Tag Archives: emotion

cognitive achievement that comes at an emotional cost

November 11, 2010

By Steve Bradt, Harvard Staff Writer

People spend 46.9 percent of their waking hours thinking about something other than what they’re doing, and this mind-wandering typically makes them unhappy. So says a study that used an iPhone Web app to gather 250,000 data points on subjects’ thoughts, feelings, and actions as they went about their lives.

The research, by psychologists Matthew A. Killingsworth and Daniel T. Gilbertof Harvard University, is described this week in the journal Science.

“A human mind is a wandering mind, and a wandering mind is an unhappy mind,” Killingsworth and Gilbert write. “The ability to think about what is not happening is a cognitive achievement that comes at an emotional cost.”

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Social learning theory

Social learning theory (Albert Bandura) posits that learning is a cognitive process that takes place in a social context and can occur purely through observation or direct instruction, even in the absence of motor reproduction or direct reinforcement.[1] In addition to the observation of behavior, learning also occurs through the observation of rewards and punishments, a process known as vicarious reinforcement. The theory expands on traditional behavioral theories, in which behavior is governed solely by reinforcements, by placing emphasis on the important roles of various internal processes in the learning individual.[2]

Prior to 1960, published theories of learning were heavily influenced by theories of classic conditioning, operant conditioning, and the psychoanalytic concept of drives.[3] In 1959,Noam Chomsky published his criticism[4] of B.F. Skinner‘s book Verbal Behavior.[5] In his review, Chomsky stated that pure stimulus-response theories of behavior could not account for the process of language acquisition, an argument that contributed significantly to psychology’s cognitive revolution.

Within this context, Albert Bandura studied learning processes that occurred in interpersonal contexts and were not adequately explained by theories of operant conditioning or existing models of social learning, such as the work of Julian Rotter.[1] Specifically, Bandura argued that “the weaknesses of learning approaches that discount the influence of social variables are nowhere more clearly revealed than in their treatment of the acquisition of novel responses.”[1] Skinner’s explanation of the acquisition of new responses relied on the process of successive approximation, which required multiple trials, reinforcement for components of behavior, and gradual change.[6] Rotter’s theory proposed that the likelihood of a behavior occurring was a function of the subjective expectancy and value of the reinforcement.[7] This model assumed a hierarchy of existing responses and thus did not (according to Bandura[1]) account for a response that had not yet been learned. Bandura began to conduct studies of the rapid acquisition of novel behaviors via social observation, the most famous of which were the Bobo doll experiments.

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In 1961 Bandura conducted a controversial experiment known as the Bobo doll experiment, to study patterns of behavior , at least in part, by social learning theory, and that similar behaviors were learned by individuals shaping their own behavior after the actions of models.

The experiment was criticized by some on ethical grounds, for training children towards aggression. Bandura’s results from the Bobo Doll Experiment changed the course of modern psychology, and were widely credited for helping shift the focus in academic psychology from pure behaviorism to cognitive psychology. The experiment is among the most lauded and celebrated of psychological experiments.

The nucleus accumbens

The nucleus accumbens (NAc or NAcc), also known as the accumbens nucleus or as the nucleus accumbens septi (Latin fornucleus adjacent to the septum) is a region in the basal forebrain rostral to the preoptic area of the hypothalamus.[1] The nucleus accumbens and the olfactory tubercle collectively form the ventral striatum, which is part of the basal ganglia.[2] Each cerebral hemisphere has its own nucleus accumbens, which can be divided into two structures: the nucleus accumbens core and the nucleus accumbens shell. These substructures have different morphology and functions.

Different NAcc subregions (core vs shell) and neuron subpopulations within each region (D1-type vs D2-type medium spiny neurons) are responsible for different cognitive functions.[3][4] As a whole, the nucleus accumbens has a significant role in the cognitive processing of aversion, motivation, pleasure, reward and reinforcement learning;[5][6][7] hence, it has a significant role inaddiction.[6][7] It plays a lesser role in processing fear (a form of aversion), impulsivity, and the placebo effect.[8][9][10] It is involved in the encoding of new motor programs as well.[6]

Major inputs to the nucleus accumbens include the prefrontal cortex, basolateral amygdala, and dopaminergic neurons located in the ventral tegmental area (VTA), which connect via the mesolimbic pathway. Thus the nucleus accumbens is often described as one part of a cortico–basal ganglia–thalamic loop.[11]

Dopaminergic input from the VTA modulate the activity of neurons within the nucleus accumbens. These neurons are activated directly or indirectly by euphoriant drugs (e.g.,amphetamine, opiates, etc.) and by participating in rewarding experiences (e.g., sex, music, exercise, etc.).[12][13]

Another major source of input comes from the CA1 and ventral subiculum of the hippocampus to the dorsomedial area of the nucleus accumbens. The neurons of the hippocampus have a noteworthy correlation to slight depolarizations of cells in the nucleus accumbens, which makes them more positive and therefore more excitable. The correlated cells of these excited states of the medium spiny neurons in the nucleus accumbens are shared equally between the subiculum and CA1. The subiculum neurons are found to hyperpolarize (increase negativity) while the CA1 neurons “ripple” (fire > 50 Hz) in order to accomplish this priming.[14]

The nucleus accumbens is one of the few regions that receive histaminergic projections from the tuberomammillary nucleus (the sole source of histamine neurons in the brain).[15]

Output

The output neurons of the nucleus accumbens send axon projections to the basal ganglia and the ventral analog of the globus pallidus, known as the ventral pallidum (VP). The VP, in turn, projects to the medial dorsal nucleus of the dorsal thalamus, which projects to the prefrontal cortex as well as the striatum. Other efferents from the nucleus accumbens include connections with the tail of the ventral tegmental area,[16] substantia nigra, and the reticular formation of the pons.[1]

Neurotransmitters

Dopamine: Dopamine is related to recreational drugs including amphetamines, cocaine, and morphine, which increase extracellular levels of dopamine in both the NAc shell and the NAc core, but the effect of these increases is more pronounced in the shell. Only amphetamine at high levels increases extracellular levels of dopamine to similar levels in both the shell and the core. All of this points to a ‘functional heterogeneity’ in the nucleus accumbens between the shell region and the core region.[26] Similarly to drug rewards, non-drug rewards also increase levels of extracellular dopamine in the NAc shell, but drug induced DA increase is more resilient to habituation when exposed repeatedly to drug-stimuli, unlike non-drug rewarding stimuli induced dopamine increases, which do succumb to habituation. Recent[when?] studies have shown that the repeated influence of drug-inducing DA projection has an abnormal strengthening effect on stimulus-drug associations and increases the drug-reward stimuli’s resistance to extinction. This may be a contributing factor to addiction. This effect was more pronounced in the NAc shell than in the NAc core.[19][27]

Phenethylamine and tyramine: Phenethylamine and tyramine are trace amine compounds which are synthesized in several types of CNS neurons, including all dopamine neurons.[28] Specifically, these neurotransmitters act within the dopaminergic inputs to the NAcc. These substances regulate the presynaptic release of dopamine through their interactions with VMAT2 and TAAR1, analogous to amphetamine.

Glucocorticoids and dopamine: Glucocorticoid receptors are the only corticosteroid receptors in the nucleus accumbens shell. L-DOPA, steroids, and specifically glucocorticoids are currently known to be the only known endogenous compounds that can induce psychotic problems, so understanding the hormonal control over dopaminergic projections with regards to glucocorticoid receptors could lead to new treatments for psychotic symptoms. A recent study demonstrated that suppression of the glucocorticoid receptors led to a decrease in the release of dopamine, which may lead to future research involving anti-glucocorticoid drugs to potentially relieve psychotic symptoms.[29]

Glucocorticoids (GCs) are a class of corticosteroids, which are a class of steroid hormones. Glucocorticoids are corticosteroids that bind to the glucocorticoid receptor (GR),[1] that is present in almost every vertebrate animal cell. The name glucocorticoid (glucose +cortex + steroid) is composed from its role in regulation of glucose metabolisms synthesis in the adrenal cortex, and its steroidalstructure (see structure to the right). A less common synonym is glucocorticosteroid.

GCs are part of the feedback mechanism in the immune system which reduces certain aspects of immune function, such as reduction of inflammation. They are therefore used in medicine to treat diseases caused by an overactive immune system, such as allergies, asthma, autoimmune diseases, and sepsis. GCs have many diverse (pleiotropic) effects, including potentially harmful side effects, and as a result are rarely sold over the counter.[2] They also interfere with some of the abnormal mechanisms in cancer cells, so they are used in high doses to treat cancer. This includes: inhibitory effects on lymphocyte proliferation as in the treatment of lymphomas and leukemias; and the mitigation of side effects of anticancer drugs.

GCs affect cells by binding to the glucocorticoid receptor (GR). The activated GR complex, in turn, up-regulates the expression of anti-inflammatory proteins in the nucleus (a process known as transactivation) and represses the expression of proinflammatory proteins in the cytosol by preventing the translocation of other transcription factors from the cytosol into the nucleus (transrepression).[2]

Glucocorticoids are distinguished from mineralocorticoids and sex steroids by their specific receptors, target cells, and effects. In technical terms, “corticosteroid” refers to both glucocorticoids and mineralocorticoids (as both are mimics of hormones produced by the adrenal cortex), but is often used as a synonym for “glucocorticoid.” Glucocorticoids are chiefly produced in the zona fasciculataof the adrenal cortex, whereas mineralocorticoids are synthesized in the zona glomerulosa.

Cortisol (or hydrocortisone) is the most important human glucocorticoid. It is essential for life, and it regulates or supports a variety of important cardiovascular, metabolic, immunologic, and homeostatic functions. Various synthetic glucocorticoids are available; these are used either as replacement therapy in glucocorticoid deficiency or to suppress the immune system.

Glucocorticoids act on the hippocampus, amygdala, and frontal lobes. Along with adrenaline, these enhance the formation of flashbulb memories of events associated with strong emotions, both positive and negative.[5] This has been confirmed in studies, whereby blockade of either glucocorticoids or noradrenaline activity impaired the recall of emotionally relevant information. Additional sources have shown subjects whose fear learning was accompanied by high cortisol levels had better consolidation of this memory (this effect was more important in men). The effect that glucocorticoids have on memory may be due to damage specifically to the CA1 area of the hippocampal formation. In multiple animal studies, prolonged stress (causing prolonged increases in glucocorticoid levels) have shown destruction of the neurons in this area of the brain, which has been connected to memory performance.[6][7][8]

Glucocorticoids have also been shown to have a significant impact on vigilance (attention deficit disorder) and cognition (memory). This appears to follow the Yerkes-Dodson curve, as studies have shown circulating levels of glucocorticoids vs. memory performance follow an upside-down U pattern, much like the Yerkes-Dodson curve. For example, long-term potentiation (LTP; the process of forming long-term memories) is optimal when glucocorticoid levels are mildly elevated, whereas significant decreases of LTP are observed after adrenalectomy (low-GC state) or after exogenous glucocorticoid administration (high-GC state). Elevated levels of glucocorticoids enhance memory for emotionally arousing events, but lead more often than not to poor memory for material unrelated to the source of stress/emotional arousal.[9] In contrast to the dose-dependent enhancing effects of glucocorticoids on memory consolidation, these stress hormones have been shown to inhibit the retrieval of already stored information.[10] Long-term exposure to glucocorticoid medications, such as asthma and anti-inflammatory medication, has been shown to create deficits in memory and attention both during and, to a lesser extent, after treatment,[11][12] a condition known as “steroid dementia.”[13]

GABA: A recent study on rats that used GABA agonists and antagonists indicated that GABAA receptors in the NAc shell have inhibitory control on turning behavior influenced by dopamine, and GABAB receptors have inhibitory control over turning behavior mediated by acetylcholine.[19][30]

Glutamate: Studies have shown that local blockade of glutamatergic NMDA receptors in the NAcc core impaired spatial learning.[31] Another study demonstrated that both NMDA and AMPA (both glutamate receptors) play important roles in regulating instrumental learning.[32]

Serotonin (5-HT): Overall, 5-HT synapses are more abundant and have a greater number of synaptic contacts in the NAc shell than in the core. They are also larger and thicker, and contain more large dense core vesicles than their counterparts in the core.

Reward and reinforcement

The nucleus accumbens, being one part of the reward system, plays an important role in processing rewarding stimuli, reinforcing stimuli (e.g., food and water), and those which are both rewarding and reinforcing (addictive drugs, sex, and exercise).[6][33] The nucleus accumbens is selectively activated during the perception of pleasant, emotionally arousing pictures and during mental imagery of pleasant, emotional scenes.[34][35] A 2005 study found that it is involved in the regulation of emotions induced by music,[36]perhaps consequent to its role in mediating dopamine release. The nucleus accumbens plays a role in rhythmic timing and is considered to be of central importance to the limbic-motor interface (Mogensen).[citation needed]

In the 1950s, James Olds and Peter Milner implanted electrodes into the septal area of the rat and found that the rat chose to press a lever which stimulated it. It continued to prefer this even over stopping to eat or drink. This suggests that the area is the “pleasure center” of the brain and is involved in reinforcement learning.[37] In rats, stimulation of the ventral tegmental area causes the release of dopamine in the nucleus accumbens much in the same way as addictive drugs and natural reinforcers, such as water or food, initiate the release of dopamine in the nucleus accumbens.[38] The same results have been seen in human subjects in functional imaging studies. For example, increased dopamine concentration is seen in the extracellular fluid of the nucleus accumbens when subjects believed they were being given money[citation needed], and increased activation (i.e., increased fMRI BOLD signal-change) was observed among heterosexual males viewing pictures of attractive women.[39]

Aversion

Activation of D1-type MSNs in the nucleus accumbens is involved in reward, whereas the activation of D2-type MSNs in the nucleus accumbens promotes aversion.[4]

Maternal behavior

An fMRI study conducted in 2005 found that when mother rats were in the presence of their pups the regions of the brain involved in reinforcement, including the nucleus accumbens, were highly active.[40] Levels of dopamine increase in the nucleus accumbens during maternal behavior, while lesions in this area upset maternal behavior.[41] When women are presented pictures of unrelated infants, fMRIs show increased brain activity in the nucleus accumbens and adjacent caudate nucleus, proportionate to the degree to which the women find these infants “cute”.[42]

Placebo effect

Activation of the NAcc has been shown to occur in the anticipation of effectiveness of a drug when a user is given a placebo, indicating a contributing role of the nucleus accumbens in the placebo effect.[9][52]

A smile

A smile is a facial expression formed primarily by flexing the muscles at the sides of the mouth.[1] Some smiles include a contraction of the muscles at the corner of the eyes, an action known as a “Duchenne smile”. Smiles performed without the eye contraction can be perceived as “fake”.

Among humans, smiling is an expression denoting pleasure, sociability, happiness, or amusement. It is distinct from a similar but usually involuntary expression of anxiety known as a grimace. Although cross-cultural studies have shown that smiling is a means of communication throughout the world,[2] there are large differences between different cultures, with some using smiles to convey confusion or embarrassment.

A smile seems to have a favorable influence upon others and makes one likable and more approachable.[3] In the social context, smiling and laughter have different functions in the order of sequence in social situations:

  • Smiling is not a pre-laughing device and is a common pattern for paving the way to laughter;
  • Smiling can be used as a response to laughter in the previous turn.[4]

Smiling is a signaling system that evolved from a need to communicate information of many different forms. One of these is advertisement of sexual interest. Female smiles are appealing to heterosexual males, increasing physical attractiveness and enhancing sex appeal. However, recent research indicates a man’s smile may or may not be most effective in attracting heterosexual women, and that facial expressions such as pride or even shame might be more effective. The researchers ignored the role of smiles in other sexual preferences.[5]

Cultural differences

A Smiling boy from Bangladesh.

While smiling is perceived as a positive emotion most of the time, there are many cultures that perceive smiling as a negative expression and consider it unwelcoming. Too much smiling can be viewed as a sign of shallowness or dishonesty.[6] In other parts of Asia, people may smile when they are embarrassed or in emotional pain. Some people may smile at others to indicate a friendly greeting. A smile may be reserved for close friends and family members. Many people in the former Soviet Union area consider smiling at strangers in public to be unusual and even suspicious behavior.

While conducting research on the physiology of facial expressions in the mid-19th century, French neurologist Guillaume Duchenneidentified two distinct types of smiles. A Duchenne smile involves contraction of both the zygomatic major muscle (which raises the corners of the mouth) and the orbicularis oculi muscle (which raises the cheeks and forms crow’s feet around the eyes).[9]

A non-Duchenne smile involves only the zygomatic major muscle.[10] “Research with adults initially indicated that joy was indexed by generic smiling, any smiling involving the raising of the lip corners by the zygomatic major…. More recent research suggests that smiling in which the muscle around the eye contracts, raising the cheeks high (Duchenne smiling), is uniquely associated with positive emotion.”[11]

The Pan Am smile, also known as the “Botox smile”, is the name given to a fake smile, in which only the zygomatic major muscle is voluntarily contracted to show politeness. It is named after the now defunct airline Pan American World Airways, whose flight attendants would always flash every passenger the same perfunctory smile.[12] Botox was introduced for cosmetic use in 2002.[13] Chronic use of Botox injections to deal with eye wrinkle can result in the paralysis of the small muscles around the eyes, preventing the appearance of a Duchenne smile.

In animals

In animals, the exposure of teeth, which may bear a resemblance to a smile and imply happiness, often conveys other signals. The baring of teeth is often used as a threat or warning display—known as a snarl—or a sign of submission. For chimpanzees, it can also be a sign of fear. However, not all animal displays of teeth convey negative acts or emotions. For example, Barbary macaques demonstrate an open mouth display as a sign of playfulness which likely has similar roots and purposes as the human smile.[14]