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The Big and Bangin' Pseudo-Advanced Drug Chemistry, Pharmacology and More Thread, V.2

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Your body down-regulates how much gaba it needs to make naturally since when benzo's bind to the gaba receptor they enhance the potency/efficacy of natural gaba at doing its job. Less gaba is needed to inhibit while the benzos are acting, and when you discontinue use you are left with a gaba down-regulation that takes a while to return to normal levels. Gaba being the chief inhibitory neurotransmitter in the brain, when heavily down-regulated and abrubtly discontinued can lead to over-activity causing withdrawals, all the way from rebound anxiety to grand mal seizures, and possibly death.

from wiki-

http://en.wikipedia.org/wiki/Benzodiazepine_withdrawal_syndrome
Benzodiazepines potentiate the action of the neurotransmitter GABA. When this potentiation is sustained by long-term use, neuroadaptations occur which result in decreased GABA activity and increased excitability of the glutamate system. When benzodiazepines are stopped, these neuroadaptations are "unmasked", leading to excitability of the nervous system and the appearance of withdrawal symptoms. Increased glutamate excitatory activity during withdrawal is believed to result in kindling phenomena.[82] Those who have a prior history of withdrawing from benzodiazepines are found to be less likely to succeed the next time around.[83] Repeated benzodiazepines withdrawals, like with alcohol withdrawal, may lead to sensitization or kindling of the CNS, possibly leading to worsening cognition and symptomatology and making each subsequent withdrawal period worse.
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In BZD/Barb/alcohol W/D, your GABA-A receptores are insufficiently activated to endogenous GABA. Benzos/barbs (and to some extent alcohol) all make GABA-A receptors *more sensitive* to GABA and so when they are used for a long time your body decreases production. When you withdraw your body's levels of GABA won't be enough to activate receptors properly.

GABA-A is a mian inhibitory neurotransmitter (stops seizures etc and other silly brain activity) so you could see why this would be bad
 
sekio said:
In BZD/Barb/alcohol W/D, your GABA-A receptores are insufficiently activated to endogenous GABA. Benzos/barbs (and to some extent alcohol) all make GABA-A receptors *more sensitive* to GABA and so when they are used for a long time your body decreases production. When you withdraw your body's levels of GABA won't be enough to activate receptors properly.

GABA-A is a mian inhibitory neurotransmitter (stops seizures etc and other silly brain activity) so you could see why this would be bad
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Oh, also, how do the seizures KILL you? The only time I've heard of seizures killing epileptic people is when they happen while the person is driving, crossing a street, or something else dangerous.

And, how about GABA-B? What is that for?
 
The seizures kill you from exhaustion, aspiration of vomit, or respiratory collapse. Or of course from injuries 2nd to it.

GABA-B is a mostly unrelated subclass of receptors that bind GABA as well, but they don't have effects like "classical" sedatives (benzos/barbs) - although they are inhibitory when activated - and lack a benzodiazepine/barbiturate binding site. Example of agonists: phenibut, baclofen.
 
Can you clarify "respiratory collapse"?

I fair amount of people who die from seizure have bitten off their tongue and choked on it too, just adding.

Phenibut does activate GABA-A at high doses from what I can recall.
 
Anybody know why pregabalin at high doses yields some heavy closed eye visuals? This effect has been reported a few times and it tends to be of a movie-like nature in that you can see how themes develop.
 
GHB does something similar for me. They are typically quite colourful, and if they progress past neon RGB static then they're quite realistic. They only come very close to the knockout dose though.
 
Transform said:
GHB does something similar for me. They are typically quite colourful, and if they progress past neon RGB static then they're quite realistic. They only come very close to the knockout dose though.
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It must be something else than the purported GABA analogue property of pregabalin, right? Last I read on pregabalin, it is still not 100% on how it works but I read up on it long time ago. Would love an educated opinion from you guys. I actually decided to try a high dose with no tolerance (500mgs) and 4 hours into the trip I was watching an actual movie (from the CEVs) though I could only hold it for 30-40 mins before I was going into full sleep. NO OEVs though.

I am wondering what sub-receptors and other receptors yield CEVs aside from the typical 5HT sub-receptors.
 
How can one speed up the process of adapting to a natural GABA level post continuous benzo use?

Also

How do the GABA-B receptors effect dopamine?
 
thenightwatch said:
the only CEV i ever got from pregabalin was i shut my eyes and i was magically transported to a beach at night time =p was quite vivd
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LOL. What I got was some stuff similar to static noise on TV which in minutes progressed to objects morphing into other objects (the fuck??) and then it looked like I was watching all of this from a theatre. If I moved my eyes when they were closed, the objects would transform automatically, which makes me think if these CEVs are due to the eye movement which may be caused as one drifts into full sleep (no idea, just suggesting??).

Ive read other people comparing it to ketamine and to me it feels like the CEVs I'd get from a low dose of mushrooms.
 
sekio said:
Not with the classical ones, no
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Does this then suggest as a corollary that tolerance to GABA-agonists (be they allosteric modulators at GABAA or B) is mediated nearly exclusively via receptor downregulation, and not downregulation of the endogenous synthesis of GABA?

ebola
 
From my understanding the mu-G-coupled protein receptor doesn't have the same transporter re-uptake pump system like the monoamines (dopamine, serotonin, norepinephrine) do.
 
There are definitely chemicals that prevent the breakdown of engogenous opioids, not sure how effective they are in man though
 
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