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 […]

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.


The amygdalae

The amygdalae (singular: amygdala; /əˈmɪɡdələ/; also corpus amygdaloideum; Latin, from Greek ἀμυγδαλή, amygdalē, ‘almond’, ‘tonsil’[1]) are two almond-shaped groups of nuclei located deep and medially within the temporal lobes of the brain in complex vertebrates, including humans.[2] Shown in research to perform a primary role in the processing of memory, decision-making, andemotional reactions, the amygdalae […]

The amygdalae (singular: amygdala; /??m??d?l?/; also corpus amygdaloideum; Latin, from Greek ????????, amygdal?, ‘almond’, ‘tonsil’[1]) are two almond-shaped groups of nuclei located deep and medially within the temporal lobes of the brain in complex vertebrates, including humans.[2] Shown in research to perform a primary role in the processing of memory, decision-making, andemotional reactions, the amygdalae are considered part of the limbic system.[3]

Amygdalar development

There is considerable growth within the first few years of structural development in both male and female amygdalae. Within this early period, female limbic structures grow at a more rapid pace than do males. Amongst female subjects, the amygdala reaches its full growth potential approximately 1.5 years before the peak of male development. The structural development of the male amygdala occurs over a longer period than in women. Despite the early development of female amygdalae, they reach their growth potential sooner than males, whose amygdalae continue to develop. The larger relative size of the male amygdala may be attributed to this extended developmental period.

In addition to longer periods of development, other neurological and hormonal factors may contribute to sex-specific developmental differences. The amygdala is rich in androgen receptors – nuclear receptors that bind to testosterone. Androgen receptors play a role in the DNA binding that regulates gene expression. Though testosterone is present within the female hormonal systems, women have lower levels of testosterone than men. The abundance of testosterone in the male hormonal system may contribute to development. In addition, the grey matter volume on the amygdala is predicted by testosterone levels, which may also contribute to the increased mass of the male amygdala.

In addition to sex differences, there are observable developmental differences between the right and left amygdala in both males and females. The left amygdala reaches its developmental peak approximately 1.5–2 years prior to the right amygdala. Despite the early growth of the left amygdala, the right increases in volume for a longer period of time. The right amygdala is associated with response to fearful stimuli as well as face recognition. It is inferred that the early development of the left amygdala functions to provide infants the ability to detect danger.[12]

In childhood, the amygdala is found to react differently to same-sex versus opposite-sex individuals. This reactivity decreases until a person enters adolescence, where it increases dramatically at puberty.[13]

Gender distinction

The amygdala is one of the best-understood brain regions with regard to differences between the sexes. Larger male than female amygdalae have been demonstrated in children ages 7–11,[14] in adult humans,[15] and in adult rats.[16]

In addition to size, other differences between men and women exist with regards to the amygdala. Subjects’ amygdala activation was observed when watching a horror film andsubliminal stimuli. The results of the study showed a different lateralization of the amygdala in men and women. Enhanced memory for the film was related to enhanced activity of the left, but not the right, amygdala in women, whereas it was related to enhanced activity of the right, but not the left, amygdala in men.[17] One study found evidence that on average, women tend to retain stronger memories for emotional events than men.[18]

The right amygdala is also linked with taking action as well as being linked to negative emotions,[19] which may help explain why males tend to respond to emotionally stressful stimuli physically. The left amygdala allows for the recall of details, but it also results in more thought rather than action in response to emotionally stressful stimuli, which may explain the absence of physical response in women.

Emotional learning

In complex vertebrates, including humans, the amygdalae perform primary roles in the formation and storage of memories associated with emotional events. Research indicates that, during fear conditioning, sensory stimuli reach the basolateral complexes of the amygdalae, particularly the lateral nuclei, where they form associations with memories of the stimuli. The association between stimuli and the aversive events they predict may be mediated by long-term potentiation,[22][23] a sustained enhancement of signaling between affected neurons.[24] There have been studies that show that damage to the amygdala can interfere with memory that is strengthened by emotion. One study examined a patient with bilateral degeneration of the amygdala. He was told a violent story accompanied by matching pictures and was observed based on how much he could recall from the story. The patient had less recollection of the story than patients with functional amygdala, showing that the amygdala has a strong connection with emotional learning.[25]

Memories of emotional experiences imprinted in reactions of synapses in the lateral nuclei elicit fear behavior through neuronal connections with the central nucleus of the amygdalae and the bed nuclei of the stria terminalis (BNST). The axon terminals from sensory neurons form synapses with dendritic spines on neurons from the central nucleus.[26] The central nuclei are involved in the genesis of many fear responses such as defensive behavior (freezing or escape responses), autonomic nervous system responses (changes in blood pressure and heart rate/tachycardia), neuroendocrine responses (stress-hormone release), etc. Damage to the amygdalae impairs both the acquisition and expression of Pavlovian fear conditioning, a form of classical conditioning of emotional responses.[24]

The amygdalae are also involved in appetitive (positive) conditioning. It seems that distinct neurons respond to positive and negative stimuli, but there is no clustering of these distinct neurons into clear anatomical nuclei.[27][28] However, lesions of the central nucleus in the amygdala have been shown to reduce appetitive learning in rats. Lesions of the basolateral regions do not exhibit the same effect.[29] Research like this indicates that different nuclei within the amygdala have different functions in appetitive conditioning.[30][31]

Memory modulation

The amygdala is also involved in the modulation of memory consolidation. Following any learning event, the long-term memory for the event is not formed instantaneously. Rather, information regarding the event is slowly assimilated into long-term (potentially lifelong) storage over time, possibly via long-term potentiation. Recent studies suggest that the amygdala regulates memory consolidation in other brain regions. Also, fear conditioning, a type of memory that is impaired following amygdala damage, is mediated in part by long-term potentiation.[22][23]

During the consolidation period, the memory can be modulated. In particular, it appears that emotional arousal following the learning event influences the strength of the subsequent memory for that event. Greater emotional arousal following a learning event enhances a person’s retention of that event. Experiments have shown that administration of stress hormones to mice immediately after they learn something enhances their retention when they are tested two days later.[32]

The amygdala, especially the basolateral nuclei, are involved in mediating the effects of emotional arousal on the strength of the memory for the event, as shown by many laboratories including that of James McGaugh. These laboratories have trained animals on a variety of learning tasks and found that drugs injected into the amygdala after training affect the animals’ subsequent retention of the task. These tasks include basic classical conditioning tasks such as inhibitory avoidance, where a rat learns to associate a mild footshock with a particular compartment of an apparatus, and more complex tasks such as spatial or cued water maze, where a rat learns to swim to a platform to escape the water. If a drug that activates the amygdalae is injected into the amygdalae, the animals had better memory for the training in the task.[33] If a drug that inactivates the amygdalae is injected, the animals had impaired memory for the task.

Buddhist monks who do compassion meditation have been shown to modulate their amygdala, along with their temporoparietal junction and insula, during their practice.[34] In anfMRI study, more intensive insula activity was found in expert meditators than in novices.[35] Increased activity in the amygdala following compassion-oriented meditation may contribute to social connectedness.[36]

Amygdala activity at the time of encoding information correlates with retention for that information. However, this correlation depends on the relative “emotionalness” of the information. More emotionally arousing information increases amygdalar activity, and that activity correlates with retention. Amygdala neurons show various types of oscillationduring emotional arousal, such as theta activity. These synchronized neuronal events could promote synaptic plasticity (which is involved in memory retention) by increasing interactions between neocortical storage sites and temporal lobe structures involved in declarative memory.[37]

Research using Rorschach test blot 03 finds that the number of unique responses to this random figure links to larger sized amygdalae. The researchers note, “Since previous reports have indicated that unique responses were observed at higher frequency in the artistic population than in the nonartistic normal population, this positive correlation suggests that amygdalar enlargement in the normal population might be related to creative mental activity.”[38]

Neuropsychological correlates of amygdala activity

Early research on primates provided explanations as to the functions of the amygdala, as well as a basis for further research. As early as 1888, rhesus monkeys with a lesioned temporal cortex (including the amygdala) were observed to have significant social and emotional deficits.[39] Heinrich Klüver and Paul Bucy later expanded upon this same observation by showing that large lesions to the anterior temporal lobe produced noticeable changes, including overreaction to all objects, hypoemotionality, loss of fear, hypersexuality, and hyperorality, a condition in which inappropriate objects are placed in the mouth. Some monkeys also displayed an inability to recognize familiar objects and would approach animate and inanimate objects indiscriminately, exhibiting a loss of fear towards the experimenters. This behavioral disorder was later named Klüver-Bucy syndrome accordingly,[40] and later research proved it was specifically due to amygdala lesions. Monkey mothers who had amygdala damage showed a reduction in maternal behaviors towards their infants, often physically abusing or neglecting them.[41] In 1981, researchers found that selective radio frequency lesions of the whole amygdala caused Klüver-Bucy syndrome.[42]

With advances in neuroimaging technology such as MRI, neuroscientists have made significant findings concerning the amygdala in the human brain. A variety of data shows the amygdala has a substantial role in mental states, and is related to many psychological disorders. Some studies have shown children with anxiety disorders tend to have a smaller left amygdala. In the majority of the cases, there was an association between an increase in the size of the left amygdala with the use of SSRIs (antidepressant medication) or psychotherapy. The left amygdala has been linked to social anxiety, obsessive and compulsive disorders, and post traumatic stress, as well as more broadly to separation and general anxiety.[43] In a 2003 study, subjects with borderline personality disorder showed significantly greater left amygdala activity than normal control subjects. Some borderline patients even had difficulties classifying neutral faces or saw them as threatening.[44] Individuals with psychopathy show reduced autonomic responses, relative to comparison individuals, to instructed fear cues.[45] In 2006, researchers observed hyperactivity in the amygdala when patients were shown threatening faces or confronted with frightening situations. Patients with more severe social phobia showed a correlation with increased response in the amygdala.[46] Similarly, depressed patients showed exaggerated left amygdala activity when interpreting emotions for all faces, and especially for fearful faces. Interestingly, this hyperactivity was normalized when patients were administered antidepressant medication.[47] By contrast, the amygdala has been observed to respond differently in people with bipolar disorder. A 2003 study found that adult and adolescent bipolar patients tended to have considerably smaller amygdala volumes and somewhat smaller hippocampal volumes.[48] Many studies have focused on the connections between the amygdala and autism.[49]

Studies in 2004 and 2006 showed that normal subjects exposed to images of frightened faces or faces of people from another race will show increased activity of the amygdala, even if that exposure is subliminal.[50][51] However, the amygdala is not necessary for the processing of fear-related stimuli, since persons in whom it is bilaterally damaged show rapid reactions to fearful faces, even in the absence of a functional amygdala.[52]

Recent research suggests that parasites, in particular toxoplasma, form cysts in the brain of rats, often taking up residence in the amygdala. This may provide clues as to how specific parasites may contribute to the development of disorders, including paranoia.[53]

Future studies have been proposed to address the role of the amygdala in positive emotions, and the ways in which the amygdala networks with other brain regions.[54]

Sexual orientation

Recent studies have suggested possible correlations between brain structure, including differences in hemispheric ratios and connection patterns in the amygdala, and sexual orientation. Homosexual men tend to exhibit more female-like patterns in the amygdala than heterosexual males do, just as homosexual females tend to show more male-like patterns in the amygdala than heterosexual women do. It was observed that amygdala connections were more widespread from the left amygdala in homosexual males, as is also found in heterosexual females. Amygdala connections were more widespread from the right amygdala in homosexual females, as in heterosexual males.[55][55][56]

Social interaction

Amygdala volume correlates positively with both the size (the number of contacts a person has) and the complexity (the number of different groups to which a person belongs) of social networks.[57][58] Individuals with larger amygdalae had larger and more complex social networks. They were also better able to make accurate social judgments about other persons’ faces.[59] The amygdala’s role in the analysis of social situations stems specifically from its ability to identify and process changes in facial features. It does not, however, process the direction of the gaze of the person being perceived.[60][61]

The amygdala is also thought to be a determinant of the level of a person’s emotional intelligence. It is particularly hypothesized that larger amygdalae allow for greater emotional intelligence, enabling greater societal integration and cooperation with others.[62]

The amygdala processes reactions to violations concerning personal space. These reactions are absent in persons in whom the amygdala is damaged bilaterally.[63]Furthermore, the amygdala is found to be activated in fMRI when people observe that others are physically close to them, such as when a person being scanned knows that an experimenter is standing immediately next to the scanner, versus standing at a distance.[63]

Aggression

Animal studies have shown that stimulating the amygdala appears to increase both sexual and aggressive behavior. Likewise, studies using brain lesions have shown that harm to the amygdala may produce the opposite effect. Thus, it appears that this part of the brain may play a role in the display and modulation of aggression.[64]

Fear

There are cases of human patients with focal bilateral amygdala lesions, due to the rare genetic condition Urbach-Wiethe disease.[65][66] Such patients fail to exhibit fear-related behaviors, leading one, Patient S.M., to be dubbed the “woman with no fear”. This finding reinforces the conclusion that the amygdala “plays a pivotal role in triggering a state of fear”.[67]

Alcoholism and binge drinking

The amygdala appears to play a role in binge drinking, being damaged by repeated episodes of intoxication and withdrawal.[68] Alcoholism is associated with dampened activation in brain networks responsible for emotional processing[clarification needed], including the amygdala.[69] Protein kinase C-epsilon in the amygdala is important for regulating behavioral responses to morphine, ethanol, and controlling anxiety-like behavior. The protein is involved in controlling the function of other proteins and plays a role in development of the ability to consume a large amount of ethanol.[70][71]

Anxiety

There may also be a link between the amygdala and anxiety.[72] In particular, there is a higher prevalence of females that are affected by anxiety disorders. In an experiment,degu pups were removed from their mother but allowed to hear her call. In response, the males produced increased serotonin receptors in the amygdala but females lost them. This led to the males being less affected by the stressful situation.

The clusters of the amygdala are activated when an individual expresses feelings of fear or aggression. This occurs because the amygdala is the primary structure of the brain responsible for flight or fight response. Anxiety and panic attacks can occur when the amygdala senses environmental stressors that stimulate fight or flight response.

The amygdala is directly associated with conditioned fear. Conditioned fear is the framework used to explain the behavior produced when an originally neutral stimulus is consistently paired with a stimulus that evokes fear. The amygdala represents a core fear system in the human body, which is involved in the expression of conditioned fear. Fear is measured by changes in autonomic activity including increased heart rate, increased blood pressure, as well as in simple reflexes such as flinching or blinking.

The central nucleus of the amygdala has direct correlations to the hypothalamus and brainstem – areas directly related to fear and anxiety. This connection is evident from studies of animals that have undergone amygdalae removal. Such studies suggest that animals lacking an amygdala have less fear expression and indulge in non-species-like behavior. Many projection areas of the amygdala are critically involved in specific signs that are used to measure fear and anxiety.

Mammals have very similar ways of processing and responding to danger. Scientists have observed similar areas in the brain – specifically in the amygdala – lighting up or becoming more active when a mammal is threatened or beginning to experience anxiety. Similar parts of the brain are activated when rodents and when humans observe a dangerous situation, the amygdala playing a crucial role in this assessment. By observing the amygdala’s functions, people can determine why one rodent may be much more anxious than another. There is a direct relationship between the activation of the amygdala and the level of anxiety the subject feels.

Feelings of anxiety start with a catalyst – an environmental stimulus that provokes stress. This can include various smells, sights, and internal feelings that result in anxiety. The amygdala reacts to this stimuli by preparing to either stand and fight or to turn and run. This response is triggered by the release of adrenaline into the bloodstream. Consequently, blood sugar rises, becoming immediately available to the muscles for quick energy. Shaking may occur in an attempt to return blood to the rest of the body. A better understanding of the amygdala and its various functions may lead to a new way of treating clinical anxiety.[73]

Posttraumatic stress disorder

There seems to be a connection with the amygdalae and how the brain processes posttraumatic stress disorder. Multiple studies have found that the amygdalae may be responsible for the emotional reactions of PTSD patients. One study in particular found that when PTSD patients are shown pictures of faces with fearful expressions, their amygdalae tended to have a higher activation than someone without PTSD.[74]

Political orientation

Amygdala size has been correlated with cognitive styles with regard to political thinking. A study found that “greater liberalism was associated with increased gray matter volume in the anterior cingulate cortex, whereas greater conservatism was associated with increased volume of the right amygdala.”[75]


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 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]


Anki

Anki is a program which makes remembering things easy. Because it’s a lot more efficient than traditional study methods, you can either greatly decrease your time spent studying, or greatly increase the amount you learn. Anyone who needs to remember things in their daily life can benefit from Anki. Since it is content-agnostic and supports … Continue reading Anki

Anki is a program which makes remembering things easy. Because it’s a lot more efficient than traditional study methods, you can either greatly decrease your time spent studying, or greatly increase the amount you learn.

Anyone who needs to remember things in their daily life can benefit from Anki. Since it is content-agnostic and supports images, audio, videos and scientific markup (via LaTeX), the possibilities are endless.
For example:

  • Learning a language
  • Studying for medical and law exams
  • Memorizing people’s names and faces
  • Brushing up on geography
  • Mastering long poems
  • Even practicing guitar chords!

Memory

Hermann Ebbinghaus (January 24, 1850 – February 26, 1909) was a German psychologist who pioneered the experimental study of memory, and is known for his discovery of the forgetting curve and the spacing effect. He was also the first person to describe thelearning curve.[1] He was the father of the eminent neo-Kantian philosopher Julius Ebbinghaus.

Hermann Ebbinghaus (January 24, 1850 – February 26, 1909) was a German psychologist who pioneered the experimental study of memory, and is known for his discovery of the forgetting curve and the spacing effect. He was also the first person to describe thelearning curve.[1] He was the father of the eminent neo-Kantian philosopher Julius Ebbinghaus.


memories in DNA

Parental olfactory experience influences behavior and neural structure in subsequent generations Brian G Dias & Kerry J Ressler Full text PDF Abstract Using olfactory molecular specificity, we examined the inheritance of parental traumatic exposure, a phenomenon that has been frequently observed, but not understood. We subjected F0 mice to odor fear conditioning before conception and found […]

Parental olfactory experience influences behavior and neural structure in subsequent generations

Abstract

Using olfactory molecular specificity, we examined the inheritance of parental traumatic exposure, a phenomenon that has been frequently observed, but not understood. We subjected F0 mice to odor fear conditioning before conception and found that subsequently conceived F1 and F2 generations had an increased behavioral sensitivity to the F0-conditioned odor, but not to other odors. When an odor (acetophenone) that activates a known odorant receptor (Olfr151) was used to condition F0 mice, the behavioral sensitivity of the F1 and F2 generations to acetophenone was complemented by an enhanced neuroanatomical representation of the Olfr151 pathway. Bisulfite sequencing of sperm DNA from conditioned F0 males and F1 naive offspring revealed CpG hypomethylation in the Olfr151 gene. In addition, in vitro fertilization, F2 inheritance and cross-fostering revealed that these transgenerational effects are inherited via parental gametes. Our findings provide a framework for addressing how environmental information may be inherited transgenerationally at behavioral, neuroanatomical and epigenetic levels.

 

Thursday, October 22, 2015

New research from Emory University School of Medicine, in Atlanta, has shown that it is possible for some information to be inherited biologically through chemical changes that occur in DNA. During the tests they learned that that mice can pass on learned information about traumatic or stressful experiences – in this case a fear of the smell of cherry blossom – to subsequent generations.

According to the Telegraph, Dr Brian Dias, from the department of psychiatry at Emory University, said: ”From a translational perspective, our results allow us to appreciate how the experiences of a parent, before even conceiving offspring, markedly influence both structure and function in the nervous system of subsequent generations.

“Such a phenomenon may contribute to the etiology and potential intergenerational transmission of risk for neuropsychiatric disorders such as phobias, anxiety and post-traumatic stress disorder.”

This suggests that experiences are somehow transferred from the brain into the genome, allowing them to be passed on to later generations.

  • 1 December 2013

Experiments showed that a traumatic event could affect the DNA in sperm and alter the brains and behaviour of subsequent generations.

A Nature Neuroscience study shows mice trained to avoid a smell passed their aversion on to their “grandchildren”.

Experts said the results were important for phobia and anxiety research.

The animals were trained to fear a smell similar to cherry blossom.

The team at the Emory University School of Medicine, in the US, then looked at what was happening inside the sperm.

They showed a section of DNA responsible for sensitivity to the cherry blossom scent was made more active in the mice’s sperm.

Both the mice’s offspring, and their offspring, were “extremely sensitive” to cherry blossom and would avoid the scent, despite never having experienced it in their lives.

Changes in brain structure were also found.

“The experiences of a parent, even before conceiving, markedly influence both structure and function in the nervous system of subsequent generations,” the report concluded.


memories in DNA

Parental olfactory experience influences behavior and neural structure in subsequent generations Brian G Dias & Kerry J Ressler Full text PDF Abstract Using olfactory molecular specificity, we examined the inheritance of parental traumatic exposure, a phenomenon that has been frequently observed, but not understood. We subjected F0 mice to odor fear conditioning before conception and found […]

Parental olfactory experience influences behavior and neural structure in subsequent generations

Abstract

Using olfactory molecular specificity, we examined the inheritance of parental traumatic exposure, a phenomenon that has been frequently observed, but not understood. We subjected F0 mice to odor fear conditioning before conception and found that subsequently conceived F1 and F2 generations had an increased behavioral sensitivity to the F0-conditioned odor, but not to other odors. When an odor (acetophenone) that activates a known odorant receptor (Olfr151) was used to condition F0 mice, the behavioral sensitivity of the F1 and F2 generations to acetophenone was complemented by an enhanced neuroanatomical representation of the Olfr151 pathway. Bisulfite sequencing of sperm DNA from conditioned F0 males and F1 naive offspring revealed CpG hypomethylation in the Olfr151 gene. In addition, in vitro fertilization, F2 inheritance and cross-fostering revealed that these transgenerational effects are inherited via parental gametes. Our findings provide a framework for addressing how environmental information may be inherited transgenerationally at behavioral, neuroanatomical and epigenetic levels.

 

Thursday, October 22, 2015

New research from Emory University School of Medicine, in Atlanta, has shown that it is possible for some information to be inherited biologically through chemical changes that occur in DNA. During the tests they learned that that mice can pass on learned information about traumatic or stressful experiences – in this case a fear of the smell of cherry blossom – to subsequent generations.

According to the Telegraph, Dr Brian Dias, from the department of psychiatry at Emory University, said: ”From a translational perspective, our results allow us to appreciate how the experiences of a parent, before even conceiving offspring, markedly influence both structure and function in the nervous system of subsequent generations.

“Such a phenomenon may contribute to the etiology and potential intergenerational transmission of risk for neuropsychiatric disorders such as phobias, anxiety and post-traumatic stress disorder.”

This suggests that experiences are somehow transferred from the brain into the genome, allowing them to be passed on to later generations.

  • 1 December 2013

Experiments showed that a traumatic event could affect the DNA in sperm and alter the brains and behaviour of subsequent generations.

A Nature Neuroscience study shows mice trained to avoid a smell passed their aversion on to their “grandchildren”.

Experts said the results were important for phobia and anxiety research.

The animals were trained to fear a smell similar to cherry blossom.

The team at the Emory University School of Medicine, in the US, then looked at what was happening inside the sperm.

They showed a section of DNA responsible for sensitivity to the cherry blossom scent was made more active in the mice’s sperm.

Both the mice’s offspring, and their offspring, were “extremely sensitive” to cherry blossom and would avoid the scent, despite never having experienced it in their lives.

Changes in brain structure were also found.

“The experiences of a parent, even before conceiving, markedly influence both structure and function in the nervous system of subsequent generations,” the report concluded.


experiencing less as we record more

Photographing More, Experiencing Less Put Down The Camera And Watch The Show … Really? The idea that we are experiencing less as we record more got psychologist Linda Henkel thinking. Her father was a photographer, and she wanted to explore how photographs … Continue reading

photos

Photographing More, Experiencing Less

The idea that we are experiencing less as we record more got psychologist Linda Henkel thinking. Her father was a photographer, and she wanted to explore how photographs shape our memories.

Henkel, who researches human memory at Fairfield University in Connecticut, began an experiment by sending groups of students to the university’s art museum. The students observed some objects and photographed others. Then, back at the laboratory, they were given a memory test.

Henkel found what she called a “photo-taking impairment effect.”

“The objects that they had taken photos of — they actually remembered fewer of them, and remembered fewer details about those objects. Like, how was this statue’s hands positioned, or what was this statue wearing on its head. They remembered fewer of the details if they took photos of them, rather than if they had just looked at them,” she says.

Henkel says her students’ memories were impaired because relying on an external memory aid means you subconsciously count on the camera to remember the details for you.


Unconscious Decision Making

Published on Jul 26, 2012 Instinct is the driving force behind human decision making. Irrationality must be recognized if we’re going to get beyond the risks of not being built as thinking machines, says David Ropeik. David P. Ropeik is … Continue reading

Published on Jul 26, 2012 Instinct is the driving force behind human decision making. Irrationality must be recognized if we’re going to get beyond the risks of not being built as thinking machines, says David Ropeik. David P. Ropeik is an international consultant, author, teacher, and speaker on risk perception and risk communication.[1] He is also creator and director of Improving Media Coverage of Risk, a training program for journalists. He is a regular contributor to Big Think,[2] Psychology Today,[3] Cognoscenti,[4] and the Huffington Post.[5] http://bigthink.com


Published on Nov 26, 2012 Animation describing the Universal Principles of Persuasion based on the research of Dr. Robert Cialdini, Professor Emeritus of Psychology and Marketing, Arizona State University. Dr. Robert Cialdini & Steve Martin are co-authors (together with Dr. Noah Goldstein) of the New York Times, Wall Street Journal and Business Week International Bestseller Yes! 50 Scientifically Proven Ways to be Persuasive. US Amazon http://tinyurl.com/afbam9g UK Amazon http://tinyurl.com/adxrp6c IAW USA: http://www.influenceatwork.com IAW UK: http://www.influenceatwork.co.uk/


Nobel Prize winning neuropsychiatrist Eric Kandel describes new research which hints at the possibility of a biological basis to the unconscious mind. Directed / Produced by Elizabeth Rodd and Jonathan Fowler

Eric Richard Kandel (born November 7, 1929) is an American neuropsychiatrist. He was a recipient of the 2000 Nobel Prize in Physiology or Medicine for his research on the physiological basis of memory storage in neurons. He shared the prize with Arvid Carlsson and Paul Greengard.

Kandel, who had studied psychoanalysis, wanted to understand how memory works. His mentor, Harry Grundfest, said, “If you want to understand the brain you’re going to have to take a reductionist approach, one cell at a time.” So Kandel studied the neural system of the sea slug Aplysia californica, which has large nerve cells amenable to experimental manipulation and is a member of the simplest group of animals known to be capable of learning.[1]

Starting in 1966 James Schwartz collaborated with Kandel on a biochemical analysis of changes in neurons associated with learning and memory storage. By this time it was known that long-term memory, unlike short-term memory, involved the synthesis of new proteins. By 1972 they had evidence that the second messenger molecule cyclic AMP (cAMP) was produced in Aplysia ganglia under conditions that cause short-term memory formation (sensitization). In 1974 Kandel moved his lab moved to Columbia University and became founding director of the Center for Neurobiology and Behavior. It was soon found that the neurotransmitter serotonin, acting to produce the second messenger cAMP, is involved in the molecular basis of sensitization of the gill-withdrawal reflex. By 1980, collaboration with Paul Greengard resulted in demonstration that cAMP-dependent protein kinase, also known as protein kinase A (PKA), acted in this biochemical pathway in response to elevated levels of cAMP. Steven Siegelbaum identified a potassium channel that could be regulated by PKA, coupling serotonin’s effects to altered synaptic electrophysiology. In 1983 Kandel helped form the Howard Hughes Medical Research Institute at Columbia devoted to molecular neural science. The Kandel lab then sought to identify proteins that had to be synthesized to convert short-term memories into long-lasting memories. One of the nuclear targets for PKA is the transcriptional control protein CREB (cAMP response element binding protein). In collaboration with David Glanzman and Craig Bailey, Kandel identified CREB as being a protein involved in long-term memory storage. One result of CREB activation is an increase in the number of synaptic connections. Thus, short-term memory had been linked to functional changes in existing synapses, while long-term memory was associated with a change in the number of synaptic connections. Some of the synaptic changes observed by Kandel’s laboratory provide examples of Hebbian learning. One article describes the role of Hebbian learning in the Aplysia siphon-withdrawal reflex.[4] The Kandel lab has also performed important experiments using transgenic mice as a system for investigating the molecular basis of memory storage in the vertebrate hippocampus.[5][6][7] Kandel’s original idea that learning mechanisms would be conserved between all animals has been confirmed. Neurotransmitters, second messenger systems, protein kinasesion channels, and transcription factors like CREB have been confirmed to function in both vertebrate and invertebrate learning and memory storage.[8][9]

Kandel is a professor of biochemistry and biophysics at the College of Physicians and Surgeons at Columbia University. He is a Senior Investigator in the Howard Hughes Medical Institute. He was also the founding director of the Center for Neurobiology and Behavior, which is now the Department of Neuroscience at Columbia University. Kandel’s popularized account chronicling his life and research, In Search of Memory: The Emergence of a New Science of Mind,[2] was awarded the 2006 Los Angeles Times Book Awardfor Science and Technology.


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