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Heroin Gabapentin blocking/dulling heroin effects

M

mazda01

Bluelighter
Joined
Nov 7, 2015
Messages
121
Curious if anyone else has experienced anything of this sort before. I would normally be good with a few small bumps (corner of credit card) of medium quality H but for the last few days I haven't felt much at all. I've been on a run lately with H (5 days of consecutive use) and had a script for gabapentin that I could fill and when I was anticipating not being able to get anymore H i filled the gaba script and took about 3.2 grams, 1.6g seperated by about an hour for the stacking effect but then I ended up scoring some H. I got really fucked up off the gaba (drunk feeling, stumbling around, etc etc) but when I took some H I didn't end up feeling anything. I went through the whole $20 bag in about 4 hours taking small bumps and never felt a thing from the H.

So the next day I got another $20 worth of H but this time I had only taken 1.6g total of gaba before I did the H and this time felt a little something from the H like euphoria, slight itch etc etc but nothing to what I was feeling when I didn't use gaba at all.

This is really shocking to me because I did check bluelight for answers and most I could find were some people actually saying that gaba potentiated opiates, not block them. SO I am just curious if anyone else has expereinced this or could inform me of why this happened. THanks
 
Folks say gabapentin and pregabalin potentiate opioids/opiates but that's not my experience....if you're naïve or close to naive to those drugs then yeah they'll get you fucked up but there's a difference between feeling multiple drugs stacked together and taking one drug that inhibits an enzyme that metabolizes the other drug hence longer and or stronger action of said drug.

Honestly when I could get euphoria from opioids other drugs like pregabalin, weed and even benzos I found that they would blunt the opiate euphoria which is a subtle euphoria when compared with meth and MDMA in my opinion.
 
Gabapentin does actually have an interaction with morphine, I forget if the gabapentin increases the BA of the morphine, or if the morphine increases gabapentin's BA. The information is in the prescribing effects. Either way, I find Gabapentins' psychoactive properties very uncomfortable feeling and like you said, kind of blunts the effects of the opiate.
 
Could it just be the H? Perhaps your medium grade turned into low grade, or you're doing too much.

Let me explain....
If I wait 6-8 hours between H doses, I feel a rush but if I constantly dose, I plateau, and don't feel squat really.

Perhaps it is the Gaba, but I'd try dosing the H several hours after the initial dose to see if that's the issue.
 
I just experienced this again, i was doing H without any gaba because I went through my script so fast. I was getting nice and high. Well i just got the refill and was doing H yesterday. I wanted to see if it truely was the gaba so i took 900mg of gaba which was 3 hours after my last sniff of 2 tooth pick sized lines of some good H (well it's better than I've had other times I could just tell by the size of lines i needed to get off) Anyway, about 6 hours after my last dose of H (while the 900mg of gaba was kicking in) i snorted some more H, 2 tooth pick sized lines and I didn't really get high. I think the gaba just dulls my senses and I don't get off like I normally would without the gaba.

So im going to keep the gaba for when I need it, when i don't have any H and i'm kicking. It works best for that. Then when I can get some more H (like tomorrow i'll be able to) I won't dose any gaba tomorrow morning and i'll be picking up around noon. Hopefully the gaba will be outta my system but I have taken a lot today. I've taken 900mg 4 different times today total and I plan on taking one more dose of that around 9pm to sleep since I didn't have any dope today and I've been dosing everyday for about a week. Before I got the gaba i was kicking without the H, it was a very light kick but i felt like shit, couldn't sleep, couldn't sit still, running nose, eyes watering, yawning etc etc. It's amazing it only takes a week straight use all day to get physically dependent on this shit. I've used, kicked, used, kicked, used so many times i guess my body is quick to be dependent on this shit. Probably cause i never give my brain time to heal and use it's on endorphins. I don't know, i'm no scientist. lol

Anyway, i just wanted to follow up and let people know in my experience gaba CAN dull the effects of H.
 
In my opinion the a2 adrenergic antagonist properties of gabapentin at 3.2 gram dose would make me feel fine during withdrawals even tired at that . So I think 3.2 grams is such a high dose that the H you're doing doesn't make a difference cause of your adrenals being wacked out idk my theory I'm probably wrong
 
^Kind of going along what the above poster said, I find that with high dosages of gabapentin, the feeling of intoxication would overcome the high of the opiate, which is much subtler/less abrasive. I used to take huge dosages of gabapentin too which would sometimes cause me to feel like I had taken some amphetamine while drunk, and I would try to ease that feeling by using benzo's which never really worked; the gabapentin would basically mask there effects.
 
I think GABAergics, the blunter the better, block some effect of an opiate. I bet having Fioricet with Codeine when you never take it would be awesome. Like take it only on your birthday or Christmas. Somewhere the GABAergic and the opiate/opioid, system cross paths. Either, giving the same effects or doing something similar. Ill experament with this with my next refill of pregabalin. Benzos easily blunt opiate effects. It seems like the GABAergic, is the worse system to mess with.
 
Speed King said:
Benzos easily blunt opiate effects.
Click to expand...
oh this I definitely disagree with, for me benzo's synergize my opiate high. maybe not synergize but it adds to the sedation effect that's for sure. it allows me to nod when I otherwise wouldn't.

and just like I had hoped, i picked up some more H today (same stuff/quality) and didn't take my morning gaba dose and I was able to get high as I normally would from 2 small tooth picked sized lines.
 
There are quite a few possibilities why the gabapentinoids blunt the effects narcotics...

And yeah, benzos are widely accepted as great potentiators for narcotics. The reason I think that gabapentin and other similer GABAergics that don't involve GABAa activity blunt the effect is because of their paradoxical ability to fire action potentials during their hyperpolarizations. All the gabapentinoids do this. Be it the GABAb receptors ligands like baclofen or phenibut, or (I'm of the opinion they affect GABAb but there's no definitive proof they do or don't) pregabalin, and in this case gabapentin.

All of them activate inward rectifying potassium channels - directly or indirectly (GIRK channels and Kir channels but it's unlikely the Kir channels are causing the effects: it's more likely they do actually activate the GABAb GIRK cannel) - which causes great inhibition and hyperpolarization of the cell. But this inhibition brings the voltage just low enough to start firing off specific calcium channels sporadically, allowing for excitatory effects to take place. Low threshold spikes. . This is the reason the GABAb receptor causes stimulating, sometimes hypomanic effects, whilst the GABAa receptor is mostly inhibitory.

I think this is the reason that they blunt the effects of opioids. The mu opioid receptor is also a GIRK channel, but it has no effect on the t type channels itself.

A functional link between T-type calcium channels and mu-opioid receptor expression in adult primary sensory neurons:

(http://www.ncbi.nlm.nih.gov/pubmed/19250340)

Their calcium channel blocking activity probably has something to do with it as well, as the high voltage gated channels are blocked by all of them, inhibiting the release of neurotransmitters including dopamine. That's why they're used as mood stabilizers as well.


Different effects of L-, N- and T-type calcium channel blockers on striatal dopamine release measured by microdialysis in freely moving rats:

http://www.sciencedirect.com/science/article/pii/019701869290072Y

The increase of GABA synthesis and synaptic availability caused by gabapentin probably limits dopamine release in the VTA, since GABA and dopamine are usually coupled together.

Direct link between GABA activation and dopamine suppression:

http://www.news-medical.net/news/20...GABA-activation-and-dopamine-suppression.aspx
 
theGirlWithBlueHair said:
There are quite a few possibilities why the gabapentinoids blunt the effects narcotics...

And yeah, benzos are widely accepted as great potentiators for narcotics. The reason I think that gabapentin and other similer GABAergics that don't involve GABAa activity blunt the effect is because of their paradoxical ability to fire action potentials during their hyperpolarizations. All the gabapentinoids do this. Be it the GABAb receptors ligands like baclofen or phenibut, or (I'm of the opinion they affect GABAb but there's no definitive proof they do or don't) pregabalin, and in this case gabapentin.

All of them activate inward rectifying potassium channels - directly or indirectly (GIRK channels and Kir channels but it's unlikely the Kir channels are causing the effects: it's more likely they do actually activate the GABAb GIRK cannel) - which causes great inhibition and hyperpolarization of the cell. But this inhibition brings the voltage just low enough to start firing off specific calcium channels sporadically, allowing for excitatory effects to take place. Low threshold spikes. . This is the reason the GABAb receptor causes stimulating, sometimes hypomanic effects, whilst the GABAa receptor is mostly inhibitory.

I think this is the reason that they blunt the effects of opioids. The mu opioid receptor is also a GIRK channel, but it has no effect on the t type channels itself.

A functional link between T-type calcium channels and mu-opioid receptor expression in adult primary sensory neurons:

(http://www.ncbi.nlm.nih.gov/pubmed/19250340)

Their calcium channel blocking activity probably has something to do with it as well, as the high voltage gated channels are blocked by all of them, inhibiting the release of neurotransmitters including dopamine. That's why they're used as mood stabilizers as well.


Different effects of L-, N- and T-type calcium channel blockers on striatal dopamine release measured by microdialysis in freely moving rats:

http://www.sciencedirect.com/science/article/pii/019701869290072Y

The increase of GABA synthesis and synaptic availability caused by gabapentin probably limits dopamine release in the VTA, since GABA and dopamine are usually coupled together.

Direct link between GABA activation and dopamine suppression:

http://www.news-medical.net/news/20...GABA-activation-and-dopamine-suppression.aspx
Click to expand...
well damn, now there's some science behind it all. thank you very much for this information.
 
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