinking about reward motivation in psychology and neuroscience was dominated by two concepts: drive and drive reduction Hull, ; Miller, Drive was typically conceived as an aversive state that goaded behavior into action to reduce the unpleasant drive hunger, thirst, sex, drug withdrawal, etc.

Drive reduction served as reward in this motivational framework; not as a positive pleasure or incentive, but in a negative reinforcement sense of eliminating the aversive drive. This is why anesthetics make us so happy. Natural motivations were viewed by drive-reduction theory as generators of aversive states, triggered by signals for physiological homeostatic needs low nutrient reserves for hunger, dehydration for thirst or of other forms of deprivation lack of sex, withdrawal from addictive drugs, etc.

Hull, ; Miller, Today, drive reduction theories can still be found in a few cases, such as theories of drug addiction based on withdrawal symptoms, or in the conclusions of a few recent neuroscience studies of hunger or thirst. For example, in drug addiction, the opponent-process theory posited negative hedonic states of withdrawal and dysphoria to be the chief force driving addicts to take drugs Solomon and Corbit, , a view that still has adherents Koob and Volkow, ; Keramati et al.

Modern proponents suggest that downregulation or loss of brain dopamine D2 receptors one of the two main types of neuronal receptors for dopamine make addicts experience less pleasure in their lives than other people Koob and Volkow, ; Keramati et al. Consequently, these theorists argue that addicts must take addictive drugs to achieve normal levels of dopamine stimulation and pleasure. However, this hedonic deficiency view has been critiqued on grounds that dopamine receptor downregulation is probably a consequence of drug taking rather than the original cause of addiction, on grounds that dopamine does not actually cause pleasure nor does dopamine downregulation cause pleasure deficits, and on grounds that addictions persist after withdrawal syndromes go away Berridge and Robinson, Recent studies of hunger and thirst neuronal circuitry provide a few more examples that drive reduction ideas persist today.

Hunger neurons are thought to include those in the hypothalamus that release agouti-related peptide AgRP , and stimulating those neurons cause mice to eat. However, a mouse may subsequently avoid a flavor that was paired with the AgRP neuronal stimulation that made it eat, leading some authors to suggest that stimulated hunger is necessarily an aversive drive that the mouse later associates with the flavor Betley et al.

However, other neuroscientists have found that mice will actually work to turn on their hypothalamic AgRP neurons that previously made them eat, indicating that the increased appetite can be dissociated from negative valence, and even take on a positive valence in the right conditions Chen et al.

This makes a pure drive reduction theory of AgRP hunger less plausible, similar as to what happened for hypothalamic reward electrodes discussed below. Recently, a thirst drive-reduction hypothesis was suggested by authors of a study similar to the first AgRP one for hunger Allen et al.

These thirst-study authors found that artificial stimulation of neurons in the hypothalamus made mice drink, but that mice would work to turn off the stimulation if given a choice, thus leading the authors to suggest that thirst is essentially aversive.

Yet if history repeats itself, the aversiveness of the hypothalamic neuronal activation may in future turn out to be separable from its ability to trigger drinking Toates, ; Berridge, If so, aversiveness above could in part due to relatively extreme or unnatural parameters of the earlier neural stimulation. The crucial test will be if future studies with other stimulation parameters can eventually tease apart drinking elicitation from aversive effects — possibly even finding that activation of the drinking neurons can become sought under some circumstances.

That could help dissolve these new drive-reduction explanations into a future incentive motivation explanation for the same hypothalamic circuitry. Of course they can, giving drive-reduction theories an eternally intuitive appeal. Perhaps the single most compelling piece of evidence that moved motivation theory away from negative drive theories to positive incentive theories of motivation came from s studies of reward and hunger motivation caused by brain electrode stimulation — mostly at sites in the lateral hypothalamus that indirectly also activated mesolimbic dopamine systems Olds and Milner, ; Valenstein et al.

It quickly became clear that brain reward electrodes were not only rewarding in the sense that rats and people worked eagerly to activate them , but the same electrodes were also often powerfully motivating in the sense of apparently turning on natural motivations.

That is, simply giving free stimulations of the electrodes, without making them work for it, caused rats to suddenly start eating, or start drinking, or begin engaging in sex, or parental behaviors, etc. Valenstein et al.

Similarly in human psychiatric patients who had been implanted with similar brain electrodes, activation of a reward electrode caused sudden sexual urges, or urges to drink, or other intense motivations, in addition to supporting button pressing to self-stimulate their electrodes Moan and Heath, The finding that the same electrode was both rewarding in the sense of being sought after and motivating confounded expectations based on drive theories.

According to drive theories, the intense motivations had to be aversive. According to drive reduction theories, reward was produced by reducing motivations, not by increasing drives. Thus behavioral neuroscientists of the time expected that an electrode that increased sex or hunger or thirst motivations, would be a punishing electrode.

They expected that a reward electrode would reduce drive, and so stop any ongoing eating, drinking, or sex behavior — never stimulate those motivations.

To drive theorists, a reward electrode that also increased motivation is an inexplicable paradox Miller, ; Olds, ; Stuber and Wise, How can that paradox be resolved? The fact that an electrode that caused eating behavior or drinking, or sex, etc. Since the rewarding electrode actually increased the apparent drive to eat, reward needed to be understood as a phenomenon that was independent from drive reduction.

The paradox was eventually solved by incentive motivation theory described below. Other evidence has indicated similarly that the aversiveness of drives does not actually motivate much behavior, even for hunger and thirst. Nor is the reduction of an aversive drive actually the chief target of those motivations.

For example, when in a place that has been repeatedly associated with hunger, or paired with thirst, one might expect a re-encounter of that place to trigger Pavlovian conditioned cue-triggered hunger or thirst again, and increase eating or drinking.

That should happen if re-activation of the aversive need-state or drive motivates eating or drinking behavior. But that does not happen. For example, rats typically fail to increase eating in a place previously paired with hunger drive, nor to increase drinking in a place paired with thirst drive Huston, ; Mineka et al.

Pavlovian cues for hunger fail to elicit ingestive behaviors, that is, unless those cues were additionally paired with the opportunity to eat while hungry, or the opportunity to drink while thirsty. However, if that extra pairing with food consumption while hungry is given, then later the Pavlovian food cue can evoke conditioned eating even if encountered when the rat is no longer hungry Weingarten, ; Holland et al.

That is, a food incentive cue elicits eating, but a hunger cue does not. Similarly, for thirst,: encountering a place paired with thirst drive does not alter behavior, but encountering a cue for water will evoke intense increases in activity in thirsty rats, as though searching for water Campbell, In these cases, cues for the incentive stimulus evoke motivation in a state, whereas cues for the drive state by itself do not.

Hunger acts to enhance the incentive value of food, and thirst enhances the incentive value of water — but in the absence of incentives or their learned expectation, neither need state effectively motivates behavior as posited by aversive drive theory. Not only is drive a weak motivator by itself, but drive reduction turns out to be surprisingly impotent as a reward by itself.

Reduction of a hunger or thirst drive is usually not enough to reinforce behavior, unless an incentive stimulus is also involved. For example, rats that can deliver nutrients directly to their stomach via feeding through a gastric fistula in some studies fail to bar press for the nutrients at all Holman, However, if opportunity to taste a mouthful of saccharin at the same time as a gastric nutrient infusion, then the rats do learn to bar press for the combination the sweet taste by itself is similarly insufficient, revealing an importance of interaction between incentive stimulus and physiological state, captured by Bindra-Toates rules of incentive motivation described below Holman, Similarly, hungry rats merely walked slowly to a place where they expect intra-gastric milk, but eagerly ran to a place where they could drink and taste the milk while hungry Miller and Kessen, And drive reduction is not even satiating: reducing a physiological drive often does not effectively reduce the motivated behavior.

For example, delivering daily calories intravenously to dogs, who were also allowed to eat actual food normally if they wished, did not suppress their daily eating intake: the dogs continued to eat customary amounts of food in addition to their full doses of intravenous nutrients, and so soon became obese Turner et al. What is the alternative to drive theories? Incentive motivation theories posit that motivation is directed toward affectively positive incentives, and that brain motivation systems modulate those incentive values Toates, ; Berridge, Incentive motivation is focused on reward, which involve three categories of mechanism: wanting, liking and learning.

Hedonic hotspots are anatomically small pleasure-generating islands of brain tissue, tucked within larger limbic structures, such as nucleus accumbens and limbic cortex Figures 2 , 3.

The size of each hotspot discovered so far is only a cubic millimeter or so in volume in the brain of a rat. In the brain of a person, a hotspot would be expected to be about a cubic centimeter in volume, extrapolating from the size difference between whole brains. Microinjections of the same glutamate-blocking drug DNQX elicit opposite motivations at different sites. Both incentive motivation and fearful motivation require local mesolimbic dopamine.

Based on Reynolds and Berridge and Richard and Berridge Neurochemically, these hotspots respond with hedonic amplification to opioid, endocannabinoid, orexin and related neurotransmitter signals — but never dopamine. Several of these hedonic hotspots have been found in the brain scattered from cortex to brainstem Figure 1. Hotspots are found in limbic areas of prefrontal cortex such as in orbitofrontal cortex, in insula cortex, and in subcortical structures such as nucleus accumbens, ventral pallidum the chief target of nucleus accumbens , and the brainstem pons.

The distributed hotspots appear to act together as a functionally interconnected network, so that stimulating one hotspot with a drug microinjection causes other hotspots to be recruited into neurobiological activation too Smith and Berridge, ; Castro and Berridge, Unanimous activation of multiple hotspots together appears required in order to amplify sensory pleasures.

Cognitive wanting is goal-oriented, and based typically on declarative memories and on cognitive expectations of act-outcome relations, and less tied to mesolimbic dopamine-related systems. By contrast, incentive salience has distinct signature features: often being cue-triggered as a temporary peak of desire to obtain or consume an associated reward Berridge, , Sometimes the cues may even become targets of consumption themselves.

Incentive salience is responsible for many incentive motivation phenomena described above, including the apparent paradox that the same brain stimulation can be both motivating i. Sarah Mae Sincero Oct 15, Motivation and Emotion. Retrieved Nov 11, from Explorable. The text in this article is licensed under the Creative Commons-License Attribution 4. That is it. You can use it freely with some kind of link , and we're also okay with people reprinting in publications like books, blogs, newsletters, course-material, papers, wikipedia and presentations with clear attribution.

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