List of Facebook Log-In / APP Errors & What They Might Mean (Various FB Errors)

1.) ACCOUNT TEMPORARILY UNAVAILABLE

Your account is currently unable to use Facebook for Websites. For more information, please log in to www.facebook.com and follow the instructions you see there.

More often that not, I find that this error has to do with a security issue, specifically the IP Address you are using to sign-in with on facebook. However, a secondary issue could be your account is temporarily locked by repeated failed log-in attempts.

CHECK

• Are you using your phone, on a data network you have never used before to use the application or to log-in with your facebook account?
• Are you using a VPN, Proxy, or some other IP Changing program?
• Are you on vacation, or logging in from another state or country than usual?
• Do you give your password to anyone else, do you have access to your actual facebook account or are you locked out from it?
• Are you logging in with a different browser than usual, especially on a different operating system?
• Do you have device registry enabled on your facebook, and other security features? NOTE : These can be changed in your account / security settings on facebook.

The Mysterious Serotonin 5-HT5A Receptors and their Function as Mediators of an "Unidentified Current" : Effects on Behavior and Sleep Patterns Explored

The Native Serotonin5-HT5A Receptor

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 Electrophysiological Characterization in Rodent Cortex and 5-HT1A-Mediated Compensatory Plasticity in the Knock-Out Mouse
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Nathalie M. Goodfellow,1 Craig D. C. Bailey,1 and Evelyn K. Lambe1,2
1
Department of Physiology and Department of Obstetrics and Gynaecology, University of Toronto, Toronto, Ontario, M5S 1A8, Canada
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~BEFORE ANYTHING ELSE, YES, HUMANS HAVE THIS RECEPTOR~

The 5-HT5A receptor is the least understood serotonin (5-HT) receptor. Here, we electrophysiologically identify and characterize a native5-HT5A receptor current in acute ex vivo brain slices of adult rodent prefrontal cortex.
In the presence of antagonists for the previouslycharacterized 5-HT1A and 5-HT2 receptors, a proportion of layer V pyramidal neurons continue to show 5-HT-elicited outward currentsin both rats and mice.

These 5-HT currents are suppressed by the selective 5-HT5A antagonist, SB-699551, and are not observed in 5-HT5A receptor knock-out mice. Further characterization reveals that the 5-HT5A current is activated by submicromolar concentrations of 5-HT,is inwardly rectifying with a reversal potential near the equilibrium potential for K (potassium) ions, and is suppressed by blockers of Kir3 channels.

Finally, we observe that genetic deletion of the inhibitory 5-HT5A receptor results in an unexpected, large increase in the inhibitory 5-HT1A receptor currents. The presence of functional prefrontal 5-HT5A receptors in normal rodents along with compensatory plasticity in5-HT5A receptor knock-out mice testifies to the significance of this receptor in the healthy prefrontal cortex.

Of all receptors I have researched, this one is indeed, mysterious! 

The interesting thing about this receptor , is not only is it a compensatory autoreceptor, it's unidentified currents seem to have both excitory and inhibitory effects. Mice lacking the 5-HT5A receptor, as in genetic deletion or knock out, did not display an anxiety-phenotype, nor did they respond to auditory startle. (!) (!)
In addition, the extracellular levels of serotonin were higher, indicating that 5-HT5A's are definitely autoreceptors regulating serotonin release.

The lack of startle in 5-HT5A knockout mice, and lack of anxiety is probably due to less inhibition and more overall serotonin release on the more localized areas where other inhibitory receptors are present(!), because either less 5-HT5A activation, as with blockade, or genetic deletion/knockout pushes more serotonin ESPECIALLY on the 5-HT1A receptor in order to compensate for the increases in serotonin, thus, by the 5-HT1A receptor, which also inhibits serotonin, the brain upregulates the activity of it to protect against excessive serotonin from 5-HT5A autoreceptor blockade, in the process of doing this however, the secondary effects of 5-HT1A activation, such as adenylyl cyclase inhibition become especially pronounced, leading to depressed nervous system responses.

This is also consistent with 5-HT1A agonists decreasing anxiety and some stress responses.

 because either less 5-HT5A activation, as with blockade, or genetic deletion/knockout pushes more serotonin ESPECIALLY on the 5-HT1A receptor 

5-HT5A may be involved as well in the startle response induced by serotonin. This has been my experience as well, that using a partial agonist to this receptor, such as valerian extract, had greatly stopped stimulants from causing me to be jumpy.Therefore, it must be that the cross noradrenergic-serotonergic activation of 5-HT5A is one mechanism in which stimulants may increase nervousness.

So , therefore, it can be said that 5-HT5A antagonism leads to indirect agonism of 5-HT1A---Receptors.



This receptor, the serotonin 5-HT5A is unique in that it's inhibitory , calming effects come from the REDUCTION OF CYCLIC AMP(!), whereas the startle and anxiety provoking effects come from it's inhibition of serotonin activity on other more inhibitory receptors.



We can conclude then that 5-HT5A receptors in the SPN and other areas can do the following when activated.

• Reduce serotonin release as an autoreceptor, and downregulate 5-HT1A's to compensate for the reduction of serotonin. 5-HT5A and 5-HT1A are inter-reactive receptors, and act on a behavioral parallel , eyeing each other down for signaling, when one receptor is activated, the other autoreceptor decreases etc.
• They are negatively coupled to adenylyl cyclase, so activating them reduces cyclic AMP!
• They increase behavioral excitation in response to loud noises, probably by acting locally to reduce serotonin activity where it would normally reduce these responses, or by reducing cAMP in discernment areas of the temporal lobe and vestibular neuronal networks.

THUS, A PLAUSIBLE MECHANISM, OF HOW TO REDUCE OR DOWNREGULATE 5-HT1A RECEPTORS, WOULD BE THE ACTIVATION OF 5-HT5A serotonin receptors.

ALSO IN REGARDS TO VALERIAN, THE FOLLOWING.

CITATION

https://www.mja.com.au/journal/2004/181/7/effectiveness-complementary-and-self-help-treatments-anxiety-disorders

Makes sense that the specific effects of VALERINIC ACID / VALERIAN EXTRACT in terms of partial agonism of 5-HT5A would be.

• Antagonize the autoreceptor part, raising serotonin, while agonizing the receptors in the SPN to reduce cyclic AMP.
• Modulating other autoreceptors as a direct interactive or downstream effect of modulating 5-HT5A activity.

Estrogen Effects on Serotonergic and Dopaminergic Neurotransmission (Estrogen in the Brain)

I'm just throwing this together now, figured it would be helpful.

This is a summary of how estrogen, including that derived from or converted from testosterone, by means of aromatase, affects central 5-HT (Serotonin) and dopaminergic neurotransmission.

In the references you will find specific brain region alterations induced by estrogen, and how this may correlate to brain function.
This is all relevant if you want to achieve optimal brain health - including intellectual capacity and general cognition.(!)

• Estrogen downregulates somatodendritic 5-HT1A (!) autoreceptors (presynaptic) in the raphe nuclei, leading to enhanced serotonin release in these areas, however, it also increased cortical post-synaptic 5-HT1A receptors - which can induce cortisol and prolactin release and blunt sexual functions(!). (However, estrogen decreases hypothalamic 5-HT1A receptors(!)

• Estrogen also downregulated 5-HT1A in the limbic areas(!).
• Estrogen also downregulates 5-HT1A receptors in the amygdala, hippocampus, perirhinal cortex, and motor cortex (!) , but when combined with progesterone, the 5-HT1A receptors in the hippocampus increased, with no change in other areas.
• Estrogen also stimulates a significant increase in the density of 5-hydroxytryptamine2A (5-HT2A) binding sites in anterior frontal, cingulate and primary olfactory cortex and in the nucleus accumbens, areas of the brain concerned with the control of mood, mental state, cognition, emotion and behavior(!) (!). This can lead to excitation, anxiety, and potentiation of hallucinogenic drugs.
• Estrogen increases SERT (serotonin reuptake transporter) (!) - leading to enhanced reuptake and less serotonin activity in the synapse - this means that although estrogen may increase serotonin through the above autoreceptor modulation , it ends up not mattering too much in the face of less usability. Thus , high estrogen levels rapidly deplete serotonin from the synapse, leading to reduced efficiency and activity of serotonin. Low estrogen levels would create higher serotonin in the synapse, but less receptors , mainly of the excitory types to bind to. One could presume, that both high and low estrogen would reduce positive effects of SSRI-antidepressants, and increase negative side-effects.
• Estrogen competitively inhibits serotonin 5-HT3 receptor activity.(!)(!)
• Estrogen stimulates the expression of serotonin 5-HT4 (causing excitation and prolactin release), 5-HT5A (can disrupt sleep patterns), and 5-HT6 receptor mRNA (causing cognitive disruptions).(!)
• Estrogen increases dopamine D(2) receptors in the striatum(!).

Thus, estrogen is largely ANTI-COGNITIVE, ANTI-INTELLECTUAL, and does not really provide much benefit at all in terms of these two areas of neurotransmission ......

However, a small amount of estrogen may be necessary to maintain dopamine receptor expression in men and women.
Varying amounts of estrogen per gender, of course....

The greek and roman warriors of old certainly didn't have estrogen dominance - and they were master strategists and intellectuals ---- though I s'pose some of them could be dumb on occasion!

Therefore in terms of serotonergic activity, low estrogen would equate to the following changes.
The fields marked in blue are positive effects of low estrogen, while red is negative, generally.
Purple is neutral, or determined more so by the person.

• More serotonin in the synapse, due to less SERT (transporters), and thus , lessened reuptake of serotonin.
• Increased 5-HT1A receptors in many brain regions, including the hypothalamus, leading to decreased central nitrergic and dopaminergic activity as well as serotonergic neuron activity.
• Decreased serotonin 5-HT2A receptor expression. (leading to less cortisol and prolactin, generally good thing)
• Decreased 5-HT4, 5-HT6, 5-HT5A receptors, especially in pituitary.
• Decreased dopamine D2 in the striatum.
• Increased 5-HT3 receptor binding and activity. (can cause nausea, excitation,pain)
• Decreased serotonin production from tryptophan.
• MORE MONOAMINE OXIDASE (MAO-A)

THUS ALL ROUND LESS SEROTONIN PRODUCTION AND ACTIVITY WITH LOW ESTROGEN HOWEVER.......IN THE PRESENCE OF NORMALIZING TRYPTOPHAN HYDROXYLASE ACTIVITY  - SEROTONIN MAY BE EASIER CHRONICALLY ENHANCED BY LOW ESTROGEN , EXCEPT THAT THE MAIN RECEPTORS SEROTONIN WOULD THEORETICALLY BIND TO WHEN ONE HAS LOW ESTROGEN WOULD BE.


LOW ESTROGEN WOULD MEAN THESE RECEPTORS BELOW WOULD BE MORE AVAILABLE WHILE ALL OTHERS ARE DECREASED.

• 5-HT1A
• 5-HT1B
• 5-HT1D
• 5-HT3
• 5-HT7

THUS, LOW  ESTROGEN RESULTS IN DECREASED.

• 5-HT2A/2C
• 5-HT4
• 5-HT5A
• 5-HT6

Thus, low estrogen by means of all above may have very broad effects, there may be an increase in some forms of intellectual capacity, but a central reduction in glutamatergic tone and a generally lethargic state - which is more pronounced in women ....however, in men, DHT and other androgens can modulate thinking and cognitive function - however, low estrogen in men, may in some, still lead to depression or the need for caffeine and other stimulants............


IN MY EXPERIENCE, BOTH HIGH AND LOW ESTROGEN CHANGES THE TYPE OF FOOD I LIKE.


When estrogen is on the lower side , nearly undetectable, as with when I was on a cut or aromatase inhibitor, I eat more salty and spicy foods, but when estrogen became high in my large experiments with prohormones, I seemed to cling to carbohydrate type foods and sugary foods!

I do find it easier to eat cleaner with lower estrogen, and also alcohol is not desirable not one bit when estrogen is on the lower side, however, my need for caffeine and stimulants increases at times when estro goes into the undetectable or near undetectable range.

( how does estrogen affect men's brains human )

Similar and Legal Variants of the "ECA Stack" Discussion with Cyber-Outlaw "Corageon"

One stack that has worked particularly well for me, while on a cut, has been my own custom, legal, ECA alternative.....


That alternative consists of...

• Caffeine 200mg / PW
• Yohimbine 7.5mg / PW
• Albuterol / 11 puffs.

The science behind this, is that Caffeine occupies adenosine, increases calcium uptake , and then inhibits phosphodiestearases, while Yohimbine gives a better pump, more thermal energy production, and helps shed fat. Albuterol synergizes with the yohimbine to also increase vasodilation, and to increase nervous system strength and muscle contractions.

http://www.ncbi.nlm.nih.gov/pubmed/12323115

http://www.ncbi.nlm.nih.gov/pubmed/1851466

http://www.ncbi.nlm.nih.gov/pubmed/9545623


Testing Potential Synergistic Effects of Albuterol and Caffeine on Metabolic Rate

http://www.mindandmuscle.net/forum/42931-hitting-all-ppars

The particular products I use are below.

Cheap, and effective.

                                                            

What is hCG & Where to buy it Online? {PCT GUIDES 101}

hCG is a hormone produced by the syncytiotrophoblast, a portion of the placenta following implantation.[1][2]. It is often isolated and extracted from a pregnant mare's urine. Though this may sound gross, it is also purified so that it is free of contaminants and yet, maintains it's biological function. 

Bodybuilders may utilize the natural fertility boosting, gonadotropic effect to restore testicle size after a steroid cycle, or to help maintain libido and testicle size on cycle...though, depending on the compounds used, one would likely have trouble maintaining testicle size if the program is harsh enough; regardless of hCG dosage[3].

hCG may restore testosterone production and sex drive after a cycle. It mimics the action of LH ; luteinizing hormone; a gonadotropin , and thus acts directly on the testes to signal testosterone production to start again.


hCG is different than other PCT compounds, in that , unlike clomid, it has no direct effect on any hormone receptor, and it is NOT a pill, nor is it meant to be continued for months at a time.

It is available for INTRAMUSCULAR    OR     SUBCUTANEOUS INJECTION ONLY!

hCG also has the potential to do a few other things differently.

• hCG may raise progesterone and pregnenolone; two important neurosteroids that may help alleviate anxiety and stress related issues(!)(!).
• It can increase estrogen as well though, possibly more so than some other compounds(!).
• It doesn't raise LH, it mimics it. 
• It may help promote fat loss (!) (!) in conjunction with a healthy diet and exercise regimen, however, these reports are merely anecdotal, and not proven, an additional study showed no significant difference between hCG and caloric restriction{!}.
• May help users maintain muscle mass after a cycle(!) (!).

WHERE TO BUY HCG ONLINE

You may buy hCG below, by clicking the image. This is real brand hCG, just doing a simple google search will tell you all about "Pregnyl" the most popular brand!

I have used this product personally. I vouch for it's effectiveness.

CLICK HERE to buy hCG online @ the cheapest possible price. 

List of Purchasable DRI's - Dopamine Reuptake Inhibitors - Both Pharma / Natural - Where to Get DRIs Online

Let me assure you, there is a point to dopamine reuptake inhibition - also known as DAT INHIBITION. 

The benefits of doing this are many.

• Increase short-term memory.
• Alleviate depression.
• Increase cognitive function, including active memory.
• Increase creativity.
• Increase libido.
• Increase motivation.
• BETTER QUALITY OF LIFE.

The first major , natural DOPAMINE REUPTAKE INHIBITOR IS....

"FLOWERING QUINCE EXTRACT"

http://www.ncbi.nlm.nih.gov/pubmed/18485464

 Pharmacol Biochem Behav. 2008 Sep;90(3):363-71. doi: 10.1016/j.pbb.2008.03.014. Epub 2008 Mar 30.

Dopamine transporter inhibitory and antiparkinsonian effect of common flowering quince extract.

Zhao G1, Jiang ZH, Zheng XW, Zang SY, Guo LH.

Author information

Abstract

Common flowering quince (FQ) is the fruit of Chaenomeles speciosa (Sweet) Nakai. FQ-containing cocktails have been applied to the treatment of neuralgia, migraine, and depression in traditional Chinese medicine. The present study assessed whether FQ is effective in dopamine transporter (DAT) regulation and antiparkinsonism by utilizing in vitro and in vivo assays, respectively. FQ at concentrations of 1-1000 microg/ml concentration-dependently inhibited dopamine uptake by Chinese hamster ovary (CHO) cells stably expressing DAT (D8 cells) and by synaptosomes. FQ had a slight inhibitory action on norepinephrine uptake by CHO cells expressing the norepinephrine transporter and no inhibitory effect on gamma-aminobutyric acid (GABA) uptake by CHO cells expressing GABA transporter-1 or serotonin uptake by the serotonin transporter. A viability assay showed that FQ mitigated 1-methyl-4-phenylpyridinium-induced toxicity in D8 cells. Furthermore, in behavioral studies, FQ alleviated rotational behavior in 6-hydroxydopamine-treated rats and improved deficits in endurance performance in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice. Furthermore, immunohistochemistry revealed that FQ markedly reduced the loss of tyrosine hydroxylase-positive neurons in the substantia nigra in MPTP-treated mice. In summary, FQ is a selective, potent DAT inhibitor and has antiparkinsonian-like effects that are mediated possibly by DAT suppression. FQ has the potential to be further developed for Parkinson's disease treatment.

PMID:

 

18485464

 

[PubMed - indexed for MEDLINE]

THE SECOND NATURAL - HERBAL - DOPAMINE REUPTAKE INHIBITOR IS....

!CATUABA EXTRACT!

http://www.ncbi.nlm.nih.gov/pubmed/15991001

Psychopharmacology (Berl). 2005 Oct;182(1):45-53. Epub 2005 Sep 29.

Antidepressant-like effects of Trichilia catigua (Catuaba) extract: evidence for dopaminergic-mediated mechanisms.

Campos MM1, Fernandes ES, Ferreira J, Santos AR, Calixto JB.

Author information

Abstract

RATIONALE:

Currently available therapy for depression treatment is often associated with several undesirable side effects, and it is effective only in a certain portion of the population. Therefore, the identification of alternative therapeutic tools for the treatment of depression is still needed.

OBJECTIVE:

The present study analyzed the possible antidepressant-like effects of the Brazilian medicinal plant, Trichilia catigua, in rodents. Attempts were also made to investigate some of the possible mechanisms implicated in its actions.

METHODS:

The antidepressant-like effects of T. catigua extract were assessed in two species of rodents (mice and rats) by means of in vivo (forced swimming test) and in vitro (monoamine reuptake and release in synaptosomal preparations) approaches.

RESULTS:

Acute oral treatment with the extract of T. catigua produced antidepressant-like effects in the forced swimming model in both mice and rats. Anti-immobility actions of T. catigua extract in mice were significantly reversed by haloperidol or by chlorpromazine, but not by pimozide, ketanserin, spiroxatrine or p-chlorophenylalanine. In vitro, T. catigua extract concentration-dependently inhibited the uptake and increased the release of serotonin, and especially of dopamine, from rat brain synaptosomal preparations.

CONCLUSIONS:

The present study provides convincing evidence for a dopamine-mediated antidepressant-like effect of the active principle(s) present in the hydroalcoholic extract of T. catigua in mice and rats when in vivo and in vitro strategies were employed. Therefore, a standardized T. catigua extract or its purified constituents could be of potential interest for the treatment of depressive disorders.

PMID:

 

15991001

 

[PubMed - indexed for MEDLINE]

Catuaba Extract 4:1 - 60 500mg VegiCaps - Stearate Free, Bottled in Glass

PHARMACEUTICAL DOPAMINE REUPTAKE INHIBITORS

BUY ANTI DEPRESSANT WELLBUTRIN ONLINE. CLICK IMAGE BELOW TO GO TO SITE IT'S BY THE PILL, SO YOU CAN BUY ONE, FIVE OR 100.

Symptoms and Signs of Serotonin 5-HT1A Receptor OVER-ACTIVATION & Activity / Too Much 5-HT1A

:::::::::::::::::::::NOTE::::::::::::::::::::::::

By no means are these symptoms ONLY caused by 5-HT1A activation, and there are indeed, many causes of too much 5-HT1A activation, this article should only be a reference point to compare a SET OF SYMPTOMS with your own - but one should not assume that this is the reason without corresponding bloodwork/urine screening; AT LEAST ON 5-H1AA ( a serotonin metabolite) - to determine if the autoreceptor inhibition of serotonin release is the issue. However, this does not mean that you can't have high serotonin levels and 5-ht1A activation, because it doesn't necessarily translate to peripheral or liver related degradation of serotonin - which is handled by monoamine oxidase and other enzymes.

:::::::::::::::::::::NOTE::::::::::::::::::::::::

The symptoms of serotonin 5-HT1A overactivation would be summarized as follows.

• ANTICIPATORY ANXIETY; e.g "can't wait for" behavior, impatient in lines, awaiting the arrival of goods causing anxiety, or anxiously awaiting paycheck. (part of why serotonin can cause anxiety)
• Emotional dampening; bluntness,shallow faced, expressionless, indifferent. This is because of serotonin 5-hT1A's interactions with the opioidergic systems, as well inhibition of amygdala dopamine and glutamate activity which normally act to facilitate these emotions.
• Low / Slow Sexual response, low libido, delayed ejaculation, erectile dysfunction, hypoactive sexual desire/arousal in women.
• LONG-TERM MEMORY PROBLEMS, PROBLEMS WITH CONCENTRATION, ESPECIALLY IN ACTIVE MEMORY, AND MEMORY CONSOLIDATION TASKS.
• PARADOXICAL AGGRESSION, NORMALLY THIS RECEPTOR IS ANTI AGGRESSIVE ITSELF, BUT....BECAUSE IT IS AN AUTORECEPTOR, IT MAY ACTUALLY INCREASE AGGRESSION BY LOWERING OTHER NEUROTRANSMITTERS THAT ACT TO INHIBIT IT.