45 replies to this topic

[medievil]

Fendiline as first example is a positive GABAB modulater (PAM) like benzo's are gabaa pam's, its a calcium channel blocker.


Will keep updating this thread, also will add threads about the differened channels like the calcium channels, what they do and the therapeutic implications.


Dipyridamole is a GABA increases because of its adenosing reuptake inhibition, its also a global PDE inhibitor that increases, cAMP, cGMP and nitric oxide, it has anxiolytic, neuroprotective, cognitive enhancing effects and more, ppl should try it in the cilltep stack. Cafeine reverses the effects of adenosing reuptake if you are not interested in that.

Its otc here so ppl can buy it off me if anyone is interested, be quick tough limited offer.

I use it in my regime and it definatly enhances learning wich is good, i need to have a shitload of info for the site i want next to my future shop to attract customers hehe, it can all still take awhile but knowledge will make me money in the future.

Edited by medievil, 28 February 2013 - 08:12 PM.

[medievil]

[Effect of neuroleptics and antidepressants on the process of gamma-aminobutyric acid-H3 uptake by isolated rat brain nerve endings].

[Article in Russian]
Raevskiĭ KS, Maĭsov NI.

Abstract

The effects of phenothiazine neuropleptics--chlorpromazine, trifluoperazine, fluphenazine and of antidepressants-imipramine and phthoracizine on theGABA-H3 accumulation by synaptosomes of the rat cerebral cortex were studied. All neuroleptics were found to inhibit the process of neurotransmitter uptake by the brain synaptosomes. Antidepressants were less potent. Chlorpromazine had the highest inhibitory effect on GABAuptake and phthoracizine--the lowest. It is suggested that the influence of neurolptics on GABA uptake could play a certain role in the mode of a synaptic action of these drugs.

Farmakol Toksikol. 1975 Sep-Oct;38(5):537-40.
[Effect of psychotropic substances on the uptake of [H3]-gamma-aminobutyric acid by rat brain synaptosomes].

[Article in Russian]
Maĭsov NI, Tolmacheva NS, Raevskiĭ KS.

Abstract

The in vitro effects of some neuroleptics and antidepressants on the accumulation of [3H]/-GABA by the synaprosomes of the rat brain cortex were studied. Chloropromazine, trifluoperazine, fluphenazine, perphenazine, thioproperazine, haloperidol, trifluperidol, droperidol, imipramine, haloanison and phthoracyzine were found (in order of a decreasing activity) to inhibit the [3H]/-GABA uptake of synaptosomes. Neuroleptics, except for a new drug carbidine, proved to be more potent inhibitors than antidepressants are. The tranquilized diazepan failed to have any effect on the [3H]/-GABAuptake. The rats synaptosomes treated with chlorpromazine and imipramine were found to display a decreased ability to accumulate [3H]/-GABA. The suppressive effect of psychotropic agents on the [3H]/-GABA uptake by synaptosomes is suggested to be due, at least partly, to their known inhibitory influence on the Na+, K+-dependent ATPase.

[The effect of psychotropic substances on synaptosomal uptake of gamma-aminobutyric H3-acid and the activity of Na,K-ATPase].

[Article in Russian]
Maĭsov NI, Sandalov IuG, Glebov RN, Raevskiĭ KS.

Abstract

The centrally acting drugs belonging to different groups--fluphenazine, trifluperidol, phthoracyzine, imipramine, diazepam, apomorphine, fentanyl, diphneylhydantoin, nonachlazine displayed in vitro an inhibitory effect on the uptake of gamma-aminobutyric acid by rat brain synaptosomes. A decrease in the activity of synaptosomal Na,K-ATPase was found in most cases. Drugs that failed to alter GABA uptake were as a rule found to be ineffective in relation to the enzyme activity (carbidine, morphine). GABA uptake was not affected by certain drugs inhibiting the Na,K-ATPase activity (azabuperon, tetrabenazine). It is supposed that the drugs used had at least two possible sites of action - Na,K-ATPase itself and hypothetic GABAtransmembrane carrier.

The methylene blue derived neuroleptics, alimemazine does this too and found it quite gabaergic in effects.

[SpawnMoreOverlords]

Interesting...

I'm about to receive a shipment of liquid Baclofen, which is reported to be similar to Phenibut but shorter acting and more reliable in its effects. I especially like the effect gabaergics produce when combined with racetams. Would like to experiment with other gabaB agonists that are not benzos in the future as well.

[medievil]

Baclofen sucks compared to phenibut, imo because it blocks calcium channels and depletes glutamate a property wich phenibut hasnt got im guessing as it feels more like GHB, so i was researching how to hijack that calcium channel blockade.

[medievil]

Muscimol is a direct GABAA agonist.

Valproic acid inhibits gaba breakdown, tiagabine is a gaba reuptake inhibitor, gabatril also increases but makes you blind wich augments the anxiolytic effects as you dont see the ppl that give you anxiety. Lamictal, carbemazine, oxycarbemazepine also inhibit gaba breakdown.

Phenibut is a PEA antagonist, im sure that somehow blocks gabab's depleting effect on glutamate.

[Galaxyshock]

I'm interested in GABA-upregulating substances. Temporary discomfort to feel better later and in the long-run should be a healthier method (well this is how exercising works), in this case if more GABA is desired we should also consider GABA-antagonists or similar modulators. Instead of getting there directly and suffering of rebounds and possible addiction/withdrawals... Kava is interesting as it's supposably both GABAergic anxiolytic and yet induces GABAa-upregulation. We know adaptogens like Ginseng have GABA and Glutamate-modulating activity but not specific information what they exactly do. GABAb-upregulation is another quite poorly studied field. Supposably certain MAOIs and PEA have GABAb-antagonistic activity and are candidates for that.

I'm thinking a combination of GABA-antagonist and an NMDA-antagonist or some different mechanism of action anxiolytic/neuroprotective (Lysine?) could be a long-term therapeutic method for treating anxiety without getting one in substance addiction or withdrawals - it would actually leave the patient better after discontinuatiion..

[medievil]

Ive been using dxm as i needed like 4 tabs of 6mg bromazepam, so far noticed rather dramatic tolerance reduction but can be placebo, either way i got enough with halves or one every 6 hours instead of 4.

Ive been using dxm as i needed like 4 tabs of 6mg bromazepam, so far noticed rather dramatic tolerance reduction but can be placebo, either way i got enough with halves or one every 6 hours instead of 4.

[SpawnMoreOverlords]

Medievil any ideas how those effects that you've mentioned would affect the actual experience taking it, as compared to phenibut ? I've heard a lot of experience reports on it and it seems that people who got positive effects from phenibut also got nearly the same effects from Baclofen. Biggest advantage of baclofen is that it does not produce tolerance as compared to phenibut. Theres very few reports of people who combined baclofen and racetams(While phenibut is super enhanced by racetams for me, and lots of other people), and those who did, report amazing experiences from that combination. Personally I'm going to experiment with it while also being on Piracetam+Noopept and I expect great results from it. I know phenibut + just piracetam produced subtle but crisp euphoria(not unlike mdma, just less intense) and total lack of anxiety - great for socializing, interviews, etc.

Edited by SpawnMoreOverlords, 01 March 2013 - 09:12 PM.

[medievil]

Hmm ive heared alot of ppl saying the opposite, that baclofen isnt recreational like phenibut, it does help a friends depression that only responds to phenibut and GHB, but then without feeling anything, i cant feel baclofen either.

Im shizorelated tough and have lower glutamate levels, so extra depletion may deplete some positives for me too. Keep us updated on your experience.

[MrHappy]

I found a list:

Hypnotics/sedatives (N05C)

GABAA agonists/PAMs:

Barbiturates: Allobarbital, Amobarbital, Aprobarbital, Barbital, Butabarbital, Butobarbital, Cyclobarbital, Ethallobarbital, Heptabarb, Hexobarbital, Mephobarbital, Methohexital, Pentobarbital, Phenallymal, Phenobarbital, Propylbarbital, Proxibarbal, Reposal, Secobarbital, Talbutal, Thiamylal, Thiopental, Vinbarbital, Vinylbital
Benzodiazepines: Brotizolam, Clonazepam, Cinolazepam, Climazolam, Doxefazepam, Estazolam, Flunitrazepam, Flurazepam, Flutoprazepam, Haloxazolam, Loprazolam, Lorazepam,Lormetazepam, Midazolam, Nimetazepam, Nitrazepam, Quazepam, Temazepam, Triazolam
Carbamates: Carisoprodol, Ethinamate, Hexapropymate, Meprobamate, Methocarbamol, Procymate, Tybamate
Neuroactive Steroids: Acebrochol, Allopregnanolone, Alphadolone, Alphaxolone, Eltanolone, Ganaxolone, Hydroxydione, Minaxolone, Org 20599, Org 21465, Tetrahydrodeoxycorticosterone
Nonbenzodiazepines: CL-218,872, Eszopiclone, Indiplon, JM-1232, Lirequinil, Necopidem, Pazinaclone, ROD-188, Saripidem, Suproclone, Suriclone, SX-3228, U-89843A, U-90042, Zaleplon, Zolpidem, Zopiclone
Phenols: Fospropofol, Propofol
Piperidinediones: Glutethimide, Methyprylon, Pyrithyldione, Piperidione
Quinazolinones: Afloqualone, Cloroqualone, Diproqualone, Etaqualone, Mebroqualone, Mecloqualone, Methaqualone, Methylmethaqualone, Nitromethaqualone, SL-164
Volatiles/gases: 2M2B, Acetophenone, Acetylglycinamide chloral hydrate, Centalun, Chloral hydrate, Ethanol (Alcohol), Paraldehyde, Trichloroethanol
Others: Bromide (Lithium bromide, Potassium bromide, Sodium bromide), Chloralose, Chloralodol, Clomethiazole, Dichloralphenazone, Ethchlorvynol, Etomidate, Gaboxadol, Loreclezole, Methylpentynol, Metomidate, Org 25435, Petrichloral, Sulfonmethane, Triclofos, Valerenic acid (Valerian)

GABAB agonists:

1,4-Butanediol, Aceburic acid, GABOB, GHB (Sodium oxybate), GBL, GVL

Edited by MrHappy, 02 March 2013 - 12:05 PM.

[medievil]

Haha yeah those are the obvious one's, atleast the more known direct tranquelisers and its all scattered i was going trough that before to find the rare interesting things too.

[Galaxyshock]

Theanine blocks mGlu1 and thus upregulates GABAB.

http://www.ncbi.nlm....les/PMC2726695/

[medievil]

Why the fuck did no sup company extract muscimol and solled it? it would be the gabaa version of phenibut, another disaster too tough but id like to see it available.

ANy information how i cna extract this safely myself, with the emphasis on safely as it also contains a toxin.

[medievil]

Seems like ppl did it before, wonder how much i could yield out one extraction, wont bother if its not worth it.

[xsiv1]

Seems like ppl did it before, wonder how much i could yield out one extraction, wont bother if its not worth it.

There is some wonderfully intelligent chemists on herbsmaxforum or something like that. I'm sure a moderator there named Toastus would know. They've devised a unique way to extend PEA's effects for far longer than what you'll typically find reading anecdotal reports like combining it with Selegline or Quercetin etc. Anyways, it's something to consider. I myself reacted very positively to Phenibut and it lasted for quite some time..taking it with Piracetam mostly. Sharpness personified. It pooped out and I had to taper off. I've tried Baclofen on several occasions and hate it. It seems like it lacks any of the dopamine agonism that Phenibut possesses. Makes you kind of just flat and dull feeling if not dysphoric. For me, it's completely void of any recreational or nootropic value. It will relax your muscle and possesses anxiolytic qualities. You may not develop the tolerance to it..as phenibut has a very steep tolerance ramp. Unfortunately, unless used sparingly - like Phenibut, Baclofen also possesses dependence qualities and must be tapered off. The one thing about Baclofen, if you're getting it from a pharm, is you typically know it's clean and void of heavy metals etc..otherwise it's crap. It may work nicely when combined with DLPA or the CILTEP regimen, otherwise meh.

[medievil]

Baclofen i like for its anti addictive property's, phenibut been taking a year before allways kept working with stims, on its own never did much for me, cant imagine tapering off, just switch to valiium for a week painless.

Where here has tried valproic acid, does it feel gabaergic and does it take the edge of stims?

[Thorsten3]

Seems like ppl did it before, wonder how much i could yield out one extraction, wont bother if its not worth it.

There is some wonderfully intelligent chemists on herbsmaxforum or something like that. I'm sure a moderator there named Toastus would know. They've devised a unique way to extend PEA's effects for far longer than what you'll typically find reading anecdotal reports like combining it with Selegline or Quercetin etc. Anyways, it's something to consider. I myself reacted very positively to Phenibut and it lasted for quite some time..taking it with Piracetam mostly. Sharpness personified. It pooped out and I had to taper off. I've tried Baclofen on several occasions and hate it. It seems like it lacks any of the dopamine agonism that Phenibut possesses. Makes you kind of just flat and dull feeling if not dysphoric. For me, it's completely void of any recreational or nootropic value. It will relax your muscle and possesses anxiolytic qualities. You may not develop the tolerance to it..as phenibut has a very steep tolerance ramp. Unfortunately, unless used sparingly - like Phenibut, Baclofen also possesses dependence qualities and must be tapered off. The one thing about Baclofen, if you're getting it from a pharm, is you typically know it's clean and void of heavy metals etc..otherwise it's crap. It may work nicely when combined with DLPA or the CILTEP regimen, otherwise meh.

My experience with baclofen mirrors yours, well, the acute effects, anyway. After the dull, flat feeling wears off after some hours, I would then get a euphoric 'rebound' reaction. Not sure what is the cause of this, but is the reason I would only take baclofen in the late evening. I did this so I would then see positive effects the next day. It was a decent anti-depressant, for me, when used this way.

I only tried it a few times, though.

[medievil]

GABAB antagonists are investigated as antidepressants, so kinda makes sense.

[medievil]

Full papers please:
"Curr Pharm Des. 1999 May;5(5):317-43.
Ligands for the benzodiazepine binding site--a survey.
Teuber L, Wätjens F, Jensen LH.
Source
NeuroSearch A/S, 26B Smedeland, Glostrup, DK-2600, Denmark.
Abstract
Gamma-Aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the mammalian Central Nervous System (CNS). GABA participates in the regulation of neuronal excitability through interaction with specific membrane proteins (the GABAA receptors). The binding of GABA to these postsynaptic receptors, results in an opening of a chloride channel integrated in the receptor which allows the entry of Cl- and consequently leads to hyperpolarization of the recipient cell. The action of GABA is allosterically modulated by a wide variety of chemical entities which interact with distinct binding sites at the GABAA receptor complex. One of the most thoroughly investigated modulatory site is the benzodiazepine binding site. The benzodiazepines constitute a well-known class of therapeutics displaying hypnotic, anxiolytic and anticonvulsant effects. Their usefulness, however, is limited by a broad range of side effects comprising sedation, ataxia, amnesia, alcohol and barbiturate potentiation, tolerance development and abuse potential. Consequently, there has been an intensive search for modulatory agents with an improved profile, and a diversity of chemical entities distinct from the benzodiazepines, but with GABA modulatory effects have been identified. The existence of endogenous ligands for the GABAA receptor complex beside GABA has often been described, but their role in the regulation of GABA action is still a matter of controversy. The progress of molecular biology during the last decade has contributed enormously to the understanding of benzodiazepine receptor pharmacology. A total of 14 GABAA receptor subunits have been cloned from mammalian brain and have been expressed/co-expressed in stable cell lines. These transfected cells constitute an important tool in the characterization of subtype selective ligands. In spite of the rapidly expanding knowledge of the molecular and pharmacological mechanisms involved in GABA/benzodiazepine related CNS disorders, the identification of clinically selective acting drugs is still to come."

"Mol Neurobiol. 1998 Aug;18(1):35-86.
The diversity of GABAA receptors. Pharmacological and electrophysiological properties of GABAA channel subtypes.
Hevers W, Lüddens H.
Source
Department of Psychiatry, University of Mainz, Germany.
Abstract
The amino acid gamma-aminobutyric-acid (GABA) prevails in the CNS as an inhibitory neurotransmitter that mediates most of its effects through fast GABA-gated Cl(-)-channels (GABAAR). Molecular biology uncovered the complex subunit architecture of this receptor channel, in which a pentameric assembly derived from five of at least 17 mammalian subunits, grouped in the six classes alpha, beta, gamma, delta, sigma and epsilon, permits a vast number of putative receptor isoforms. The subunit composition of a particular receptor determines the specific effects of allosterical modulators of the GABAARs like benzodiazepines (BZs), barbiturates, steroids, some convulsants, polyvalent cations, and ethanol. To understand the physiology and diversity of GABAARs, the native isoforms have to be identified by their localization in the brain and by their pharmacology. In heterologous expression systems, channels require the presence of alpha, beta, and gamma subunits in order to mimic the full repertoire of native receptor responses to drugs, with the BZ pharmacology being determined by the particular alpha and gamma subunit variants. Little is known about the functional properties of the beta, delta, and epsilon subunit classes and only a few receptor subtype-specific substances like loreclezole and furosemide are known that enable the identification of defined receptor subtypes. We will summarize the pharmacology of putative receptor isoforms and emphasize the characteristics of functional channels. Knowledge of the complex pharmacology of GABAARs might eventually enable site-directed drug design to further our understanding of GABA-related disorders and of the complex interaction of excitatory and inhibitory mechanisms in neuronal processing."

"Vopr Med Khim. 1997 Nov-Dec;43(6):576-83.
[New GABA-A receptor blockers: attempts to find more powerful clozapine-like selective GABA antagonists].
[Article in Russian]
Squires RF, Saederup E.
Source
Nathan S. Kline Institute for Psychiatric Research, Orangeburg, New York 10962, USA.
Abstract
Because clozapine and a number of other antipsychotic, as well as antidepressant drugs selectively block subsets of GABAA receptors, we have routinely screened 1100 compounds since 1983 for GABA antagonistic effects on 35S-TBPS binding, with a view to finding more potent clozapine-like selective GABAA receptor blockers. About 225 GABA antagonists were identified. Among compounds not previously published, four groups of tricyclic compounds (phenothiazines, phenoxazines, acridines and phenazines) contained GABAA receptor blockers, with acridines and oxidized phenothiazines in general being the most potent. Other active groups include cocaine derivatives, xanthines, indoles and phenethylamine derivatives. A large group of miscellaneous structures includes all known GABAA receptor blockers, as well as some antihistamines, antitussives, antimalarial/antiprotozoals, potential antidepressant, and a large non-therapeutic category consisting of diverse chemical structures. The amino steroid R5135 remains the most potent GABAA receptor blocker by far (EC50 = 5.7 nM, delta Bopt = 130%), and is non-aromatic. Pitrazepin, the next-most potent GABAA receptor blocker (EC50 = 360 nM), also fully reverses the inhibitory effect of 1 microM GABA on 35S-TBPS binding, but is 63-fold less potent than R5135. Appropriately positioned amidino groups, ring (aromatic) nitrogen, ether and keto groups can contribute to the potency of GABAA receptor blockade. Clozapine-like selective GABAA receptor blockers with EC50 values in the low nanomolar range remain to be identified. Such compounds may have potent antipsychotic effects."

I greatly reward with points, no idea whats alot too ill do as many characters i can type lol

[xsiv1]

Seems like ppl did it before, wonder how much i could yield out one extraction, wont bother if its not worth it.

There is some wonderfully intelligent chemists on herbsmaxforum or something like that. I'm sure a moderator there named Toastus would know. They've devised a unique way to extend PEA's effects for far longer than what you'll typically find reading anecdotal reports like combining it with Selegline or Quercetin etc. Anyways, it's something to consider. I myself reacted very positively to Phenibut and it lasted for quite some time..taking it with Piracetam mostly. Sharpness personified. It pooped out and I had to taper off. I've tried Baclofen on several occasions and hate it. It seems like it lacks any of the dopamine agonism that Phenibut possesses. Makes you kind of just flat and dull feeling if not dysphoric. For me, it's completely void of any recreational or nootropic value. It will relax your muscle and possesses anxiolytic qualities. You may not develop the tolerance to it..as phenibut has a very steep tolerance ramp. Unfortunately, unless used sparingly - like Phenibut, Baclofen also possesses dependence qualities and must be tapered off. The one thing about Baclofen, if you're getting it from a pharm, is you typically know it's clean and void of heavy metals etc..otherwise it's crap. It may work nicely when combined with DLPA or the CILTEP regimen, otherwise meh.

My experience with baclofen mirrors yours, well, the acute effects, anyway. After the dull, flat feeling wears off after some hours, I would then get a euphoric 'rebound' reaction. Not sure what is the cause of this, but is the reason I would only take baclofen in the late evening. I did this so I would then see positive effects the next day. It was a decent anti-depressant, for me, when used this way.

I only tried it a few times, though.

Very interesting. May I ask what dose you used in the late evening? I have a bunch of it and after using it sparingly a handful of times, I almost discarded it as not for me. I've never tried using it later in the evening though.

[medievil]

A few days ago i found meds that had gabab antagonism as a side effect but completely lost it, will try to find it again, prob therapeutic for you guys.

This is giving me a headache but we can pretty much modulate everything allready, like most antihistamines have something unigue and interesting, try to find it tough haha. Good sometimes my ocd fuels me like crazy with amp.

[xsiv1]

Baclofen i like for its anti addictive property's, phenibut been taking a year before allways kept working with stims, on its own never did much for me, cant imagine tapering off, just switch to valiium for a week painless.

Where here has tried valproic acid, does it feel gabaergic and does it take the edge of stims?

Haven't tried VA, but I must ask, because I had enough valium to kill a horse so I couldn't imagine utilizing it during the day where my work requires critical decision-making and analytical thinking often scrutinizing records of "health service" type patient data. I've never actually found any positive mood-enhancing effect from any benzodiazepine. They all inevitably make me feel tired and sleepy. I've tried, experimentally, slightly higher doses and it only quickened my desire to sleep. I just can't imagine having to use diazepam even for a week to get off phenibut. I got off it anyways but it surely wasn't entirely comfortable. It wasn't horrific either though...quite manageable.

[medievil]

Benzo's dont even make me tired in massive doses, just take the edge of stims or otherwise make me feel neutral during withdrawal, no matter how much i take, like 20mg of xanax or so can make me lose my memory not saying im totally immume.

They dont enhance my mood either just modulate shit or reverse withdrawals, i dont find benzo's recreational, just my cushin in my bed to sleep relaxed instead of on the floor so to speak with amp wich is too harsh on its own.

[medievil]

Eur J Neurosci. 2000 Sep;12(9):3433-6.
Presynaptic inhibition by muscimol through GABAB receptors.

Yamauchi T, Hori T, Takahashi T.

Source

Department of Neurophysiology, University of Tokyo Faculty of Medicine, Hongo, Tokyo 113-0033, Japan.

Abstract

The gamma-aminobutyric acid type A (GABAA) receptor agonist muscimol is widely used as a tool for reducing neuronal activities particularly in experiments in vivo. At the synapse formed by the calyx of Held in the rat brainstem slice, the GABAA receptor agonist muscimol (> 10 microM) attenuated the amplitude of excitatory post synaptic currents (EPSCs) accompanied by an increase in the coefficient of variation of EPSCs, suggesting its presynaptic inhibitory effect. This muscimol effect was not affected by bicuculline but occluded the presynaptic inhibitory effect of the GABAB receptor agonist baclofen and was abolished by the type B GABA (GABAB) receptor-specific antagonist (+)-5, 5-dimethyl-2-morpholineaceticacid (SCH 50911; 20 microM). We conclude that muscimol activates presynaptic GABAB receptors thereby attenuating synaptic transmission.

Muscimol is a gabab agonist! def want to try now as we dont have many of those.

[xsiv1]

Eur J Neurosci. 2000 Sep;12(9):3433-6.
Presynaptic inhibition by muscimol through GABAB receptors.

Yamauchi T, Hori T, Takahashi T.

Source

Department of Neurophysiology, University of Tokyo Faculty of Medicine, Hongo, Tokyo 113-0033, Japan.

Abstract

The gamma-aminobutyric acid type A (GABAA) receptor agonist muscimol is widely used as a tool for reducing neuronal activities particularly in experiments in vivo. At the synapse formed by the calyx of Held in the rat brainstem slice, the GABAA receptor agonist muscimol (> 10 microM) attenuated the amplitude of excitatory post synaptic currents (EPSCs) accompanied by an increase in the coefficient of variation of EPSCs, suggesting its presynaptic inhibitory effect. This muscimol effect was not affected by bicuculline but occluded the presynaptic inhibitory effect of the GABAB receptor agonist baclofen and was abolished by the type B GABA (GABAB) receptor-specific antagonist (+)-5, 5-dimethyl-2-morpholineaceticacid (SCH 50911; 20 microM). We conclude that muscimol activates presynaptic GABAB receptors thereby attenuating synaptic transmission.

Muscimol is a gabab agonist! def want to try now as we dont have many of those.

GabaA no?

Excellent source: http://www.iamshaman...ta-muscaria.htm

Edited by xsiv1, 08 March 2013 - 05:54 PM.

[xsiv1]

Benzo's dont even make me tired in massive doses, just take the edge of stims or otherwise make me feel neutral during withdrawal, no matter how much i take, like 20mg of xanax or so can make me lose my memory not saying im totally immume.

They dont enhance my mood either just modulate shit or reverse withdrawals, i dont find benzo's recreational, just my cushin in my bed to sleep relaxed instead of on the floor so to speak with amp wich is too harsh on its own.

How is your sleep now?

[medievil]

my sleep was allways good never had insomnia in my life.

[medievil]

Above was just a metaphor.

I admit i have to think klonopin with my stims as desoxy is long lasting, klono makes me kinda sedated all day but not overly so i can sleep when i want, still feel energetic too. Sometimes a extra hand wont hurt too tonight ill try chamomile before sleep to induce a faster onset.

[Thorsten3]

Seems like ppl did it before, wonder how much i could yield out one extraction, wont bother if its not worth it.

There is some wonderfully intelligent chemists on herbsmaxforum or something like that. I'm sure a moderator there named Toastus would know. They've devised a unique way to extend PEA's effects for far longer than what you'll typically find reading anecdotal reports like combining it with Selegline or Quercetin etc. Anyways, it's something to consider. I myself reacted very positively to Phenibut and it lasted for quite some time..taking it with Piracetam mostly. Sharpness personified. It pooped out and I had to taper off. I've tried Baclofen on several occasions and hate it. It seems like it lacks any of the dopamine agonism that Phenibut possesses. Makes you kind of just flat and dull feeling if not dysphoric. For me, it's completely void of any recreational or nootropic value. It will relax your muscle and possesses anxiolytic qualities. You may not develop the tolerance to it..as phenibut has a very steep tolerance ramp. Unfortunately, unless used sparingly - like Phenibut, Baclofen also possesses dependence qualities and must be tapered off. The one thing about Baclofen, if you're getting it from a pharm, is you typically know it's clean and void of heavy metals etc..otherwise it's crap. It may work nicely when combined with DLPA or the CILTEP regimen, otherwise meh.

My experience with baclofen mirrors yours, well, the acute effects, anyway. After the dull, flat feeling wears off after some hours, I would then get a euphoric 'rebound' reaction. Not sure what is the cause of this, but is the reason I would only take baclofen in the late evening. I did this so I would then see positive effects the next day. It was a decent anti-depressant, for me, when used this way.

I only tried it a few times, though.

Very interesting. May I ask what dose you used in the late evening? I have a bunch of it and after using it sparingly a handful of times, I almost discarded it as not for me. I've never tried using it later in the evening though.

Sorry bud, this was about two years ago. I cannot recall the dosages. I was taking it in liquid format, but I guess it probably was no more than 50mg. I took it three times, usually around the 18.00 mark. The acute effects were usually quite depressive, but with improvements in certain markers of anxiety. I would then fall asleep and wake up the next day in a great mood. My libido was always elevated too, but this also come with minor sexual dysfunction (nothing dramatic, would just take a while to come sometimes, lol).

For me, the results were interesting because being a former GBL abuser I am more than aware of what horrible rebound effects can occur from the acute GABAB stimulation. However, due to the fact i only used it three times, I don't think I would qualify on giving a positive anecdote to it. For all I know, perhaps you would get into trouble with it, from long term use?

I don't know. I guess baclofen's agonism at GABAB is far less than GHB. As an example, towards the end of my 'GBL abuse era', just one dose of GBL taken in the morning, would give me withdrawal effects lasting into the night (insomina, sweats, aches/cramps). When I trialled baclofen it was during a brief break I had during my GBL period. No side effects from what I could notice. But for all I know, they could have manifested with continued usage.

Edited by Thorsten2, 08 March 2013 - 08:46 PM.

[xsiv1]

Is it weird to know that when I take ephedrine (30mgs) and have a coffee, the crash I experience that occurs just about an hour before bedtime helps me fall asleep faster than on a day that I don't take such a combo before my workout?