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The Role of Hypothalamic Neuropeptides in Neurogenesis and Neuritogenesis

hypos peptides and neuritos

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#1 medievil

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Posted 27 February 2016 - 01:50 PM


Another find on reddit which ppl may like to discuss here

 

The Role of Hypothalamic Neuropeptides in Neurogenesis and Neuritogenesis  
 

The hypothalamus is a source of neural progenitor cells which give rise to different populations of specialized and differentiated cells during brain development. Newly formed neurons in the hypothalamus can synthesize and release various neuropeptides. Although term neuropeptide recently undergoes redefinition, small-size hypothalamic neuropeptides remain major signaling molecules mediating short- and long-term effects on brain development. They represent important factors in neurite growth and formation of neural circuits. There is evidence suggesting that the newly generated hypothalamic neurons may be involved in regulation of metabolism, energy balance, body weight, and social behavior as well. Here we review recent data on the role of hypothalamic neuropeptides in adult neurogenesis and neuritogenesis with special emphasis on the development of food intake and social behavior related brain circuits.

 
Abstract

 

 
Hmm the abstract doesnt copy in here for some reason, clicking well have to do then
 
 
Abstract

The hypothalamus is a source of neural progenitor cells which give rise to different populations of specialized and differentiated cells during brain development. Newly formed neurons in the hypothalamus can synthesize and release various neuropeptides. Although term neuropeptide recently undergoes redefinition, small-size hypothalamic neuropeptides remain major signaling molecules mediating short- and long-term effects on brain development. They represent important factors in neurite growth and formation of neural circuits. There is evidence suggesting that the newly generated hypothalamic neurons may be involved in regulation of metabolism, energy balance, body weight, and social behavior as well. Here we review recent data on the role of hypothalamic neuropeptides in adult neurogenesis and neuritogenesis with special emphasis on the development of food intake and social behavior related brain circuits.


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#2 medievil

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Posted 27 February 2016 - 03:12 PM

Is it me or are there less people posting here then there used to be? seems like im all over the place here while i allways used to post this much.



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#3 medievil

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Posted 27 February 2016 - 07:25 PM

Why does this forum label me a irresponsible drug addict? for years ive studied the effects of drug abuse and have been posting harm reduction information with regards to most drugs such as the use of memantine for tolerance, i was the first on bluelight to post that GHB is neurotoxic, before that everyone kept assuming it was not.

 

All the advice i give here can be backed up with references and the latest researchm while maybe i do take drugs in a irresponsible way sometimes that is my business, and is not something i promote in any way, in fact ive allways used harm reduction and got away with years of drug addiction without any long term side effects, that said when i am being prescribed dexamphetamine my drug abuse vanishes and i turn into a weekly recreational drug user which ive allways been untill i triggered unbearable anhedonia with test due to triggeriing shizophrenia.

 

I know many drug abusers which are irresponsible and they dont compare to me as they dont practice strategies with regards to harm reduction.

 

I made a mistake of trying to sell meds here which got screwed up but that hasnt got any relevance to my drug use.

 

Whoever labeled me this should explain to me why exactly, and what is so irresponsible to my drug abuse? i beleive with targetting the issues of drugs, tolerance and withdrawals while using the side effects experienced to provide harm reduction information to others is not irresponsible, so id like to hear the rationale behind this, im sure it is someone that takes nootropic combos that have no science behind them and provide advice they have red somewhere on the get smart with nuutropics and become a genius supersite.



#4 medievil

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Posted 27 February 2016 - 07:35 PM

I bet its one of those guys recommending choline sources with racetams while it should be know by know that racetams dont need choline sources and that those can induce depression, which mister responsible probably doesnt warn about, also piracetam actually reduces choline content, in that aspect increased choline can be beneficial but here people sometimes make out that adding a choline source is something which somehow activates racetams and makes them effectiven..lol.

 

Come out mister responsible and lets take a look at the advices and scientific information here post.

 



#5 playground

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Posted 27 February 2016 - 08:29 PM

nice find Medi-Evil.

 

Readers of this thread my download the full-text of the author's more recent version

of this paper by visiting this link:  (Dated January 2016)

https://www.research..._Neuritogenesis

 

I love this idea that the hypothalmus acts as a progenitor of new neurons both during early neonatal development __and__ into *adulthood*.

And hence is a source of neurogenesis in _adult_ brains. 

The implications for dementia and TBI (Traumatic Brain Injury) patents is obvious.

 

So the obvious question is, how do you stimulate this hypothalamus neurogenesis ?

See Table 1.

The key entry is towards the bottom: 

Corticotrophin-releasing hormone

We have a recombinant version of this hormone called corticorelin

(See wikipedia)

 

 

 



#6 gamesguru

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Posted 27 February 2016 - 10:06 PM

this opens new leads, with specific strategies.



#7 playground

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Posted 28 February 2016 - 08:03 AM

After sleeping on this article.  I woke up this morning with new eyes.

 

The article makes reference to this website:

 

     www.neuropeptides.nl

 

The front page notes this:

 


 

Neuropeptides are small protein-like molecules used by neurons to communicate with each other. They are neuronal signaling molecules. The brain largely functions by virtue of neuropeptides.

Neuropeptides are expressed and released by neurons, and mediate or modulate neuronal communication by acting on cell surface receptors. The human genome contains about 90 genes that encode precursors of neuropeptides. Neuropeptides can be clustered in at least 10 subfamilies according to structural feature

The Neuropeptide Database is the internet resource to data about all known neuropeptides, their genes, precursors and expression in the brain.

 

 

Inside the database you can see families of neuropeptides.

See here:

 

http://www.neuropept...ides linked.htm

 

If it is true, as the blurb above says, that neuropeptides are the means of intra-brain communication.

Then all we need to do is figure out which neuropeptides carry a 'neurogenesis' message.

 

With my new eyes, this morning, I've come to these perspectives.

 

1.  We need the neuropeptide equivalent of human growth hormone(HGH).

Why ? 

(a) Because HGH is the master 'growth' switch. Every other growth factor

or co-factor is created _because_ the HGH signal was sent somewhere up stream.

(b) Because if you look at a graph of human growth hormone production

it looks exactly like a graph of human neurogenesis throughout life.

Massive amounts are produced prior to birth, then gradually less and less

throughout life.  This is also the pattern for neurogenesis.

So, prime face, HGH is causing, directly or indirectly, neurogenesis.

 

See the graph below:

 

http://postimg.org/image/y78jcjn7r/

 

2.  The neuropeptides that are closely associated with HGH are IGF-1 and IGF-2.

IGF-1 controls growth in adults. 

IGF-2 controls growth in infants.

Neurogenesis is off the scale in neonates.

Neurogenesis is marginal in adults.

The most promising candidate as an agent of neurogenesis is IGF-2.

 

IGF-1 and IGF-2 are both available commercially.

IGF-1 == Somatomedin C.

IGF-2 == Somatomedin A.

(Makes me wonder what Somatomedin B is)

 

I found this abstract on PubMed:

 

Emerging evidence of insulin-like growth factor 2 as a memory enhancer: a unique animal model of cognitive dysfunction with impaired adult neurogenesis.

Abstract

In the current aging society, cognitive dysfunction is one of the most serious issues that should be urgently resolved. It also affects a wide range of age groups harboring neurological and psychiatric disorders, such as Alzheimer's disease and schizophrenia. Although the molecular mechanism of memory impairment still remains to be determined, neuronal loss and dysfunction has been revealed to mainly attribute to its pathology. The discovery of neural stem cells in the adult brain that are proliferating and able to generate functional neurons has given rise to the idea that neuronal loss could be rescued by manipulating endogenous neural progenitor and stem cells. To this end, we must characterize them in detail and their developmental programming must be better understood. A growing body of evidence has indicated that insulin-like peptides are involved in learning and memory and maintenance of neural progenitor and stem cells, and clinical trials of insulin as a memory enhancer have begun. In contrast to the expectation of insulin and IGF1, the roles of IGF2 in cognitive ability have been poorly understood. However, recent evidence demonstrated in rodents suggests that IGF2 may play a pivotal role in adult neurogenesis and cognitive function. Here, we would like to review the rapidly growing world of IGF2 in cognitive neuroscience and introduce the evidence that its deficit is indeed involved in the impairment of the hippocampal neurogenesis and cognitive dysfunction in the model mouse of 22q11.2 deletion syndrome, which deletes Dgcr8, a critical gene for microRNA processing.

 

 

I would really, really like to read the full text of this paper.

Can someone, anyone, please help with that ?

I would be very grateful :)

 

Here's another article:

 

IGF2 ameliorates amyloidosis, increases cholinergic marker expression and raises BMP9 and neurotrophin levels in the hippocampus of the APPswePS1dE9 Alzheimer's disease model mice.
Abstract

The development of an effective therapy for Alzheimer's disease (AD) is a major challenge to biomedical sciences. Because much of early AD pathophysiology includes hippocampal abnormalities, a viable treatment strategy might be to use trophic factors that support hippocampal integrity and function. IGF2 is an attractive candidate as it acts in the hippocampus to enhance memory consolidation, stimulate adult neurogenesis and upregulate cholinergic marker expression and acetylcholine (ACh) release. We performed a seven-day intracerebroventricular infusion of IGF2 in transgenic APPswe.PS1dE9 AD model mice that express green fluorescent protein in cholinergic neurons (APP.PS1/CHGFP) and in wild type WT/CHGFP littermates at 6 months of age representing early AD-like disease. IGF2 reduced the number of hippocampal Aβ40- and Aβ42-positive amyloid plaques in APP.PS1/CHGFP mice. Moreover, IGF2 increased hippocampal protein levels of the ACh-synthesizing enzyme, choline acetyltransferase in both WT/CHGFP and APP.PS1/CHGFP mice. The latter effect was likely mediated by increased protein expression of the cholinergic differentiating factor, BMP9, observed in IGF2-treated mice as compared to controls. IGF2 also increased the protein levels of hippocampal NGF, BDNF, NT3 and IGF1 and of doublecortin, a marker of neurogenesis. These data show that IGF2 administration is effective in reversing and preventing several pathophysiologic processes associated with AD and suggest that IGF2 may constitute a therapeutic target for AD.

 

 

I think IGF-2 is a promising neuropeptide to consider with regard to hypothalamic neurogenesis.

 

I would like to know what a graph of IGF-2 looks like... that is, over the course of a person's lifetime.

I found a graph of IGF-1 earlier.  It basically peaks at age 20-ish.. and then fades away.

(A bit like a graph of testosterone production in men)

 

I'm guessing that the graph of IGF-2 production, looks like a graph of HGH production. 

It peaks at birth and then falls away towards the Y-axis until death.

If anyone can find such a graph, i would be very grateful if you could post it to this thread. :)

 

The next questions are: 

 

1. Is it possible to take IGF-2 intranasally, via some spray or perhaps a saline solution ?

(As you would with NGF, for example).

 

2. How much is Somatomedin A ? 

 

3. Where can it be purchased from ?

 

 

Attached Files


Edited by playground, 28 February 2016 - 09:02 AM.


#8 chemicalambrosia

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Posted 28 February 2016 - 06:01 PM

Why does this forum label me a irresponsible drug addict? for years ive studied the effects of drug abuse and have been posting harm reduction information with regards to most drugs such as the use of memantine for tolerance, i was the first on bluelight to post that GHB is neurotoxic, before that everyone kept assuming it was not.

 

All the advice i give here can be backed up with references and the latest researchm while maybe i do take drugs in a irresponsible way sometimes that is my business, and is not something i promote in any way, in fact ive allways used harm reduction and got away with years of drug addiction without any long term side effects, that said when i am being prescribed dexamphetamine my drug abuse vanishes and i turn into a weekly recreational drug user which ive allways been untill i triggered unbearable anhedonia with test due to triggeriing shizophrenia.

 

I know many drug abusers which are irresponsible and they dont compare to me as they dont practice strategies with regards to harm reduction.

 

I made a mistake of trying to sell meds here which got screwed up but that hasnt got any relevance to my drug use.

 

Whoever labeled me this should explain to me why exactly, and what is so irresponsible to my drug abuse? i beleive with targetting the issues of drugs, tolerance and withdrawals while using the side effects experienced to provide harm reduction information to others is not irresponsible, so id like to hear the rationale behind this, im sure it is someone that takes nootropic combos that have no science behind them and provide advice they have red somewhere on the get smart with nuutropics and become a genius supersite.

 

I'm pretty sure they gave you that label because you took people's money and ripped them off. The label is probably there to make it so that is less likely to happen again. Most forums would ban someone for ripping off other members. I would take it as a sign of respect for your contributions over the years that you have a label under your name instead of being banned.
 



#9 medievil

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Posted 28 February 2016 - 06:57 PM

I never ment to rip ppl off, i actually intended to send ppl those meds as under the nhs under a differened name i managed to get meds for free under its unsurance, but i could never afford enough stims and collapsed in episodes of anhedonia, also i tought i could pull this off because of cognitive impairment with shizophrenia, but then i ended in situation where i collapsed in brain torture again and had no choice to use the money for stims, but i know ppl dont understand the pain i go trough with my shizophrenia induced anhedonia, it would lead most ppl to suicide if they dont find a treatment, hence the suicide rate in shizo is 10% while most are mostly suffering from positives not negatives.

 

im not someone that rips ppl off, i would never intend to do something terrible like that, i dedicate my time to helping ppl with advice and other things, and i want to pay ppl bacl but the nhs putting me in a position of having to self medicate with expensive stimulant rcs makes it difficould, also im not an addict when i have dex prescribed, having to self medicate with powders turns me into one.

 

I do understand the reasening behind it, but ppl here know what i did and im alot less impaired to come with ideas like that as its impossible to pull off, i couldnt think far enough that i can make up so many fake names and register with docs to get the meds i wanted to sell, also im banned from all surgerys now because the healthcare system cought up with me.

 

if ppl could feel my pain theyd understand more, as i have the impression i take stims because of addiction, no im forced too to avoid absolute horror wich i can only get trough by trying to sleep all day and lie in bed



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#10 playground

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Posted 28 February 2016 - 09:06 PM

nice find Medi-Evil.

 

Readers of this thread my download the full-text of the author's more recent version

of this paper by visiting this link:  (Dated January 2016)

https://www.research..._Neuritogenesis

 

I love this idea that the hypothalmus acts as a progenitor of new neurons both during early neonatal development __and__ into *adulthood*.

And hence is a source of neurogenesis in _adult_ brains. 

The implications for dementia and TBI (Traumatic Brain Injury) patents is obvious.

 

So the obvious question is, how do you stimulate this hypothalamus neurogenesis ?

See Table 1.

The key entry is towards the bottom: 

Corticotrophin-releasing hormone

We have a recombinant version of this hormone called corticorelin

(See wikipedia)

 

Here's a paper that specifically talks about the neurogenesis in connection with Corticotrophin Releasing Hormone.

 

Corticotropin-releasing hormone exerts direct effects on neuronal progenitor cells: implications for neuroprotection.

Koutmani Y1, Politis PK, Elkouris M, Agrogiannis G, Kemerli M, Patsouris E, Remboutsika E, Karalis KP.

 

Neurogenesis during embryonic and adult life is tightly regulated by a network of transcriptional, growth and hormonal factors. Emerging evidence indicates that activation of the stress response, via the associated glucocorticoid increase, reduces neurogenesis and contributes to the development of adult diseases.As corticotrophin-releasing hormone (CRH) or factor is the major mediator of adaptive response to stressors, we sought to investigate its involvement in this process. Accordingly, we found that CRH could reverse the damaging effects of glucocorticoid on neural stem/progenitor cells (NS/PCs), while its genetic deficiency results in compromised proliferation and enhanced apoptosis during neurogenesis. Analyses in fetal and adult mouse brain revealed significant expression of CRH receptors in proliferating neuronal progenitors. Furthermore, by using primary cultures of NS/PCs, we characterized the molecular mechanisms and identified CRH receptor-1 as the receptor mediating the neuroprotective effects of CRH. Finally, we demonstrate the expression of CRH receptors in human fetal brain from early gestational age, in areas of active neuronal proliferation. These observations raise the intriguing possibility for CRH-mediated pharmacological applications in diseases characterized by altered neuronal homeostasis, including depression, dementia, neurodegenerative diseases, brain traumas and obesity.

 






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