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Next-generation mood enhancers

mood cognitive

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#1 Ruth

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Posted 04 June 2018 - 08:00 PM






https://www.scienced...899900718300947

Objectives

To investigate the antidepressant and antioxidant effects of omega-3, folic acid and n-acetylcysteine (NAC) in rats which were subjected to early or late life stress.


Methods

Early stress was induced through maternal deprivation (MD), while late life stress was induced using the chronic mild stress (CMS) protocol. Young rats which were subjected to MD and the adult rats which were subjected to CMS were treated with omega-3 fatty acids (0.72 g/kg), NAC (20 mg/kg) or folic acid (50 mg/kg) once/day, for a period of 20 days. Then, the animals' immobility times were evaluated using the forced swimming test. Oxidative stress parameters were evaluated in the brain.


Results

Depressive-like behavior induced by CMS was prevented by NAC and folic acid, and depressive-like behavior induced by MD was prevented by NAC, folic acid and omega-3. NAC, folic acid and omega-3 were able to exert antioxidant effects in the brain of rats subjected to CMS or MD. These preventive treatments decreased the levels of protein carbonylation and lipid peroxidation, and also decreased the concentrations of nitrite/nitrate and reduced the activity of myeloperoxidase activity in the rat brain which was induced by CMS or MD. NAC, folic acid and omega-3 increased superoxide dismutase and catalase activities in the rat brain subjected to early or late life stress.


Conclusions

NAC, omega-3 and folic acid may present interesting lines of treatment based on their antioxidant properties, which cause an inhibition of behavioral and brain changes that occur from stressful life events.


https://uthealth.inf...ippocampal-anti
Experimental and epidemiological studies have shown the close relationship between stressful events, depression, and cognitive impairment. Folic acid has been reported to present antidepressant-like effects in both experimental and clinical approaches. However, the mechanisms mediating such effects are not understood. In the present study, we evaluated if folic acid administration to mice could protect against restraint stress-induced depressive-like behavior and cognitive deficit. Considering that oxidative stress has been pointed as a key event involved with depressive disorders, cerebrocortical and hippocampal oxidative stress-related parameters, such as the activities of antioxidant enzymes (mainly those related to the hydroperoxide-detoxifying system) and markers of lipid peroxidation, were also investigated. Restraint stress induced depressive-like behavior in the forced swimming test and memory impairment in the object recognition test, without altering locomotor activity of mice. Folic acid (50. mg/kg, p.o.) was able to prevent the stress-induced increase on immobility time in the forced swimming test, but did not prevent memory impairment. Moreover, restraint stress increased thiobarbituric acid reactive substance levels, and catalase, glutathione peroxidase and glutathione reductase activities in the cerebral cortex and hippocampus, and superoxide dismutase activity in the hippocampus. Folic acid treatment restored the activity of the antioxidant enzymes and reduced lipid peroxidation in the hippocampus. Glutathione, a non-enzymatic antioxidant, was not altered by stress and/or folic acid administration. Together, the results of the present work reinforce the notion that folic acid displays a specific antidepressant profile in the restraint stress paradigm that may be at least partly due to its antioxidant role


Evidence for the involvement of the opioid system in the antidepressant-like effect of folic acid in the mouse forced swimming test

The opioid system has been implicated in major depression and in the mechanism of action of antidepressants.This study investigated theinvolvementoftheopioidsystemintheantidepressant-likeeffectofthe water-solubleB-vitaminfolicacidintheforcedswimmingtest(FST).Theeffectoffolicacid(10nmol/site, i.c.v.) was prevented by the pretreatment of mice with naloxone (1mg/kg, i.p., a nonselective opioid receptor antagonist), naltrindole (3mg/kg, i.p., a selective -opioid receptor antagonist), naloxonazine (10mg/kg,i.p.,aselective1-opioidreceptorantagonist,24hbefore),butnotwithnaloxonemethiodide (1mg/kg, s.c., a peripherally acting opioid receptor antagonist). In addition, a sub-effective dose of folic acid (1nmol/site, i.c.v.) produced a synergistic antidepressant-like effect in the FST with a sub-effective dose of morphine (1mg/kg, s.c.). A further approach was designed to investigate the possible relationship between the opioid system and NMDA receptors in the mechanism of action of folic acid in the FST. Pretreatment of the animals with naloxone (1mg/kg, i.p.) prevented the synergistic antidepressant-like effect of folic acid (1nmol/site, i.c.v.) and MK-801 (0.001mg/kg, i.p., a non-competitive NMDA receptor antagonist). Together the results rstly indicate that the anti-immobility effect of folic acid in the FST is mediated by an interaction with the opioid system (1 and ), likely dependent on the inhibition of NMDA receptors elicited by folic acid.

#2 Ruth

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Posted 04 June 2018 - 08:18 PM

Activation of CB1 Receptors May Provide an Effective Treatment for Obsessive Compulsive Disorder
Obsessive compulsive disorder (OCD) is an anxiety disorder characterized by mental obsessions and compulsions stemming from chemical imbalances in the brain. Drugs that facilitate serotonin transmission are commonly used to treat OCD, but they can become ineffective with prolonged use. It has been suggested that CB1 (cannabinoid type 1) receptors are an alternative drug target that could provide effective treatment. The aims of this study were to investigate more successful longer-term drug treatment options for anxiety-based symptoms of OCD and to better understand serotonin’s interaction with CB1. This study used an 11-day marble burying behavioral model with three groups of mice treated respectively with saline, WIN 55,212-2 (CB1 agonist), or Tianeptine (5-HT antagonist; Tianeptine and WIN 55,212-2 days 6-10). Mice receiving the CB1 agonist buried fewer marbles than did the control with no deterioration of effect over ten days. Mice receiving both Tianeptine and WIN 55,212-2 also buried fewer marbles. These results indicate that WIN 55,212-2 has anxiolytic properties that could be an effective treatment for the compulsive symptoms of OCD. It also suggests that CB1 receptors are situated downstream of serotonin receptors.

https://www.ncbi.nlm...pubmed/23036485
Animal models of chronic stress represent valuable tools by which to investigate the behavioral, endocrine and neurobiological changes underlying stress-related psychopathologies, such as major depression, and the efficacy of antidepressant therapies. The present study was aimed at investigating the neurochemical effects of the antidepressant tianeptine in rats exposed to the chronic stress model. To this aim, rats were subjected to 40days of chronic unpredictable stressful stimuli, after which the animals received saline or tianeptine (15mg/kg) once a day for 7days. Additionally, IL-6, IL-1, TNF-α levels and oxidative stress parameters were assessed in the prefrontal cortex (PFC), hippocampus (HPC), amygdala (AMY) and nucleus accumbens (NAc) in all of the experimental groups studied. The results indicated that chronic mild stress and tianeptine did not exercise any effects on cytokines in all of the structures studied; in the PFC and AMY thiobarbituric acid reactive substances (TBARS) levels were decreased in control rats treated with tianeptine in the HPC; superoxide dismutase (SOD) activity was found to have decreased in stressed rats treated with saline in the PFC, HPC, AMY and NAc, and tianeptine reversed this effect; catalase (CAT) activity was found to have decreased in the PFC, HPC and NAc of stressed rats treated with saline, but was shown to have increased in stressed rats treated with tianeptine, and tianeptine also reversed the decreases in CAT activity in stressed rats treated with saline, suggesting that tianeptine exerted antioxidant activity. In conclusion, the present findings open new vistas on the pharmacological activity of tianeptine, in particular, concerning its ability to attenuate oxidative stress.

https://www.longecit...adhddepression/
https://www.ncbi.nlm...les/PMC4662168/ The dopaminergic system is correlated with increased gray matter volume in the dorsolateral prefrontal cortex and striatal regions, which are associated with creativity.1) The antidepressant bupropion inhibits dopamine and norepinephrine reuptake. Buproprion led to significant improvement in our patient’s depression symptoms and significant increases in gray matter, white matter, and total brain volumes. The dopamine and norepinephrine agonist methamphetamine can also increase gray matter volume in the right putamen, which is associated with better inhibitory control.2) Apart from these dopamine-related mechanisms, bupropion probably also changes gray matter volume by preventing oxidative stress related to major depressive disorder,3) or by modulating glutamate receptor function.4) Gray matter volume might increase for several reasons: synaptic remodeling and neurogenesis;5) stimulation of neurotrophic factors by antipsychotics;6) prevention of oxidative stress or 6-OH-dopamine lesioning with subsequent increased glial cell proliferation in the frontal cortex;7) or modulation of glutamate receptor function.8)

One concern with these results is the variability of the SIENA method. A longitudinal survey comparing different segmentation methods found that SIENA gives large, heterogeneous values for brain volume changes, implying the variability of this method.9) Another study mentioned that SIENA could use the outer skull surface for both time points to reduce the effects of scanner drift and inter-scanner variability on longitudinal morphometric results.10) Therefore, our method still had some value for assessing longitudinal changes with bupropion treatment. This evidence of increased gray matter and total brain volumes with bupropion treatment has clinical implications for the possible effects of norepinephrine and dopamine reuptake inhibition on brain structure in the treatment of depression.

In conclusion, the treatment of depression with bupropion appears to be accompanied by changes in the gray matter, white matter, and total brain volumes.
https://www.reddit.c...ach_antagonism/
https://www.ncbi.nlm...pubmed/1319912/


The effects of L-alpha-glycerylphosphorylcholine (alpha-GPC) on scopolamine-induced memory impairment and on brain acetylcholine (ACh) synthesis and release were investigated in rats. Oral administration of alpha-GPC 3 h before the behavioural test prevented the learning impairment induced by scopolamine given 30 min before the acquisition of a passive avoidance response. Similarly, retrograde amnesia induced by scopolamine, given immediately after acquisition training, was also completely reversed by the drug. These effects were dose-dependent with a maximum at 300 mg/kg. The mechanism of action of this compound was investigated by measuring hippocampal ACh synthesis and release both in vivo by means of the microdialysis technique and in vitro in tissue slices. alpha-GPC dose dependently increased ACh release with a maximum at 300 mg/kg. In addition, i.v. injection of [14C]alpha-GPC resulted in [14C]ACh formation. The data suggest that the behavioural effects of alpha-GPC may be related to its property to increase hippocampal ACh synthesis and release.


PMID: 1319912
https://www.ncbi.nlm...les/PMC3669033/


Background

Eurycoma longifolia is a medicinal plant commonly called tongkat ali (TA) and “Malaysian ginseng.” TA roots are a traditional “anti-aging” remedy and modern supplements are intended to improve libido, energy, sports performance and weight loss. Previous studies have shown properly-standardized TA to stimulate release of free testosterone, improve sex drive, reduce fatigue, and improve well-being.


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Methods

We assessed stress hormones and mood state in 63 subjects (32 men and 31 women) screened for moderate stress and supplemented with a standardized hot-water extract of TA root (TA) or Placebo (PL) for 4 weeks. Analysis of variance (ANOVA) with significance set at p < 0.05 was used to determine differences between groups.


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Results

Significant improvements were found in the TA group for Tension (−11%), Anger (−12%), and Confusion (−15%). Stress hormone profile (salivary cortisol and testosterone) was significantly improved by TA supplementation, with reduced cortisol exposure (−16%) and increased testosterone status (+37%).


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Conclusion

These results indicate that daily supplementation with tongkat ali root extract improves stress hormone profile and certain mood state parameters, suggesting that this “ancient” remedy may be an effective approach to shielding the body from the detrimental effects of “modern” chronic stress, which may include general day-to-day stress, as well as the stress of dieting, sleep deprivation, and exercise training.
https://www.hindawi....i/2017/7949582/ Central nervous system (CNS) senses energy homeostasis by integrating both peripheral and autonomic signals and responding to them by neurotransmitters and neuropeptides release. Although it is previously considered an immunologically privileged organ, we now know that this is not so. Cells belonging to the immune system, such as B and T lymphocytes, can be recruited into the CNS to face damage or infection, in addition to possessing resident immunological cells, called microglia. In this way, positive energy balance during obesity promotes an inflammatory state in the CNS. Saturated fatty acids from the diet have been pointed out as powerful candidates to trigger immune response in peripheral system and in the CNS. However, how central immunity communicates to peripheral immune response remains to be clarified. Recently there has been a great interest in the neuropeptides, POMC derived peptides, ghrelin, and leptin, due to their capacity to suppress or induce inflammatory responses in the brain, respectively. These may be potential candidates to treat different pathologies associated with autoimmunity and inflammation. In this review, we will discuss the role of lipotoxicity associated with positive energy balance during obesity in proinflammatory response in microglia, B and T lymphocytes, and its modulation by neuropeptides
https://www.ncbi.nlm...pubmed/17762517 It has been shown that music might be able to improve mood state in people affected by psychiatric disorders, ameliorate cognitive deficits in people with dementia and increase motor coordination in Parkinson patients. Robust experimental evidence explaining the central effects of music, however, is missing. This study was designed to investigate the effect of music on brain neurotrophin production and behavior in the mouse. We exposed young adult mice to music with a slow rhythm (6 h/day; mild sound pressure levels, between 50 and 60 db) for 21 consecutive days. At the end of the treatment, mice were tested for passive avoidance learning and then killed for analysis of brain-derived neurotrophic factor (BDNF) and nerve growth factor with enzyme-linked immunosorbent assay (ELISA) in selected brain regions. We found that music-exposed mice showed increased BDNF, but not nerve growth factor in the hippocampus. Furthermore, we observed that music exposure significantly enhanced learning performance, as measured by the passive avoidance test. Our results demonstrate that exposure to music can modulate the activity of the hippocampus by influencing BDNF production. Our findings also suggest that music exposure might be of help in several central nervous system pathologies.
https://www.scienced...361923016300090 Previous research has shown that dorsal hippocampus plays an important role in spatial memory process. Music exposure can enhance brain-derived neurotrophic factor (BDNF) expression level in dorsal hippocampus (DH) and thus enhance spatial cognition ability. But whether music experience may affect different subregions of DH in the same degree remains unclear. Here, we studied the effects of exposure to Mozart K.448 on learning behavior in developing rats using the classical Morris water maze task. The results showed that early music exposure could enhance significantly learning performance of the rats in the water maze test. Meanwhile, the BDNF/TrkB level of dorsal hippocampus CA3 (dCA3) and dentate gyrus (dDG) was significantly enhanced in rats exposed to Mozart music as compared to those without music exposure. In contrast, the BDNF/TrkB level of dorsal hippocampus CA1 (dCA1) was not affected. The results suggest that the spatial memory improvement by music exposure in rats may be associated with the enhanced BDNF/TrkB level of dCA3 and dDG.
https://www.scienced...55041311630554X
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The global epidemic of obesity and its associated chronic diseases is largely attributed to an imbalance between caloric intake and energy expenditure. While physical exercise remains the best solution, the development of muscle-targeted “exercise mimetics” may soon provide a pharmaceutical alternative to battle an increasingly sedentary lifestyle. At the same time, these advances are fueling a raging debate on their escalating use as performance-enhancing drugs in high-profile competitions such as the Olympics.
https://www.fightagi...-mimetic-drugs/ The field of exercise mimetics is still young, but quite similar at the high level to the more established attempts to find drugs that mimic portions of the calorie restriction response. Exercise and calorie restriction are the two most obvious, well-studied, and reliable means of adjusting the operation of metabolism in order to improve health and extend healthy life span. Sadly, the long-term effects on life span in long-lived species such as our own are nowhere near as large as those exhibited by short-lived species such as laboratory mice. Nonetheless, given that exercise and calorie restriction produce benefits that are larger and more robust than anything that can be achieved for healthy people with presently available medical technology (a state of affairs that we hope will soon change), there is considerable interest in developing drugs that can achieve similar outcomes. In principle at least, these altered states of metabolism have points of control and regulation, a small number of proteins and genes that can be targeted by therapeutics.
https://www.the-scie...romotes-Memory/ Working out is good for the brain. Now, a team of scientists from the U.S. and Germany has a clearer idea why. A protein called cathepsin B, produced and secreted by muscle during exercise, is required for exercise-induced memory improvement and brain cell production in mice, the scientists reported in Cell Metabolism today (June 23). They also showed that levels of cathepsin B are positively correlated with fitness and memory in humans.

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#3 Ruth

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Posted 04 June 2018 - 08:23 PM

N-acetylcysteine as a mitochondrial enhancer: a new class of psychoactive drugs? N-acetilcisteína como potencializador mitocondrial: uma nova classe de drogas psicoativas?


The limited available agents effective on the treatment of depressive episodes in bipolar disorder warrants further research on the field. Of note, several drugs have been studied in the light of their mood stabilizing efficacy, including well known supplements commonly used as add-on therapy for a number of conditions. For the past years, attention has been given to N-acetylcysteine (NAC), a chemical with antioxidant properties primarily used as a mucolytic agent and in the treatment of paracetamol overdose. A study by Magalhães et al.1 published in this issue of RBP shows that add-on NAC therapy improved depressive symptoms and functional outcomes in bipolar disorder patients, which increases the interest in studying the mechanisms by which this drug may present neuroprotective effects. Among its known mechanisms of action, NAC-induced brain glutathione (GSH) replenishment is the most studied. Glutathione is the primary endogenous antioxidant of the cell, and has the ability to scavenge oxygen and nitrogen species, therefore maintaining the oxidative balance. In addition to restoring GSH levels, NAC modulates inflammation by exerting anti-inflammatory actions, and presents direct effects on glutamatergic and dopaminergic neurotransmission. The inflammatory-modulating effects of NAC may be important for its mood stabilizing efficacy, mainly due to the recently described relevance of systemic inflammation in bipolar disorder pathophysiology (Kapczinski et al.2). More specifically, its usefulness on depressive episodes may be linked to innovative mechanisms of action, which we speculate to be taking part throughout its treatment. Among them, modulation of cellular signaling pathways by NAC may ultimately increase mitochondrial resilience, as supported below. Chronic stress has been thought to play a key role in the pathophysiology of bipolar disorder, although the exact reasons for this association have not yet been fully clarified. The effects of stress are mediated mainly through glucocorticoids, which exert several body changes commonly known as ‘stress
response’. Dysregulation of glucocorticoids is associated with cognitive impairments and depressive disorder, supporting the notion that stress response may be impaired in affective and mood disorders. In this same vein, chronic stress has been shown to induce mitochondria dysfunction, whereas recent studies have described a biphasic effect of glucocorticoids on mitochondrial function, ultimately leading to the control of apoptosis on neuronal populations. Apoptosis may link chronic stress-induced neuronal death and inflammation, mainly through the release of damage-associated molecular patterns. All together, these features may be responsible for the systemic toxicity found in
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#4 Ruth

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Posted 04 June 2018 - 08:28 PM

2.3 NEUROTROPHIN AND NETWORK THEORIES OF ANTIDEPRESSANT ACTION
2.3.1 Antidepressant drugs The first antidepressant drugs (AD) were serendipitously discovered in the 1950’s. The monoamine oxidase (MAO) inhibitor iproniazid was tested for treatment of tuberculosis but was found to improve the mood of depressed patients receiving the medicine (Castrén, 2005). Iproniazid was soon followed by the first tricyclic antidepressant imipramine. Because both of these drugs affect the monoamine neurotransmitters it was suggested that depression may be caused by abnormal levels of monoamines that could be normalized with antidepressant treatment (Schildkraut, 1965). MAO inhibitors and tricyclic antidepressants were followed by more selective drugs targeting noradrenergic or serotonergic systems, for example the selective serotonin reuptake inhibitors (SSRI) that are widely used today.
In general, antidepressant drugs require weeks of treatment before their therapeutic effects appear. The primary pharmacological effects of the drugs on monoamines appear almost immediately suggesting that the therapeutic effects of ADs are not directly evolving from the increased monoamine levels in the synaptic cleft. Adaptation and plasticity of the neuronal networks resulting from chronic exposure to ADs could underlie the slow manifestation of the clinical therapeutic effect of ADs (Castrén, 2013). It is also interesting that monoamine depletion, which leads to a lack of serotonin or noradrenaline/dopamine in the brain, cannot produce depressive-like symptoms in healthy volunteers and does not lower mood in depressed patients (Ruhé et al. 2007). This suggests that there is no direct correlation with the brain monoamine levels and the depressed mood. However, the depletion in experimental conditions is acute and it is possible that longer depletion is required to induce depression symptoms. In subjects who had been previously treated with antidepressant drugs but are in a remission, tryptophan depletion moderately decreased the mood whereas phenylalanine/tyrosine depletion had no significant effect (Ruhé et al., 2007). In patients, who are in remission and are currently treated with antidepressant drugs, depletion of the corresponding monoamine in which the drug exerts its main effect can reinstate the depressive symptoms (e.g. tryptophan depletion in patients using SSRIs) (Ruhé et al., 2007). These results suggest that depressed patients are more susceptible to depressive symptoms because of a possible vulnerability in their monoaminergic systems. Interestingly, in healthy volunteers with a family history of major depressive disorder a slight reduction in the mood could be achieved with monoamine depletion, suggesting a genetic component involved in the sensitivity to the effects of monoamine depletion (Ruhé et al., 2007).
2.3.2 Concept of neurotrophin theory of depression and antidepressant action Neurotrophin theory of depression postulates that reduction of BDNF expression would impair the survival and connectivity of neurons resulting in neuronal atrophy, especially in brain areas vulnerable to stress and involved in the regulation of mood (e.g. hippocampus) (Duman et al., 1997). The expression levels of BDNF may be promoted following treatment with antidepressant drugs aiding the neurons in resisting the negative effects of stress to restore connectivity. In support of the neurotrophin theory of depression, reduced BDNF levels in the brain and serum of depressed patients, as well
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as increases in BDNF expression after AD treatment has been reported (Chen et al., 2001; Karege et al., 2002, 2005; Matrisciano et al., 2009; Shimizu et al., 2003).
In the blood BDNF is found in the platelets and it can be released upon stimulation induced by stress or injury (Fujimura et al., 2002). Megakaryocytes, which produce the platelets, express bdnf mRNA in humans and rats but not mice (Chacón-Fernández et al., 2016). Megakaryocytes also store BDNF protein, which is then transferred to platelets. Levels of BDNF in serum from depressed patients are found to be lower compared to healthy controls, with some studies suggesting that BDNF levels are correlated with the severity of depressive-like symptoms (Karege et al., 2002, 2005; Pandey et al., 2010). Antidepressants appear to increase BDNF levels in serum since depressed patients treated with ADs have elevated levels of BDNF in serum compared to non-treated controls, however, the ability of different ADs to affect BDNF levels seem to vary (Matrisciano et al., 2009; Shimizu et al., 2003). In support of these findings, in meta-analyses BDNF concentration has been found to be lower in the serum of depressed patients than in healthy controls or antidepressant-treated depressive patients, however, no correlation between BDNF levels and symptom severity was found (Molendijk et al., 2014; Sen et al., 2008). Low serum BDNF concentration is thought to result from decreased release of BDNF from the platelets and not from the overall decrease in blood BDNF levels (Karege et al., 2005).
In addition to blood, changes in brain BDNF levels have been observed in post mortem studies of depressed patients. Specifically, patients on antidepressant medication have increased BDNF expression in the hippocampus, whereas suicide victims have reduced BDNF and TrkB expression in the hippocampus and prefrontal cortex (Chen et al., 2001; Dwivedi et al., 2003)
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http://www.ernestros..._expression.htm Behavioral State-Related Gene Expression. Different states of behavior and consciousness—waking, sleeping, dreaming, emotions, motivation, and stress—are all associated with different patterns of behavioral state-related gene expression. Behavioral state-related gene expression is a fundamental link between psychology and biology. It is of essence in exploring the psychobiology of consciousness. Behavioral state-related gene expression is a genetic source of behavior that can be modulated with psychosocial cues and cultural rituals to facilitate health, performance, and healing.

· Activity-Dependent Gene Expression. Learning to do something new initiates cascades of molecular-genetic processes that are called activity-dependent gene expression. Activity-dependent gene expression generates the proteins and growth factors that signal stem cells residing in the brain to differentiate into newly functioning neurons with new connections between them. Likewise, stem cells that reside in tissues throughout the body receive psychogenomic signals that enable them to replace injured cells with healthy ones: this is proposed as a basic dynamic of the healing placebo response.

· The Novelty-Numinosum-Neurogenesis Effect. Novelty, enriching life experiences, and exercise associated with a positive sense of curiosity and wonder can turn on activity-dependent gene expression to construct and reconstruct the physical brain and the way it works throughout our entire lifetime. This is the psychobiological essence of the relationship between the creative psychological experience, gene expression, and neurogenesis — it is a psychosynthetic process of updating and recreating ourselves in everyday life as well as in the arts, humanities, and sciences. The novelty-numinosum-neurogenesis effect documents how highly motivated states of consciousness can turn on and focus gene expression, protein synthesis, neurotransmitters, and neurogenesis in our daily creative work of building a better brain.

· Creative Replay and Re-synthesis is the Essence of Psychotherapy. Replaying the 4-stage creative process for the re-synthesis of experience is the fundamental dynamic of psychotherapy and the healing arts. Our emerging models of creativity, optimal performance, stress, and healing engage Darwinian variation and conscious selection on all levels from mind to gene in the natural ultradian flow of human experiencing. Immediate early genes, behavioral state-related, and activity-dependent gene expression are bridges between body, brain, and mind that can be accessed to facilitate the creative replays of therapeutic hypnosis, psychotherapy, and the holistic healing arts.

· Individual Response-Ability and Ethical Self-Realization. Although it is generally recognized that we are all 99.9% alike in our genetic legacy, it is still not generally understood that there are at least three million small variations in our genes — called single nucleotide polymorphisms — that are expressed in our individuality. This implies that we all have a profoundly unique psychogenomic entitlement for the personal perceptions, potentials, and problems that we alone can recognize and realize as our ultimate response-ability. Of necessity, each person is responsible for the facilitation his or her unique psychogenomic endowment. Parents and teachers may help us find paths, but ultimately only we alone can know when we are really okay in our quests for ethical self-realization — the mindful integration of our personal psychogenomic potentials with those of society and culture.

· Social and Cultural Response-Ability. The ultimate gifts of art, music, dance, and the humanities are their evocative effects on gene expression, neurogenesis, and healing in the co-evolution of consciousness and culture. Play, imagination, fantasy, and dreams are all natural exploratory efforts in the creative replay and re-synthesis of life experiences on all levels. Gaia, gene, individual, and society co-create each other in the self-reflective replays of the ever-emergent dynamics of becoming. The ultimate response-ability of leadership on all levels is to facilitate this natural evolution of the goals, philosophies, and ethics of life.

· Positive Psychology and The New Decade of Behavior: 2000-2010. Our current Decade of Behavior (2000-2010), as announced by the American Psychological Association, is a wonderful complement to the previous Decade of the Brain (1900-2000) for integrating psyche and soma with the new spirit of Positive Psychology. Experiences of creativity, happiness, humor, uplifting surprise, awe, and that special spiritual sense of the numinousum—fascination, mysteriousness, and the tremendous—are all associated with immediate early, behavioral state-related, and activity-dependent gene expression, neurogenesis, healing, and self-realization. The ethical challenge is to discover new research methods for the deepening exploration and the practical implementation of these insights for the rediscovery and recreation of human nature. Lets all go for it!

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#5 Ruth

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Posted 04 June 2018 - 08:32 PM

https://onlinelibrar....1002/ajp.22875 Oxytocin (OT) and arginine‐vasopressin (AVP) are involved in the regulation of complex social behaviors across a wide range of taxa. Despite this, little is known about the neuroanatomy of the OT and AVP systems in most non‐human primates, and less in humans. The effects of OT and AVP on social behavior, including aggression, mating, and parental behavior, may be mediated primarily by the extensive connections of OT‐ and AVP‐producing neurons located in the hypothalamus with the basal forebrain and amygdala, as well as with the hypothalamus itself. However, OT and AVP also influence social cognition, including effects on social recognition, cooperation, communication, and in‐group altruism, which suggests connectivity with cortical structures. While OT and AVP V1a receptors have been demonstrated in the cortex of rodents and primates, and intranasal administration of OT and AVP has been shown to modulate cortical activity, there is to date little evidence that OT‐and AVP‐containing neurons project into the cortex. Here, we demonstrate the existence of OT‐ and AVP‐containing fibers in cortical regions relevant to social cognition using immunohistochemistry in humans, chimpanzees, and rhesus macaques. OT‐immunoreactive fibers were found in the straight gyrus of the orbitofrontal cortex as well as the anterior cingulate gyrus in human and chimpanzee brains, while no OT‐immunoreactive fibers were found in macaque cortex. AVP‐immunoreactive fibers were observed in the anterior cingulate gyrus in all species, as well as in the insular cortex in humans, and in a more restricted distribution in chimpanzees. This is the first report of OT and AVP fibers in the cortex in human and non‐human primates. Our findings provide a potential mechanism by which OT and AVP might exert effects on brain regions far from their production site in the hypothalamus, as well as potential species differences in the behavioral functions of these target regions.
https://bmcpsychiatr...2888-018-1740-9 The neuropeptide Oxytocin (OXT) plays a central role in birthing, mother-infant bonding and a broad range of related social behaviours in mammals. More recently, interest has extended to epigenetic programming of genes involved in oxytocinergic neurotransmission. This review brings together early findings in a rapidly developing field of research, examining relationships between DNA methylation (DNAm) of the Oxytocin Receptor Gene (OXTR) and social and emotional behaviour in human populations.





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