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If A Woman Consumes A Lot of Dietary Choline During Pregnancy:

brain acetylcholine cognitive

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#1 iseethelight

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Posted 16 September 2015 - 12:04 AM


Will it upregulate or downregulate the acetylcholine receptors of the child?  Meaning Will said child require high choline in their diet to operate at an optimal level cognitively or would he require less choline?



#2 gamesguru

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Posted 16 September 2015 - 12:41 AM

He would probably require less choline, but to be safe I wouldn't deviate far from this chart:

Prenatal choline exposure alters hippocampal responsiveness to cholinergic stimulation in adulthood

Manipulation of dietary choline levels during gestation results in enduring neurobehavioral changes in offspring that last into adulthood.  Alterations of hippocampal function and memory are among the most striking changes. Depending upon the measures assessed, prenatal choline supplementation tends to promote excitatory synaptic efficacy in hippocampal circuits while prenatal choline deficiency diminishes it.  These results suggest that GABA  receptor-mediated inhibition remains intact after prenatal choline manipulations, and that enhancement of the excitatory responsiveness of hippocampal circuits in slices from prenatally choline supplemented rats may be related in part to an increase in cholinergic tone within the CA1 circuit

 

And would anyway be somewhat insured against FAS:

Prenatal choline supplementation mitigates behavioral alterations associated with prenatal alcohol exposure in rats

These data indicate that choline supplementation during prenatal alcohol exposure may reduce the severity of fetal alcohol effects, particularly on alterations in tasks that require behavioral flexibility. These findings have important implications for children of women who drink alcohol during pregnancy.

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#3 iseethelight

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Posted 16 September 2015 - 06:42 AM

Thanks, appreciate it. My mom ate a dozen eggs every day when she was pregnant with me.I seem to overreact to choline supplements sometimes but can't really isolate since I feel good on it sometimes.



#4 gamesguru

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Posted 16 September 2015 - 02:14 PM

Most likely, overreaction = sensitivity.  I would just do 3-5 eggs a week for choline, and not touch supplements, especially GPC or the racetams (maybe piracetam/ani are OK, but approach the more potent ones with extreme caution).

That's a lot of eggs, I'd also be concerned about saturated fat

 

F1 Offspring of (F0) Female Rats Fed a High-Saturated Fat, Prenatal/Lactation Diet Remain Insulin Resistant Despite Postnatal Diet Rich in Omega-3 Polyunsaturated Fatty Acids

Prior research has shown adult diets rich in omega-3 long-chain polyunsaturated fatty acids (omega-3 LC-PUFAs) can improve adult metabolic health. Previous studies have also shown maternal overnutrition during pregnancy/lactation adversely affects metabolic functioning in adult offspring. The purpose of the current study was to investigate the interaction of these two metabolism regulating factors by assessing the effectiveness of a postweaning diet rich in omega-3 long chain-polyunsaturated fatty acids (omega-3 LC-PUFAs) to improve metabolic function in adult offspring whose mothers were fed a high-saturated fat “Western” diet during pregnancy/lactation. We compared metabolic function between offspring of three prenatal-lactation/postweaning diet lines of Sprague-Dawley rats: 1) offspring of mothers fed a high-saturated fat “Western” diet during pregnancy-lactation, then weaned to a high omega-3 LC-PUFA diet (Western/PUFA); 2) offspring of mothers fed a control diet during pregnancy-lactation, then weaned to a high omega-3 LC-PUFA diet (Control/PUFA); and 3) offspring of mothers fed a Western diet during pregnancylactation, and postweaning (Western/Western). Fasting plasma insulin, triglycerides, and insulin resistance (HOMA-IR) of Western/PUFA animals were intermediate to those of Western/Western and Control/PUFA offspring, although these differences did not reach statistical significance. This suggests the metabolic benefits of an omega-3 LC-PUFA-rich diet are insufficient to overcome the deleterious effects of a high-saturated fat prenatal-lactation diet.

 

which may not be such a bad thing if the eggs were pasture-raised an contained antioxidants, like zinc, selenium, vitamin E, and D

Prenatal high saturated fat diet modifies behavioral effects of prenatal alcohol exposure in rats

Alcohol had an opposite effect on offspring whose mothers consumed the high saturated fat diet, and had no effect on animals consuming the high polyunsaturated/no vitamin E or zinc diet. These preliminary results suggest that dietary fat may modify the behavioral effects of prenatal alcohol exposure. This effect may be the result of the stabilizing effect of saturated fats on cell membranes which increases their resistance to perturbation by alcohol.

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#5 iseethelight

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Posted 16 September 2015 - 05:04 PM

Thanks for the info. I was born in the country side so the eggs were pasture-raised, mostly from the local farmers . Piracetam makes me dizzy, choline supps , high egg consumption, bananas give me random cold chills along with the cold extremities. I also suffer from high histamine so some of these food reactions may  just be histamine reaction.



#6 gamesguru

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Posted 16 September 2015 - 05:39 PM

Thanks for the info. I was born in the country side so the eggs were pasture-raised, mostly from the local farmers . Piracetam makes me dizzy, choline supps , high egg consumption, bananas give me random cold chills along with the cold extremities. I also suffer from high histamine so some of these food reactions may  just be histamine reaction.

 

For how long now do you notice this association, between bananas and chilly extremities?  Do you sometimes get it after normal meals (w/o bananas)?  If so, I would be sure to remember to bring this to the attention of my doctor during my next physical.

Have you tried other cholinergic supplements?  I have in mind ginkgo[!], bacopa[1], [2], green tea[!], huperzine, galantamine, or even wild blueberries:

Acetylcholinesterase (AChE) activity was determined by Ellman's colorimetric method. Results showed that the PrB60-treated mice exhibited a significant improvement in learning and memory (step-through latency time of 228 ± 38 s compared to 101 ± 32 s of the control group). PrB extract administration also resulted in reduced lipid peroxidation products (38 and 79%) and higher brain ascorbic acid levels (21 and 64%) in both PrB30 and PrB60-treated groups, respectively, and higher glutathione levels (28%) in the PrB60-treated group. Furthermore, salt- and detergent soluble AChE activity significantly decreased in both PrB-treated groups. Thus, the significant cognitive enhancement observed in adult mice after short-term i.p. supplementation with the blueberry extract concentrated in polyphenols, is closely related to higher brain antioxidant properties and inhibition of AChE activity

 

As for the histamine intolerance, it is probably due in part to a deficiency of diamine oxidase, which normally degrades histamine.

Plasma Diamine Oxidase Activity Is Greater in Copper-Adequate than Copper-Marginal or Copper-Deficient Rats

plasma diamine oxidase activity (−94%) differed between rats fed copper-marginal and copper-adequate diets. Plasma diamine oxidase activity, therefore, may be a sensitive functional biomarker of suboptimal copper status.

Methyl jasmonate upregulates biosynthetic gene expression, oxidation and conjugation of polyamines, and inhibits shoot formation in tobacco thin layers.

the activity of S:-adenosylmethionine decarboxylase (SAMDC, EC 4.1.1.21), an enzyme involved in spermidine and spermine biosynthesis, was also stimulated by exposure to MJ. Northern analyses revealed MJ-induced, generally dose-dependent, increases in the mRNA levels of all three enzymes. Diamine oxidase activity was stimulated by MJ mainly in the cell wall fraction.

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#7 iseethelight

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Posted 16 September 2015 - 06:03 PM

The cold extremities and I forgot to mention, (jaw tremors) attributed to bananas usually don't happen until about 5+ hours after comsumption. I have suffered from the cold hands feet and random jaw tremors when it gets cold for years, but I wasn't able to isolate it to specific foods until about a few months ago.

 

I have tried all the Ach precursors (alpha -gpc, cdp,bitartrate, alcar),  and ache inhibitors like galantamine etc. The more potent choline prec caused depression, anger and anhedonia. 

 

I have also tried ginkgo, and used to consume lots of blueberries daily which I've stopped due to the adverse reactions mentioned before.

Ginkgo helped with the cold hands sometimes but would give me a nervous stomach and made me sweat too much. I've read about its dangers causing me to drop it from my stack.

I seem to be responding well to magnesium and vit d. I currently drink green tea and take l-tyrosine which seems to be helping with my lack of motivation a bit.

I did the braverman test over 10 times and I scored super low on GABA every single time, so I'm taking theanine with gaba and taurine for that. 


Edited by iseethelight, 16 September 2015 - 06:06 PM.


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#8 gamesguru

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Posted 17 September 2015 - 02:49 AM

Blueberries make my eczema flair up, which is my main symptom of histamine.  But I still eat them, just not copiously.

 

J Biomed Sci. 2010 Aug 24;17 Suppl 1:S14. doi: 10.1186/1423-0127-17-S1-S14.
Pharmacological characterization of GABAA receptors in taurine-fed mice.
Abstract
BACKGROUND:

Taurine is one of the most abundant free amino acids especially in excitable tissues, with wide physiological actions. Chronic supplementation of taurine in drinking water to mice increases brain excitability mainly through alterations in the inhibitory GABAergic system. These changes include elevated expression level of glutamic acid decarboxylase (GAD) and increased levels of GABA. Additionally we reported that GABAA receptors were down regulated with chronic administration of taurine. Here, we investigated pharmacologically the functional significance of decreased / or change in subunit composition of the GABAA receptors by determining the threshold for picrotoxin-induced seizures. Picrotoxin, an antagonist of GABAA receptors that blocks the channels while in the open state, binds within the pore of the channel between the beta2 and beta3 subunits. These are the same subunits to which GABA and presumably taurine binds.

METHODS:

Two-month-old male FVB/NJ mice were subcutaneously injected with picrotoxin (5 mg kg-1) and observed for a) latency until seizures began, b) duration of seizures, and c) frequency of seizures. For taurine treatment, mice were either fed taurine in drinking water (0.05%) or injected (43 mg/kg) 15 min prior to picrotoxin injection.

RESULTS:

We found that taurine-fed mice are resistant to picrotoxin-induced seizures when compared to age-matched controls, as measured by increased latency to seizure, decreased occurrence of seizures and reduced mortality rate. In the picrotoxin-treated animals, latency and duration were significantly shorter than in taurine-treated animas. Injection of taurine 15 min before picrotoxin significantly delayed seizure onset, as did chronic administration of taurine in the diet. Further, taurine treatment significantly increased survival rates compared to the picrotoxin-treated mice.

CONCLUSIONS:

We suggest that the elevated threshold for picrotoxin-induced seizures in taurine-fed mice is due to the reduced binding sites available for picrotoxin binding due to the reduced expression of the beta subunits of the GABAA receptor. The delayed effects of picrotoxin after acute taurine injection may indicate that the two molecules are competing for the same binding site on the GABAA receptor. Thus, taurine-fed mice have a functional alteration in the GABAergic system. These include: increased GAD expression, increased GABA levels, and changes in subunit composition of the GABAA receptors. Such a finding is relevant in conditions where agonists of GABAA receptors, such as anesthetics, are administered.

 
Adv Exp Med Biol. 2013;775:177-85. doi: 10.1007/978-1-4614-6130-2_15.
The effects of chronic taurine supplementation on motor learning.
Abstract

Taurine is one of the most abundant nonprotein amino acids shown to be essential for the development, survival, and growth of vertebrate neurons. We previously demonstrated that chronic taurine supplementation during neonatal development results in changes in the GABAergic system (El Idrissi, Neurosci Lett 436:19-22, 2008). The brains of mice chronically treated with taurine have decreased levels of GABA(A)β subunits and increased expression of GAD and GABA, which contributes to hyperexcitability. This down regulation of GABA(A)receptor subunit expression and function may be due to a sustained interaction of taurine with GABA(A)receptors. This desensitization decreases the efficacy of the inhibitory synapses at the postsynaptic membrane. If changes occur in the GABAergic system as a possible compensatory mechanism due to taurine administration, then it is important to study all aspects by which taurine induces hyperexcitability and affects motor behavior. We therefore hypothesized that modification of the GABAergic system in response to taurine supplementation influences motor learning capacity in mice. To test this hypothesis, the rotarod task was employed after chronic taurine supplementation in drinking water (0.05% for 4 weeks). Control animals receiving no taurine supplementation were also tested in order to determine the difference in motor learning ability between groups. Each animal was trained on the rotarod apparatus for 7 days at an intermediate speed of 24 rpm in order to establish baseline performance. On the testing day, each animal was subjected to eight different predefined speeds (5, 8, 15, 20, 24, 31, 33, and 44 rpm). From our observations, the animals that underwent chronic taurine supplementation appeared to have a diminished motor learning capacity in comparison to control animals. The taurine-fed mice displayed minor improvements after repeated training when compared to controls. During the testing session the taurine-fed mice also exhibited a shorter latency to fall, as the task requirements became more demanding.

 

 

Int Rev Neurobiol. 1996;39:53-76.
Use-dependent regulation of GABAA receptors.
Abstract

Prolonged occupancy of GABAA receptors by ligands, including GABA and benzodiazepine agonists, sets in motion a series of mechanisms that can be termed use-dependent regulation. These mechanisms can be subdivided into two distinct pathways, one for GABAA receptor downregulation and another for upregulation. Treatment of cortical neurons with GABA or benzodiazepines in cultures opens the pathway for GABAA receptor downregulation, which includes (in putative temporal order): (1) desensitization (tachyphylaxis), (2) sequestration (endocytosis) of subunit polypeptides and uncoupling of allosteric interactions between GABA and benzodiazepine binding sites, (3) subunit polypeptide degradation, and (4) repression of subunit gene expression. The end-point of GABAA receptor downregulation, a reduction in receptor number, is postulated to be established initially by degradation of the receptor protein and then maintained by a diminished level of de novo synthesis. Benzodiazepine treatment of many preparations, including cells expressing recombinant GABAA receptors, may elicit only desensitization, sequestration, or uncoupling, without a decline in receptor number. Components of the GABAA receptor downregulation pathway are also evoked by chronic administration of GABAmimetics, benzodiazepines, barbiturates, and neurosteroids in animals. This downregulation correlates with the establishment of tolerance to and physical dependence on the pharmacological effects of these drugs, suggesting a cellular model for this behavior. The upregulation of GABAA receptors is observed as one of the neurotrophic actions of GABA, primarily in cultured cerebellar granule cells. Upregulation in culture is caused by enhanced expression of genes for GABAA receptor subunits and correlates with the establishment of GABAergic circuitry in the developing cerebellum. Thus, both the upregulation and downregulation of GABAA receptors appear to represent use-dependent pathways for guiding synaptic plasticity in the vertebrate central nervous system.

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Falcarindiol Allosterically Modulates GABAergic Currents in Cultured Rat Hippocampal Neurons Abstract
np-2011-008522_0008.gif

 

"the effects on the amplitude of mIPSC and of the currents evoked by low [GABA] suggest an upregulation of agonist binding."

Falcarindiol (1), a C-17 polyacetylenic diol, shows a pleiotropic profile of bioactivity, but the mechanism(s) underlying its actions are largely unknown. Large amounts of 1 co-occur in water hemlock (Oenanthe crocata) along with the convulsant polyacetylenic toxin oenanthotoxin (2), a potent GABAA receptor (GABAAR) inhibitor. Since these compounds are structurally and biogenetically related, it was considered of interest to evaluate whether 1 could affect GABAergic activity, and for this purpose a model of hippocampal cultured neurons was used. Compound 1 significantly increased the amplitude of miniature inhibitory postsynaptic currents, accelerated their onset, and prolonged the decay kinetics. This compound enhanced also the amplitude of currents elicited by 3 μM GABA and accelerated their fading, reducing, however, currents evoked by a saturating (10 mM) GABA concentration. Moreover, kinetic analysis of responses to 10 mM GABA revealed that 1 upregulated the rate and extent of desensitization and slowed the current onset and deactivation. Taken together, these data show that 1 exerts a potent modulatory action on GABAARs, possibly by modulating agonist binding and desensitization, overall potentially decreasing the toxicity of co-occurring GABA-inhibiting convulsant toxins.

 

 

Chronic Caffeine Alters the Density of Adenosine, Adrenergic, Cholinergic, GABA, and Serotonin Receptors and Calcium Channels in Mouse Brain SUMMARY

1. Chronic ingestion of caffeine by male NIH strain mice alters the density of a variety of central receptors.

2. The density of cortical A1 adenosine receptors is increased by 20%, while the density of striatal A2A adenosine receptors is unaltered.

3. The densities of cortical β1 and cerebellar β2 adrenergic receptors are reduced by ca. 25%, while the densities of cortical α1 and α2 adrenergic receptors are not significantly altered. Densities of striatal D1 and D2 dopaminergic receptors are unaltered. The densities of cortical 5 HT1 and 5 HT2 serotonergic receptors are increased by 26–30%. Densities of cortical muscarinic and nicotinic receptors are increased by 40–50%. The density of cortical benzodiazepine-binding sites associated with GABAA receptors is increased by 65%, and the affinity appears slightly decreased. The density of cortical MK-801 sites associated with NMDA-glutaminergic receptors appear unaltered.

4. The density of cortical nitrendipine-binding sites associated with calcium channels is increased by 18%.

5. The results indicate that chronic ingestion of caffeine equivalent to about 100 mg/kg/day in mice causes a wide range of biochemical alterations in the central nervous system.

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actually inhibiting gaba long-term would be better than taking gaba+taurine, for activity levels

and overusing theanine[1] or magnesium[2] will also downregulate GABA(A)

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Neurosci Lett. 1997 Nov 14;237(1):1-4.
D2 receptor-mediated inhibition of GABA release by endogenous dopamine in the rat globus pallidus.
Abstract

Attempting to better understand the role of the dopaminergic innervation in the rat globus pallidus, we examined here whether or not endogenous dopamine modulates the release of [3H]GABA in superfused pallidal slices. The superfusion medium contained elevated (15 mM) potassium. The release of endogenous dopamine was induced by the dopamine releaser drug, methamphetamine. Methamphetamine (100 microM) inhibited by 46% the release of [3H]GABA. Methamphetamine inhibition was completely blocked by reserpinization of the rats. It was also completely blocked by the D2 dopamine receptor antagonist sulpiride (10 microM). Sulpiride alone caused a 105% increase in GABA release. The increase was not observed in slices from reserpinized rats. Quinpirole (10 microM), a D2 dopamine receptor agonist, inhibited (43%) [3H]GABA release. The results suggest that endogenous dopamine [D2] exerts an inhibitory effect on GABA release in the rat globus pallidus. The effect is mediated by D2 receptors presumably located on striatopallidal axon terminals.

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Ginkgo biloba extract (EGb 761) modulates the expression of dopamine-related genes in 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine-induced Parkinsonism in mice

ABSTRACT 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) causes nigrostriatal dopaminergic neurotoxicity and behavioral impairment in rodents similar to Parkinson's disease. The MPTP mouse model is widely used to evaluate new protective agents. EGb 761 is a well-defined mixture of active compounds extracted from Ginkgo biloba leaves according to a standardized procedure. We have shown that EGb 761 attenuates the loss of striatel dopamine levels and prevents the neurodegeneration of the nigrostriatal pathway induced by MPTP. This finding shows that neuroprotective effects of EGb 761 act, in part, on the dopamine system. Therefore, this study investigates whether EGb 761 exerts dopaminergic neuroprotection through the regulation of dopamine-related gene expression in MPTP-induced Parkinsonism. Male C57BL/6J mice were injected with MPTP (30 mg/kg, i.p.) for 5 days and later with EGb 761 (40 mg/kg, i.p.) daily for 18 days. The expression of selected genes was evaluated in the striatum and midbrain by quantitative PCR. The genes for tyrosine hydroxylase (Th), vesicular monoamine transporter 2 (Vmat2), dopamine transporter (Dat), dopamine D2 receptor (Da-d2r), and transcription factors (Pitx3 and Nurr1) related to dopamine neurotransmission were selected for the analysis. EGb 761 administration to MPTP-treated mice protected Th (41%), Vmat2 (15%), Dat (102%), Da-d2r (46%), Pitx3 (63%), and Nurr1 (148%) mRNA levels in the midbrain, all of which were up-regulated. However, EGb 761 partially reversed the MPTP effect exclusively for Th (48%) and Nurrl (96%) mRNA in the striatum. Only Th and Nurr1 mRNA and protein levels were regulated

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Eur J Pharmacol. 2003 Mar 7;464(1):1-8.
Bilobalide, a sesquiterpene trilactone from Ginkgo biloba, is an antagonist at recombinant α1β2γ2L GABA(A) receptors.
Abstract

The sesquiterpene trilactone bilobalide is one of the active constituents of the 50:1 Ginkgo biloba leaf extract widely used to enhance memory and learning. Bilobalide was found to antagonise the direct action of gamma-aminobutyric acid (GABA) on recombinant alpha(1)beta(2)gamma(2L) GABA(A) receptors. The effect of bilobalide on the direct action of GABA at alpha(1)beta(2)gamma(2L) GABA(A) receptors expressed in Xenopus laevis oocytes using two-electrode voltage-clamp method was evaluated and compared with the effects of the classical GABA(A) receptor competitive antagonist bicuculline and noncompetitive antagonist picrotoxinin. Bilobalide (IC(50)=4.6+/-0.5 microM) was almost as potent as bicuculline and pictrotoxinin (IC(50)=2.0+/-0.1 and 2.4+/-0.5 microM, respectively) at alpha(1)beta(2)gamma(2L) GABA(A) receptors against 40 microM GABA (GABA EC(50)). While bilobalide and picrotoxinin were clearly noncompetitive antagonists, the potency of bilobalide decreased at high GABA concentrations suggesting a component of competitive antagonism.

 

J Biol Chem. 2003 Dec 5;278(49):49279-85. Epub 2003 Sep 22.
 
Terpene trilactones from Ginkgo biloba are antagonists of cortical glycine and GABA(A) receptors.
Abstract

Glycine and gamma-aminobutyric acid, type A (GABA(A)) receptors are members of the ligand-gated ion channel superfamily that mediate inhibitory synaptic transmission in the adult central nervous system. During development, the activation of these receptors leads to membrane depolarization. Ligands for the two receptors have important implications both in disease therapy and as pharmacological tools. Terpene trilactones (ginkgolides and bilobalide) are unique constituents of Ginkgo biloba extracts that have various effects on the central nervous system. We have investigated the relative potency of these compounds on glycine and GABA(A) receptors. We find that most of the ginkgolides are selective and potent antagonists of the glycine receptor. Bilobalide, the single major component in G. biloba extracts, also reduces glycine-induced currents, although to a lesser extent. Both ginkgolides and bilobalide inhibit GABA(A) receptors, with bilobalide demonstrating a more potent effect. Additionally, we provide evidence that open channels are required for glycine receptor inhibition by ginkgolides. Finally, we employ molecular modeling to elucidate the similarities and differences in the structure of the terpene trilactones to account for the pharmacological properties of these compounds and demonstrate a striking similarity between ginkgolides and picrotoxinin, a GABA(A) and recombinant glycine alpha-homomeric receptor antagonist.

 

Chlorogenic acid is a common dietary polyphenol found in fruits such as plums, apples, and cherries and beverages such as tea and coffee which has been shown to have anxiolytic effects in animal studies [67, 76]. Chlorogenic acid has been demonstrated to have a number of effects on a cellular level, leading to several proposed mechanisms for its overall anxiolytic effects. In one study, the anxiolytic effect of chlorogenic acid was blocked in vivo by the benzodiazepine receptor antagonist flumazenil, suggesting that anxiety is reduced by activation of the benzodiazepine receptor [67]. In vitro, chlorogenic acid protected granulocytes from oxidative stress, which is another proposed important contributor to anxiety [67]. It has also been found to have neurotrophic effects in vitro that stimulate neuronal differentiation and neurite growth, supporting neuroplasticity, which also may contribute to its anxiolytic effects [66].

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Epicatechin mitigates anxiety in association with elevated hippocampal monoamine and BDNF levels
Epicatechin up-regulates GluR2 in cortical neurons and stimulates ERK-dependent cyclic AMP response element activity

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Effect of Magnolia officinalis and Phellodendron amurense (Relora®) on cortisol and psychological mood state in moderately stressed subjects.

Rosmarinic acid of Lemon Balm inhibits GABA transaminase [enzyme which degrades GABA]
http://onlinelibrary...r.2712/abstract

Magnolol of Lemon Balm enhances pentobarbital-induced sleeping behaviors and increases GABA(A) alpha receptor subunit density
http://www.ncbi.nlm....pubmed/19165750

Anxiolytic-like effects of 4-O-methylhonokiol of Lemon Balm via enhancement of GABAergic transmission and chloride influx
http://www.ncbi.nlm....pubmed/21501091

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Bacopa Increases GABA Receptor Functionality in the Hippocampus
http://www.wellnessr..._functionality/

GABA receptor density in the cerebral cortex: effect of Bacoside-A
http://www.ncbi.nlm....les/PMC3306740/

GABA receptor functional regulation in the hippocampus of epileptic rats: effect of Bacopa monnieri
http://www.ncbi.nlm....pubmed/20821261

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Neuregulin induces GABA(A) receptor subunit expression and neurite outgrowth in cerebellar granule cells
TrkB interacts with ErbB4 and regulates NRG1-induced NR2B phosphorylation in cortical neurons before synaptogenesis
YY162 [Ginkgo terpenoids and ginsenoside Rg3] prevents ADHD-like behavioral side effects and cytotoxicity induced by Aroclor1254 via interactive signaling between antioxidant potential, BDNF/TrkB, DAT and NET.

Exercise training and return to a well-balanced diet activate the neuregulin 1/ErbB pathway







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