33 replies to this topic

[Pereise1]

interesting info, thanks for sharing this. so nootropics depot has some good stuff? ive tried other stuff from them and they have been inconsistent. one time i get good quality stuff that works, other times not at all. i questioned them but they were reluctant to deny any problems. otherwise good point you have to try so many types of brands and extracts to know the real deal and it sucks it will cost money :(

 

I've personally had pretty good results with Nootropics Depot and their sister company Ceretropic. Unfortunately, most of their stuff is simply out of my price range at the current moment. As an update, the Tibetan Cordyceps from Paradise Herbs is some garbage, easily the weakest out of all the extracts I've bought. On the way, I spent a few hours of a "busy" work day recently reading up on Cordyceps, and it seems that Cordyceps Militaris is far superior to cultivated Cordyceps Sinesis, both in Cordycepin content and in antioxidant potential:

 

 

Comparison of protective effects between cultured Cordyceps militaris and natural Cordyceps sinensis against oxidative damage.

Abstract

The Chinese herb DongChong-XiaCao originating from Cordyceps sinensis is widely used as a traditional medicine in China for treatment of a wide variety of diseases. The extracts of Cordyceps sinensis (CSE) and Cordyceps militaris (CME) are well-known for their biological effects. In the present study, the antioxidant efficiency of CME and CSE in protecting lipid, protein, and low-density lipoprotein (LDL) against oxidative damage was investigated. CME and CSE showed weakly inhibitory effect on liposome oxidation, that of CME being superior to that of CSE. As for the protein oxidation model system, the inhibitory effect of CME on protein oxidation was inferior to that of CSE. CME and CSE at 1.0 mg/mL showed 50.5 and 67.1% inhibition of LDL oxidation, respectively. The contents of bioactive ingredients cordycepin and adenosine in CME are higher than those of CSE; however, both cordycepin and adenosine showed no significant antioxidant activity as determined by the Trolox equivalent antioxidant capacity method. Polyphenolic and flavonoid contents are 60.2 and 0.598 microg/mL in CME and 31.8 and 0.616 microg/mL in CSE, respectively, which may in part be responsible for their antioxidant activities. In addition, a polysaccharide present in CME and CSE displayed antioxidant activity, which suggested that the activity might be derived partly from polysaccharides of CME and CSE. The tendency to scavenge the ABTS(*)(+) free radical and the reducing ability of CME and CSE display concentration-dependent manners, suggesting that CME and CSE may be potent hydrogen donators. On the basis of the results obtained, the protective effects of CME and CSE against oxidative damage of biomolecules are a result of their free radical scavenging abilities.

 

 

With that in mind, I have the this cordyceps militaris extract from ebay coming in today, will report back on that. As an aside, and to keep this on topic, I've realized in what way my past mold exposure is probably messing with my brain regeneration efforts. The clavine type alkaloids, which are the most probable alkaloids in my brain as Aspergillus is the most probable mold type in question here, have numerous actions in the brain. It seems to be a hyperactivation and induced hypersensitivity of the presynaptic D2 receptors and D2-5HT2A heterodimer as well as the a1 adrenergic receptors: 

Ergot Alkaloids as Ligands

→ source (external link)

.

 

Excessive activation of the D2 receptor is bad for neuroregeneration, as per the following abstract:

 

 

Striatal D2 receptors regulate dendritic morphology of medium spiny neurons via Kir2 channels Abstract

Structural plasticity in the adult brain is essential for adaptive behaviors and is thought to contribute to a variety of neurological and psychiatric disorders. Medium spiny neurons of the striatum show a high degree of structural plasticity that is modulated by dopamine through unknown signaling mechanisms. Here, we demonstrate that over-expression of dopamine D2 receptors in medium spiny neurons increases their membrane excitability and decreases the complexity and length of their dendritic arbors. These changes can be reversed in the adult animal after restoring D2 receptors to wild-type levels, demonstrating a high degree of structural plasticity in the adult striatum. Increased excitability and decreased dendritic arborization are associated with down-regulation of inward rectifier potassium channels (Kir2.1/2.3). Down-regulation of Kir2 function is critical for the neurophysiological and morphological changes in vivobecause virally-mediated expression of a dominant negative Kir2 channel is sufficient to recapitulate the changes in D2 transgenic mice. These findings may have important implications for the understanding of basal ganglia disorders, and more specifically schizophrenia, in which excessive activation of striatal D2 receptors has long been hypothesized to be of pathophysiologic significance.

 

 

 

 

Although it seems to be a little more complicated than that (as everything), as simultaneous D2/D3 (possibly postsynaptic vs. presynaptic) actually increases dendrite arborization:

 

 

Dopamine D3 receptor-preferring agonists increase dendrite arborization of mesencephalic dopaminergic neurons via extracellular signal-regulated kinase phosphorylation.

Abstract

Clinical improvements in Parkinson's disease produced by dopamine D3 receptor-preferring agonists have been related to their neuroprotective actions and, more recently, to their neuroregenerative properties. However, it is unclear whether dopamine agonists produce their neurotrophic effects by acting directly on receptors expressed by the mesencephalic dopaminergic neurons or indirectly on receptors expressed by astrocytes, via release of neurotrophic factors. In this study, we investigated the effects of the dopamine D3 receptor-preferring agonists quinpirole and 7-hydroxy-N,N-di-propyl-2-aminotetralin (7-OH-DPAT), as well as of the indirect agonist amphetamine, on dopaminergic neurons identified by tyrosine hydroxylase immunoreactivity (TH-IR). Experiments were performed on neuronal-enriched primary cultures containing less than 0.5% of astrocytes prepared from the mouse embryo mesencephalon. After 3 days of incubation, both quinpirole (1-10 microm) and 7-OH-DPAT (5-500 nm) dose-dependently increased the maximal dendrite length (P < 0.001), number of primary dendrites (P < 0.01) and [3H]dopamine uptake (P < 0.01) of TH-IR-positive mesencephalic neurons. Similar effects were observed with 10 microm amphetamine. All neurotrophic effects were blocked by the unselective D2/D3 receptor antagonist sulpiride (5 microm) and by the selective D3 receptor antagonist SB-277011-A at a low dose (50 nm). Quinpirole and 7-OH-DPAT also increased the phosphorylation of extracellular signal-regulated kinase (ERK) within minutes, an effect blocked by pretreatment with SB-277011-A. Inhibition of the D2/D3 receptor signalling pathway to ERK was obtained with PD98059, GF109203 or LY294002, resulting in blockade of neurotrophic effects. These data suggest that dopamine agonists increase dendritic arborizations of mesencephalic dopaminergic neurons via a direct effect on D2/D3 receptors, preferentially involving D3 receptor-dependent neurotransmission.

 

 

[normalizing]

can you not forget to report your results from the cordyceps you ordered off ebay thanks im curious.

but you say you have good experience from nootropics depot, why not order their cordyceps if you really think its reliable? personally, i didnt really notice much, but then again, cordyceps is one of the most diluted herbs out there, chance of scoring good quality is hitting the lotto

[Pereise1]

can you not forget to report your results from the cordyceps you ordered off ebay thanks im curious.

but you say you have good experience from nootropics depot, why not order their cordyceps if you really think its reliable? personally, i didnt really notice much, but then again, cordyceps is one of the most diluted herbs out there, chance of scoring good quality is hitting the lotto

 

Just wanted to update, I had good results from the ebay seller, which goes by "Mushroom Shen". I bought both Cordyceps and Duanwood Reishi off of them, and both but especially the Reishi were quite potent at 2g+.

 

To keep things on topic however, I was curious about Risperidone, as it seems to potently increase slow wave sleep, which is when a huge chunk of Neurogenesis takes place:

 

 

 

Abstract

The effects of risperidone, a new antipsychotic with potent 5-hydroxytryptamine2 (5-HT2) and dopamine-D2 (DA-D2) antagonistic properties, were studied on sleep-wakefulness patterns in rats. Administration of low doses (0.01–0.16 mg/kg i.p.) resulted in a significant increase of deep slow wave sleep (SWS2) and a decrease of wakefulness (W) and light slow wave sleep (SWSl). High doses (0.63–2.5 mg/kg) produced opposite effects. Paradoxical sleep (PS) was significantly reduced over the dose range tested. The increase of SWS2 after low doses of risperidone could be related to a predominant and potent 5-HT2 receptor blocking activity.

 

 

 

So a really good combination before bed should be something like low dose Risperidone and a Sigma receptor agonist, per the following studies:

 

 

Captodiamine, a putative antidepressant, enhances hypothalamic BDNF expression in vivo by synergistic 5-HT2c receptor antagonism and sigma-1 receptor agonism.

Abstract

The putative antidepressant captodiamine is a 5-HT2c receptor antagonist and agonist at sigma-1 and D3 dopamine receptors, exerts an anti-immobility action in the forced swim paradigm, and enhances dopamine turnover in the frontal cortex. Captodiamine has also been found to ameliorate stress-induced anhedonia, reduce the associated elevations of hypothalamic corticotrophin-releasing factor (CRF) and restore the reductions in hypothalamic BDNF expression. Here we demonstrate chronic administration of captodiamine to have no significant effect on hypothalamic CRF expression through sigma-1 receptor agonism; however, both sigma-1 receptor agonism or 5-HT2c receptor antagonism were necessary to enhance BDNF expression. Regulation of BDNF expression by captodiamine was associated with increased phosphorylation of transcription factor CREB and mediated through sigma-1 receptor agonism but blocked by 5-HT2c receptor antagonism. The existence of two separate signalling pathways was confirmed by immunolocalisation of each receptor to distinct cell populations in the paraventricular nucleus of the hypothalamus. Increased BDNF induced by captodiamine was also associated with enhanced expression of synapsin, but not PSD-95, suggesting induction of long-term structural plasticity between hypothalamic synapses. These unique features of captodiamine may contribute to its ability to ameliorate stress-induced anhedonia as the hypothalamus plays a prominent role in regulating HPA axis activity.

 

ABSTRACT

Sigma-1 receptors (Sig-1Rs) are endoplasmic reticulum (ER)-resident proteins known to be involved in learning and memory. Dendritic spines in hippocampal neurons play important roles in neuroplasticity and learning and memory. This study tested the hypothesis that Sig-1Rs might regulate denritic spine formation in hippocampal neurons and examined potential mechanisms therein. In rat hippocampal primary neurons, the knockdown of Sig-1Rs by siRNAs causes a deficit in the formation of dendritic spines that is unrelated to ER Ca2+ signaling or apoptosis, but correlates with the mitochondrial permeability transition and cytochrome c release, followed by caspase-3 activation, Tiam1 cleavage, and a reduction in Rac1·GTP. Sig-1R-knockdown neurons contain higher levels of free radicals when compared to control neurons. The activation of superoxide dismutase or the application of the hydroxyl-free radical scavenger N-acetyl cysteine (NAC) to the Sig-1R-knockdown neurons rescues dendritic spines and mitochondria from the deficits caused by Sig-1R siRNA.

 

 

Edited by Pereise1, 15 September 2017 - 04:36 PM.

[normalizing]

so the mushrooms you brought were wild harvested and not commercial product sold by the guy who made the product? im surprised its potent and good, but then maybe because its wild product and not cultivated??