Oxytocin

Gene switches make prairie voles fall in love Epigenetic changes affect neurotransmitters that lead to pair-bond formation. Zoe Cormier 02 June 2013 Adv Exp Med Biol. 1998;449:215-24. Oxytocin, vasopressin, and the neuroendocrine basis of pair bond formation. Insel TR1, Winslow JT, Wang Z, Young LJ. Author information Abstract Several lines of evidence support a role […]

Gene switches make prairie voles fall in love

Epigenetic changes affect neurotransmitters that lead to pair-bond formation.

02 June 2013


Adv Exp Med Biol. 1998;449:215-24.

Oxytocin, vasopressin, and the neuroendocrine basis of pair bond formation.

Abstract

Several lines of evidence support a role for oxytocin and vasopressin in complex social behaviors, including parental care, sex behavior, and aggression. Recent studies in a monogamous mammal, the prairie vole, suggest an additional role for both peptides in the formation of pair bonds. Central administration of oxytocin facilitates and administration of an oxytocin antagonist inhibits partner preference formation in female prairie voles. Conversely, vasopressin facilitates and a V1a receptor antagonist inhibits pair bonding in males. A potential cellular basis for these effects is the species-specific pattern of expression of oxytocin and V1a receptor in reward pathways of the prairie vole brain. At a molecular level, comparative sequencing of the oxytocin and V1a receptors reveals species differences in the promoter sequences that may guide regional expression in the brain. Transgenic mice created with the 5′ flanking region of the prairie vole oxytocin receptor gene demonstrate that sequencing in this region influence the pattern of expression within the brain. The unique promoter sequences of the prairie vole OTR and V1a receptor genes and the resulting species-specific pattern of regional expression provide a potential molecular mechanism for the evolution of pair bonding behaviors and a cellular basis for monogamy.


Oxytocin (Oxt) is a hormone, neuropeptide, and medication.[3][4] As a medication, it is used to cause contraction of the uterus in order to start labor or increase the speed of labor, and to stop bleeding following delivery.[3] For this purpose, it is given either byinjection into a muscle or into a vein.[3]

The use of oxytocin as a medication can result in excessive contraction of the uterus that can cause distress in an unborn baby. Common side effects in the mother include nausea and a slow heart rate. Serious side effects include water intoxication with an excessive dose and uterus rupture. Allergic reactions may also occur.[3]

Oxytocin is normally produced in the hypothalamus.[5][6] It plays a role in social bonding, sexual reproduction in both sexes, and during and after childbirth.[7] Oxytocin is released into the bloodstream as a hormone in response to stretching of the cervix anduterus during labor and with stimulation of the nipples from breastfeeding.[6] This helps with birth, bonding with the baby, and milk production.[6][8]

Oxytocin was discovered in 1952.[9] It is on the World Health Organization’s List of Essential Medicines, the most important medications needed in a basic health system.[10] As of 2014, the wholesale cost of the medication is US$0.1–0.56 per dose.[11]

Oxytocin has peripheral (hormonal) actions, and also has actions in the brain. Its actions are mediated by specific, oxytocin receptors. The oxytocin receptor is a G-protein-coupled receptor that requires magnesium and cholesterol. It belongs to therhodopsin-type (class I) group of G-protein-coupled receptors.

Studies have looked at oxytocin’s role in various behaviors, including orgasm, social recognition, pair bonding, anxiety, and maternal behaviors.[12]

The peripheral actions of oxytocin mainly reflect secretion from the pituitary gland. The behavioral effects of oxytocin are thought to reflect release from centrally projecting oxytocin neurons, different from those that project to the pituitary gland, or that are collaterals from them.[13] Oxytocin receptors are expressed by neurons in many parts of the brain and spinal cord, including the amygdala,ventromedial hypothalamus, septum, nucleus accumbens, and brainstem.

  • Letdown reflex: In lactating (breastfeeding) mothers, oxytocin acts at the mammary glands, causing milk to be ‘let down’ intosubareolar sinuses, from where it can be excreted via the nipple.[14] Suckling by the infant at the nipple is relayed by spinal nerves to the hypothalamus. The stimulation causes neurons that make oxytocin to fire action potentials in intermittent bursts; these bursts result in the secretion of pulses of oxytocin from the neurosecretory nerve terminals of the pituitary gland.
  • Uterine contraction: Important for cervical dilation before birth, oxytocin causes contractions during the second and third stages oflabor. Oxytocin release during breastfeeding causes mild but often painful contractions during the first few weeks of lactation. This also serves to assist the uterus in clotting the placental attachment point postpartum. However, in knockout mice lacking the oxytocin receptor, reproductive behavior and parturition are normal.[15]
  • Social behavior[16][17] and wound healing: Oxytocin is also thought to modulate inflammation by decreasing certain cytokines. Thus, the increased release in oxytocin following positive social interactions has the potential to improve wound healing. A study by Marazziti and colleagues used heterosexual couples to investigate this possibility. They found increases in plasma oxytocin following a social interaction were correlated with faster wound healing. They hypothesized this was due to oxytocin reducing inflammation, thus allowing the wound to heal more quickly. This study provides preliminary evidence that positive social interactions may directly influence aspects of health.[18] According to a study published in 2014, silencing of oxytocin receptor interneurons in the medial prefrontal cortex (mPFC) of female mice resulted in loss of social interest in male mice during the sexually receptive phase of the estrous cycle.[19]
Oxytocin evokes feelings of contentment, reductions in anxiety, and feelings of calmness and security when in the company of the mate.[20] This suggests oxytocin may be important for the inhibition of the brain regions associated with behavioral control, fear, and anxiety, thus allowing orgasm to occur. Research has also demonstrated that oxytocin can decrease anxiety and protect against stress, particularly in combination with social support.[21]
  • Due to its similarity to vasopressin, it can reduce the excretion of urine slightly. In several species, oxytocin can stimulate sodium excretion from the kidneys (natriuresis), and, in humans, high doses can result in hyponatremia.
  • Oxytocin and oxytocin receptors are also found in the heart in some rodents, and the hormone may play a role in the embryonal development of the heart by promotingcardiomyocyte differentiation.[22][23] However, the absence of either oxytocin or its receptor in knockout mice has not been reported to produce cardiac insufficiencies.[15]
  • Modulation of hypothalamic-pituitary-adrenal axis activity: Oxytocin, under certain circumstances, indirectly inhibits release of adrenocorticotropic hormone and cortisol and, in those situations, may be considered an antagonist of vasopressin.[24]
  • Autism: Oxytocin may play a role in autism and may be an effective treatment for autism‘s repetitive and affiliative behaviors.[25] Oxytocin treatments also resulted in an increased retention of affective speech in adults with autism.[26] Two related studies in adults, in 2003 and 2007, found oxytocin decreased repetitive behaviors and improved interpretation of emotions. More recently, intranasal administration of oxytocin was found to increase emotion recognition in children as young as 12 who are diagnosed with autism spectrum disorders.[27] Oxytocin has also been implicated in the etiology of autism, with one report suggesting autism is correlated with genomic deletion of the gene containing the oxytocin receptor gene (OXTR). Studies involving Caucasian and Finnish samples and Chinese Han families provide support for the relationship of OXTR with autism.[26][28] Autism may also be associated with an aberrant methylation of OXTR.[26] After treatment with inhaled oxytocin, autistic patients exhibit more appropriate social behavior.[29] While this research suggests some promise, further clinical trials of oxytocin are required to demonstrate potential benefit and side effects in the treatment of autism. As such, researchers do not recommend use of oxytocin as a treatment for autism outside of clinical trials.[30]
  • Nasally administered oxytocin has also been reported to reduce fear, possibly by inhibiting the amygdala (which is thought to be responsible for fear responses).[31] Indeed, studies in rodents have shown oxytocin can efficiently inhibit fear responses by activating an inhibitory circuit within the amygdala.[32][33] Some researchers have argued oxytocin has a general enhancing effect on all social emotions, since intranasal administration of oxytocin also increases envy and Schadenfreude.[34]
  • Trust is increased by oxytocin.[35][36][37] Disclosure of emotional events is a sign of trust in humans. When recounting a negative event, humans who receive intranasaloxytocin share more emotional details and stories with more emotional significance.[36] Humans also find faces more trustworthy after receiving intranasal oxytocin. In a study, participants who received intranasal oxytocin viewed photographs of human faces with neutral expressions and found them to be more trustworthy than those who did not receive oxytocin.[35] This may be because oxytocin reduces the fear of social betrayal in humans.[38] Even after experiencing social alienation by being excluded from a conversation, humans who received oxytocin scored higher in trust on the Revised NEO Personality Inventory.[37] Moreover, in a risky investment game, experimental subjects given nasally administered oxytocin displayed “the highest level of trust” twice as often as the control group. Subjects who were told they were interacting with a computer showed no such reaction, leading to the conclusion that oxytocin was not merely affecting risk aversion.[39] When there is a reason to be distrustful, such as experiencing betrayal, differing reactions are associated with oxytocin receptor gene (OXTR) differences. Those with the CT haplotype experience a stronger reaction, in the form of anger, to betrayal.[40]
  • Oxytocin affects social distance between adult males and females, and may be responsible at least in part for romantic attraction and subsequent monogamous pair bonding. An oxytocin nasal spray caused men in a monogamous relationship, but not single men, to increase the distance between themselves and an attractive woman during a first encounter by 10 to 15 centimeters. The researchers suggested that oxytocin may help promote fidelity within monogamous relationships.[41] For this reason, it is sometimes referred to as the “bonding hormone”. There is some evidence that oxytocin promotes ethnocentric behavior, incorporating the trust and empathy of in-groups with their suspicion and rejection of outsiders.[16] Furthermore, genetic differences in the oxytocin receptor gene (OXTR) have been associated with maladaptive social traits such as aggressive behaviour.[42]
  • Affecting generosity by increasing empathy during perspective taking: In a neuroeconomics experiment, intranasal oxytocin increased generosity in the Ultimatum Game by 80%, but had no effect in the Dictator Game that measures altruism. Perspective-taking is not required in the Dictator Game, but the researchers in this experiment explicitly induced perspective-taking in the Ultimatum Game by not identifying to participants into which role they would be placed.[43] Serious methodological questions have arisen, however, with regard to the role of oxytocin in trust and generosity.[44]
Empathy in healthy males has been shown to be increased after intranasal oxytocin[45][46] This is most likely due to the effect of oxytocin in enhancing eye gaze.[47] There is some discussion about which aspect of empathy oxytocin might alter – for example, cognitive vs. emotional empathy.[48]
  • Certain learning and memory functions are impaired by centrally administered oxytocin.[49] Also, systemic oxytocin administration can impair memory retrieval in certain aversive memory tasks.[50] Interestingly, oxytocin does seem to facilitate learning and memory specifically for social information. Healthy males administered intranasal oxytocin show improved memory for human faces, in particular happy faces.[51][52] They also show improved recognition for positive social cues over threatening social cues[53][54] and improved recognition of fear.[55]
  • Sexual activity: The relationship between oxytocin and human sexual response is unclear. At least two uncontrolled studies have found increases in plasma oxytocin at orgasm – in both men and women.[56][57] Plasma oxytocin levels are notably increased around the time of self-stimulated orgasm and are still higher than baseline when measured five minutes after self arousal.[56] The authors of one of these studies speculated that oxytocin’s effects on muscle contractibility may facilitate sperm and egg transport.[56]
In a study measuring oxytocin serum levels in women before and after sexual stimulation, the author suggests it serves an important role in sexual arousal. This study found genital tract stimulation resulted in increased oxytocin immediately after orgasm.[58] Another study reported increases of oxytocin during sexual arousal could be in response to nipple/areola, genital, and/or genital tract stimulation as confirmed in other mammals.[59] Murphy et al. (1987), studying men, found oxytocin levels were raised throughout sexual arousal with no acute increase at orgasm.[60] A more recent study of men found an increase in plasma oxytocin immediately after orgasm, but only in a portion of their sample that did not reach statistical significance. The authors noted these changes “may simply reflect contractile properties on reproductive tissue”.[61]
  • Bonding: In the prairie vole, oxytocin released into the brain of the female during sexual activity is important for forming a monogamous pair bond with her sexual partner. Vasopressin appears to have a similar effect in males.[62] Oxytocin has a role in social behaviors in many species, so it likely also does in humans. In a 2003 study, both humans and dog oxytocin levels in the blood rose after five to 24 minutes of a petting session. This possibly plays a role in the emotional bonding between humans and dogs.[63]
  • Maternal behavior: Female rats given oxytocin antagonists after giving birth do not exhibit typical maternal behavior.[64] By contrast, virgin female sheep show maternal behavior toward foreign lambs upon cerebrospinal fluid infusion of oxytocin, which they would not do otherwise.[65] Oxytocin is involved in the initiation of maternal behavior, not its maintenance; for example, it is higher in mothers after they interact with unfamiliar children rather than their own.[66]
  • Drug interactions: According to some studies in animals, oxytocin inhibits the development of tolerance to various addictive drugs (opiates, cocaine, alcohol), and reduceswithdrawal symptoms.[67] MDMA (ecstasy) may increase feelings of love, empathy, and connection to others by stimulating oxytocin activity primarily via activation of serotonin5-HT1A receptors, if initial studies in animals apply to humans.[68] The anxiolytic Buspar (buspirone) may produce some of its effects via 5-HT1A receptor-induced oxytocin stimulation as well.[69][70]
  • Preparing fetal neurons for delivery: Crossing the placenta, maternal oxytocin reaches the fetal brain and induces a switch in the action of neurotransmitter GABA from excitatory to inhibitory on fetal cortical neurons. This silences the fetal brain for the period of delivery and reduces its vulnerability to hypoxic damage.[71]
  • Romantic attachment: In some studies, high levels of plasma oxytocin have been correlated with romantic attachment. For example, if a couple is separated for a long period of time, anxiety can increase due to the lack of physical affection. Oxytocin may aid romantically attached couples by decreasing their feelings of anxiety when they are separated.[20]
  • Feeding: Recent evidence has suggested that oxytocin neurons in the para-ventricular hypothalamus in the brain may play a key role in suppressing appetite under normal conditions and that other hypothalamic neurons may trigger eating via inhibition of these oxytocin neurons. This population of oxytocin neurons are absent in Prader-Willi syndrome, a genetic disorder that leads to uncontrollable feeding and obesity, and may play a key role in its pathophysiology.[72]
  • Group-serving dishonesty/deception: In a carefully controlled study exploring the biological roots of immoral behavior, oxytocin was shown to promote dishonesty when the outcome favored the group to which an individual belonged instead of just the individual.[73]
  • Intergroup bonding: Oxytocin can increase positive attitudes, such as bonding, toward individuals with similar characteristics, who then become classified as “in-group” members, whereas individuals who are dissimilar become classified as “out-group” members. Race can be used as an example of in-group and out-group tendencies because society often categorizes individuals into groups based on race (Caucasian, African American, Latino, etc.). One study that examined race and empathy found that participants receiving nasally administered oxytocin had stronger reactions to pictures of in-group members making pained faces than to pictures of out-group members with the same expression.[74] This shows that oxytocin may be implicated in our ability to empathize with individuals of different races and could potentially translate into willingness to help individuals in pain or stressful situations. Moreover, individuals of one race may be more inclined to help individuals of the same race than individuals of another race when they are experiencing pain. Oxytocin has also been implicated in lying when lying would prove beneficial to other in-group members. In a study where such a relationship was examined, it was found that when individuals were administered oxytocin, rates of dishonesty in the participants’ responses increased for their in-group members when a beneficial outcome for their group was expected.[75] Both of these examples show the tendency to act in ways that benefit people with which one feels is part of their social group, or in-group. Oxytocin is not only correlated with the preferences of individuals to associate with members of their own group, but it is also evident during conflicts between members of different groups. During conflict, individuals receiving nasally administered oxytocin demonstrate more frequent defense-motivated responses toward in-group members than out-group members. Further, oxytocin was correlated with participant desire to protect vulnerable in-group members, despite that individual’s attachment to the conflict.[76] Similarly, it has been demonstrated that when oxytocin is administered, individuals alter their subjective preferences in order to align with in-group ideals over out-group ideals.[77] These studies demonstrate that oxytocin is associated with intergroup dynamics. Further, oxytocin influences the responses of individuals in a particular group to those of another group. The in-group bias is evident in smaller groups; however, it can also be extended to groups as large as one’s entire country leading toward a tendency of strong national zeal. A study done in the Netherlands showed that oxytocin increased the in-group favoritism of their nation while decreasing acceptance of members of other ethnicities and foreigners.[16] People also show more affection for their country’s flag while remaining indifferent to other cultural objects when exposed to oxytocin.[78] It has thus been hypothesized that this hormone may be a factor in xenophobic tendencies secondary to this effect. Thus, oxytocin appears to affect individuals at an international level where the in-group becomes a specific “home” country and the out-group grows to include all other countries.

Hebbian learning

Hebbian theory is a theory in neuroscience which proposes an explanation for the adaptation of neurons in the brain during the learning process. It describes a basic mechanism for synaptic plasticity, where an increase in synaptic efficacy arises from the presynaptic cell’s repeated and persistent stimulation of the postsynaptic cell. Introduced by Donald Hebb in his 1949 book The Organization of Behavior,[1] the theory is also called Hebb’s rule, Hebb’s postulate, […]

Hebbian theory is a theory in neuroscience which proposes an explanation for the adaptation of neurons in the brain during the learning process. It describes a basic mechanism for synaptic plasticity, where an increase in synaptic efficacy arises from the presynaptic cell’s repeated and persistent stimulation of the postsynaptic cell. Introduced by Donald Hebb in his 1949 book The Organization of Behavior,[1] the theory is also called Hebb’s ruleHebb’s postulate, and cell assembly theory. Hebb states it as follows:

“Let us assume that the persistence or repetition of a reverberatory activity (or “trace”) tends to induce lasting cellular changes that add to its stability.… When anaxon of cell A is near enough to excite a cell B and repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells such that A’s efficiency, as one of the cells firing B, is increased.”[1]

The theory is often summarized as “Cells that fire together, wire together”.[2] However, this summary should not be taken literally. Hebb emphasized that cell A needs to ‘take part in firing’ cell B, and such causality can only occur if cell A fires just before, not at the same time as, cell B. This important aspect of causation in Hebb’s work foreshadowed what we now know about spike-timing-dependent plasticity, which requires temporal precedence.[3] The theory attempts to explain associative or Hebbian learning, in which simultaneous activation of cells leads to pronounced increases in synaptic strength between those cells, and provides a biological basis for errorless learning methods for education and memory rehabilitation.

Hebbian theory concerns how neurons might connect themselves to become engrams. Hebb’s theories on the form and function of cell assemblies can be understood from the following:

“The general idea is an old one, that any two cells or systems of cells that are repeatedly active at the same time will tend to become ‘associated’, so that activity in one facilitates activity in the other.” (Hebb 1949, p. 70)
“When one cell repeatedly assists in firing another, the axon of the first cell develops synaptic knobs (or enlarges them if they already exist) in contact with the soma of the second cell.” (Hebb 1949, p. 63)

Gordon Allport posits additional ideas regarding cell assembly theory and its role in forming engrams, along the lines of the concept of auto-association, described as follows:

“If the inputs to a system cause the same pattern of activity to occur repeatedly, the set of active elements constituting that pattern will become increasingly strongly interassociated. That is, each element will tend to turn on every other element and (with negative weights) to turn off the elements that do not form part of the pattern. To put it another way, the pattern as a whole will become ‘auto-associated’. We may call a learned (auto-associated) pattern an engram.” (Allport 1985, p. 44)

Hebbian theory has been the primary basis for the conventional view that when analyzed from a holistic level, engrams are neuronal nets or neural networks.

Work in the laboratory of Eric Kandel has provided evidence for the involvement of Hebbian learning mechanisms at synapses in the marine gastropod Aplysia californica.

Experiments on Hebbian synapse modification mechanisms at the central nervous system synapses of vertebrates are much more difficult to control than are experiments with the relatively simple peripheral nervous system synapses studied in marine invertebrates. Much of the work on long-lasting synaptic changes between vertebrate neurons (such aslong-term potentiation) involves the use of non-physiological experimental stimulation of brain cells. However, some of the physiologically relevant synapse modification mechanisms that have been studied in vertebrate brains do seem to be examples of Hebbian processes. One such study reviews results from experiments that indicate that long-lasting changes in synaptic strengths can be induced by physiologically relevant synaptic activity working through both Hebbian and non-Hebbian mechanisms.

Principles

From the point of view of artificial neurons and artificial neural networks, Hebb’s principle can be described as a method of determining how to alter the weights between model neurons. The weight between two neurons increases if the two neurons activate simultaneously—and reduces if they activate separately. Nodes that tend to be either both positive or both negative at the same time have strong positive weights, while those that tend to be opposite have strong negative weights.

The following is a formulaic description of Hebbian learning: (note that many other descriptions are possible)

\,w_{ij}=x_ix_j

where w_{ij}  is the weight of the connection from neuron  j  to neuron  i  and  x_i  the input for neuron  i . Note that this is pattern learning (weights updated after every training example). In a Hopfield network, connections w_{ij}  are set to zero if i=j  (no reflexive connections allowed). With binary neurons (activations either 0 or 1), connections would be set to 1 if the connected neurons have the same activation for a pattern.

Another formulaic description is:

w_{ij} = \frac{1}{p} \sum_{k=1}^p x_i^k x_j^k\, ,

where w_{ij}  is the weight of the connection from neuron  j  to neuron  i  p  is the number of training patterns, and x_{i}^k the  k th input for neuron  i . This is learning by epoch (weights updated after all the training examples are presented). Again, in a Hopfield network, connections w_{ij}  are set to zero if i=j  (no reflexive connections).

A variation of Hebbian learning that takes into account phenomena such as blocking and many other neural learning phenomena is the mathematical model of Harry KlopfKlopf’s model reproduces a great many biological phenomena, and is also simple to implement.

Generalization and stability

Hebb’s Rule is often generalized as

\,\Delta w_i = \eta x_i y,

or the change in the ith synaptic weight w_i is equal to a learning rate \eta times the ith input x_i times the postsynaptic response y. Often cited is the case of a linear neuron,

\,y = \sum_j w_j x_j,

and the previous section’s simplification takes both the learning rate and the input weights to be 1. This version of the rule is clearly unstable, as in any network with a dominant signal the synaptic weights will increase or decrease exponentially. However, it can be shown that for any neuron model, Hebb’s rule is unstable.[citation needed] Therefore, network models of neurons usually employ other learning theories such as BCM theoryOja’s rule,[4] or the Generalized Hebbian Algorithm.

Exceptions

Despite the common use of Hebbian models for LTP, there exists several exceptions to Hebb’s principles and examples that demonstrate some aspects of the theory are oversimplified. One of the most well-documented of these exceptions pertains to how synaptic modification may not simply occur only between activated neurons A and B, but to neighboring neurons as well.[5] This is due to how Hebbian modification depends on retrograde signaling in order to modify the presynaptic neuron.[6] The compound most commonly identified as fulfilling this retrograde transmitter role is nitric oxide, which, due to its high solubility and diffusibility, often exerts effects on nearby neurons.[7] This type of diffuse synaptic modification, known as volume learning, counters, or at least supplements, the traditional Hebbian model.[8]

Hebbian learning account of mirror neurons

Hebbian learning and what we know about spike timing dependent plasticity has also been used in an influential theory of how mirror neurons emerge.[9][10] Mirror neurons are neurons in that fire both when an individual performs an action and when the individual sees[11] or hears [12] another perform a similar action. The discovery of these neurons has been very influential in explaining how individuals make sense of the actions of others, by showing that when we perceive the actions of others, we activate the motor programs we would use to perform similar actions. The activation of these motor programs then adds information to the perception and help predict what the person will do next based on the perceiver’s own motor program. A challenge has been to explain how individuals come to have neurons that respond both while performing an action and while hearing or seeing another perform similar actions. Christian Keysers and David Perrett suggested that while an individual performs a particular action, the individual will see, hear and feel himself perform the action. These re-afferent sensory signals will trigger activity in neurons responding to the sight, sound and feel of the action. Because the activity of these sensory neurons will consistently overlap in time with those of the motor neurons that caused the action, Hebbian learning would predict that the synapses connecting neurons responding to the sight, sound and feel of an action and those of the neurons triggering the action should be potentiated. The same is true while people look at themselves in the mirror, hear themselves babble or are imitated by others. After repeated experience of this re-afference, the synapses connecting the sensory and motor representations of an action would be so strong, that the motor neurons would start firing to the sound or the vision of the action, and a mirror neuron would have been created. Evidence for that perspective comes from many experiments that show that motor programs can be triggered by novel auditory or visual stimuli after repeated pairing of the stimulus with the execution of the motor program (see [13] for a review of the evidence). For instance, people that have never played the piano do not activate brain regions involved in playing the piano when listening to piano music. Five hours of piano lesson, in which the participant is exposed to the sound of the piano each time he presses a key, suffices to later trigger activity in motor regions of the brain upon listening to piano music.[14] Consistent with the fact that spike timing dependent plasticity occurs only if the presynaptic neuron’s firing predicts the post-synaptic neuron’s firing,[15] the link between sensory stimuli and motor programs also only seem to be potentiated if the stimulus is contingent on the motor program.

Zen meditation

 Altern Complement Med. 2009 May;15(5):585-92. doi: 10.1089/acm.2008.0416. Zen meditation: an integration of current evidence. Chiesa A. Author information Abstract OBJECTIVE: Despite the growing interest in the neurobiological and clinical correlates of many meditative practices, in particular mindfulness meditations, no review has specifically focused on current evidence on electroencephalographic, neuroimaging, biological, and clinical evidence about an important […]

 Altern Complement Med. 2009 May;15(5):585-92. doi: 10.1089/acm.2008.0416.

Zen meditation: an integration of current evidence.

Abstract

OBJECTIVE:

Despite the growing interest in the neurobiological and clinical correlates of many meditative practices, in particular mindfulness meditations, no review has specifically focused on current evidence on electroencephalographic, neuroimaging, biological, and clinical evidence about an important traditional practice, Zen meditation.

METHODS:

A literature search was conducted using MEDLINE, the ISI Web of Knowledge, the Cochrane collaboration database, and references of selected articles. Randomized controlled and cross-sectional studies with controls published in English prior to May 2008 were included.

RESULTS:

Electroencephalographic studies on Zen meditation found increased alpha and theta activity, generally related to relaxation, in many brain regions, including the frontal cortex. Theta activity in particular seemed to be related to the degree of experience, being greater in expert practitioners and advanced masters. Moreover, Zen meditation practice could protect from cognitive decline usually associated with age and enhance antioxidant activity. From a clinical point of view, Zen meditation was found to reduce stress and blood pressure, and be efficacious for a variety of conditions, as suggested by positive findings in therapists and musicians.

CONCLUSION:

To date, actual evidence about Zen meditation is scarce and highlights the necessity of further investigations. Comparison with further active treatments, explanation of possible mechanisms of action, and the limitations of current evidence are discussed.

PMID:

 19422285

[PubMed – indexed for MEDLINE]