Tag Archives: memory


Published on May 16, 2013
The possibility that our personal memory can play strange tricks on us has been the focus of Giuliana’s research for many years. Her work, based at the University of Hull, has also examined the cognitive and behavioural consequences of suggestion. Giuliana is a recognised memory expert and has recently been part of Channel 4’s documentary The Boy Who Can’t Forget where she examined Aurelien, a boy who claims he can remember every day of his life. This condition is considered impossible by current models of memory.
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Overgeneral autobiographical memory (OGM)

Overgeneral autobiographical memory (OGM) is an inability to retrieve specific memories from one’s autobiographical memory.[1] Instead, general memories are recalled, such as repeated events or events occurring over broad periods. For example, when asked to recall a happy event, a person who exhibits OGM may say, “when I was on vacation last month” instead of remembering a single incident, such as, “my high school graduation.”[2] Research shows a correlation between OGM and certain mental illnesses, such as major depressive disorder (MDD) and posttraumatic stress disorder (PTSD).[3]

Stroop effect

In psychology, the Stroop effect is a demonstration of interference in thereaction time of a task. When the name of a color (e.g., “blue”, “green”, or “red”) is printed in a color not denoted by the name (e.g., the word “red” printed in blue ink instead of red ink), naming the color of the word takes longer and is more prone to errors than when the color of the ink matches the name of the color. The effect is named after John Ridley Stroop, who first published the effect in English in 1935.[1] The effect had previously been published in Germany in 1929.[2][3][4]The original paper has been one of the most cited papers in the history ofexperimental psychology, leading to more than 701 replications.[4] The effect has been used to create a psychological test (Stroop test) that is widely used in clinical practice and investigation.

Brain imaging techniques including magnetic resonance imaging (MRI), functional magnetic resonance imaging (fMRI), and positron emission tomography (PET) have shown that there are two main areas in the brain that are involved in the processing of the Stroop task.[7] They are the anterior cingulate cortex, and the dorsolateral prefrontal cortex.[8]More specifically, while both are activated when resolving conflicts and catching errors, the dorsolateral prefrontal cortex assists in memory and other executive functions, while the anterior cingulate cortex is used to select an appropriate response and allocate attentional resources.[9]

The posterior dorsolateral prefrontal cortex creates the appropriate rules for the brain to accomplish the current goal.[9] For the Stroop effect, this involves activating the areas of the brain involved in color perception, but not those involved in word encoding.[10] It counteracts biases and irrelevant information, for instance, the fact that the semantic perception of the word is more striking than the color in which it is printed. Next, the mid-dorsolateral prefrontal cortex selects the representation that will fulfil the goal. The relevant information must be separated from irrelevant information in the task; thus, the focus is placed on the ink color and not the word.[9] Furthermore, research has suggested that left dorsolateral prefrontal cortex activation during a Stroop task is related to an individual’s’ expectation regarding the conflicting nature of the upcoming trial, and not so much on the conflict itself. Conversely, the right dorsolateral prefrontal cortex aims to reduce the attentional conflict and is activated after the conflict is over.[8]

Moreoever, the posterior dorsal anterior cingulate cortex is responsible for what decision is made (i.e. whether you will say the incorrect answer [written word] or the correct answer [ink color]).[8] Following the response, the anterior dorsal anterior cingulate cortex is involved in response evaluation—deciding whether the answer is correct or incorrect. Activity in this region increases when the probability of an error is higher.[11]

In the neo-Piagetian theories of cognitive development, several variations of the Stroop task have been used to study the relations between speed of processing and executive functions with working memory and cognitive development in various domains. This research shows that reaction time to Stroop tasks decreases systematically from early childhood through early adulthood. These changes suggest that speed of processing increases with age and that cognitive control becomes increasingly efficient. Moreover, this research strongly suggests that changes in these processes with age are very closely associated with development in working memory and various aspects of thought.[21][22]

The amygdalae

Published on May 29, 2016
What the difference in brain structure between liberals and conservatives? And where do our political convictions come from: rational deliberation, or biological determinism? Psychiatrist Gail Saltz explains.
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Socioemotional selectivity theory

Socioemotional selectivity theory (developed by Stanford psychologist, Laura L. Carstensen) is a life-span theory of motivation. The theory maintains that as time horizons shrink, as they typically do with age, people become increasingly selective, investing greater resources in emotionally meaningful goals and activities. According to the theory, motivational shifts also influence cognitive processing. Aging is associated with a relative preference for positive over negative information in attention and memory (called the “positivity effect“).

Because they place a high value on emotional satisfaction, older adults often spend more time with familiar individuals with whom they have had rewarding relationships.[1] This selective narrowing of social interaction maximizes positive emotional experiences and minimizes emotional risks as individuals become older. According to this theory, older adults systematically hone their social networks so that available social partners satisfy their emotional needs.[1]

The theory also focuses on the types of goals that individuals are motivated to achieve. Knowledge-related goals aim at knowledge acquisition, career planning, the development of new social relationships and other endeavors that will pay off in the future. Emotion-related goals are aimed at emotion regulation, the pursuit of emotionally gratifying interactions with social partners and other pursuits whose benefits can be realized in the present.

When people perceive their future as open ended, they tend to focus on future-oriented and development- or knowledge-related goals, but when they feel that time is running out and the opportunity to reap rewards from future-oriented goals’ realization is dwindling, their focus tends to shift towards present-oriented and emotion- or pleasure-related goals.[1] Research on this theory often compares age groups (e.g., young adulthood vs. old adulthood), but the shift in goal priorities is a gradual process that begins in early adulthood. Importantly, the theory contends that the cause of these goal shifts is not age itself, i.e., not the passage of time itself, but rather an age-associated shift in time perspective.[1]

This justified shift in perspective is the rational equivalent of the psychological perceptual disorder known as “foreshortened future,” in which an individual, usually a young and physically healthy individual, unreasonably believes (either consciously or unconsciously) that his/her time horizons are more limited than they actually are, with the effect that the individual undervalues long-term goals and long-run pleasure and instead disproportionately pursues short-term goals and pleasure, thereby diverting resources from investment for the future and often even actively reducing his/her long-term prospects.

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]


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]


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]


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]

The fornix

The fornix (Latin: arch) is a C-shaped bundle of nerve fibers in the brain that carries signals from the hippocampus to themammillary bodies and then to the anterior nuclei of thalamus. The fornix is part of the limbic system. While its exact function and importance in the physiology of the brain is still not entirely clear, it has been demonstrated in humans that surgical transection – the cutting of the fornix along its body – can cause memory loss. There is some debate over what type of memory is affected by this damage, but it has been found to most closely correlate with recall memory rather than recognition memory. This means that damage to the fornix can cause difficulty in recalling long-term information such as details of past events, but it has little effect on the ability to recognize objects or familiar situations.