Smoking weed may help ease anxiety but it may prove to do the opposite due to the way cannabinoid agonism at CB1 acts as a kind of gain control mechanism within the architecture of neural circuits. CB1 is a presynaptic receptor that exhibits a rather uncommon and unusual manner of signalling. Instead of as happens at most synaptically located receptors (as opposed to e.g glial cells, and receptor-independent signalling through gap-junction channels), Usually the presynaptic neuron releases neurotransmitter in response to receiving sufficient input from the depolarization of other cells summing together until sufficient to trigger the firing of an action potential, which then stimulates that cell's presynaptic receptor in receipt of the action potential targeted by the neurotransmitter in question to release its own signalling neurotransmitters, fire off their own action potentials etc.
The CB1 cannabinoid receptor on the other hand is an oddball. Located presynaptically, CB1Rs activate in response to various different endocannabinoids, often based upon an eicosanoid fatty acid derivative of some sort, although there do exist ones which are not fatty acids. Once released from the postsynaptic neuron the endocannabinoids travel in their rare manner of retrograde transport, back to the presynaptic neuron where they bind and activate CB1, resulting in an overall decrease in neurotransmitter release, of both GABA, the prime inhibitory neurotransmitter, and glutamate, the major excitatory player.
Whilst benzos potentiate the effects of GABA at GABAa receptors, leading to increased conductance and Cl- ion flux through the heteropentameric ion channel, and thereby exerting GABAs inhibitory effect upon neuronal firing with response to excitatory input. This is reduced in benzo dependence, and indeed the downregulation/desensitization/internalization etc. of GABAa receptors and consequent awful effects of benzo WD.
If you cannot obtain a suitable benzo or other GABAa positive modulator (what are usually spoken of as agonists are in fact almost always allosteric positive modulators at GABAa rather than true orthosteric agonists (those which share a binding site with GABA itself, these are actually quite uncommon and the range of such ligands is relatively limited, vastly fewer are known than there are
allosteric regulators (like the benzos, barbs, carbamates, quinazolinones ala methaqualone, loreclezole, chlormethiazole, chloral hydrate, trional, tetronal and sulfonal, etomidate, propofol etc)
this being probably because the steric and chemical structural requirements imposed for an agonist of the GABA binding site itself are quite strict.
Benzo withdrawal isn't anything to fuck around with lightly, do not get caught short without at least sufficient supply to last until you can actually attend the earliest available appointment with a dr. This is especially valid in the case of short-acting drugs, like alprazolam and most of the other triazolobenzodiazepines, because things can go from having taken a dose sufficient to remain asymptomatic to plasma levels having dropped to dangerous territory, and because the action of benzos is anticonvulsant and anxiolytic, acute withdrawal onset can be capable of physically incapacitating the sufferer and preventing them seeking help.
There are quite a lot of benzos available now these days online on the 'research chemical'/'RC' grey market scene.
A long-acting one is what you want for doing a controlled taper, short acting drugs are usually pretty shitty options for tapering off a substance to which one has established a physical dependency. This is because one ends up with many repeated peaks and troughs in drug plasma levels, which makes for a lot less tolerable, more uncomfortable, harder to manage and CERTAINLY its not conducive to maintaining a stable steady-state plasma level without many unpleasant sudden variations.
In the case of DHC, this is annoying, with a stronger opiate, like when Tsath used to get and shoot a lot of OC80s its outright painful.
With a benzo, 'utterly horrific' is the entry-level scale of horrible experience.
Poisoninthestain is quite correct in stating that you SHOULDN'T FUCKING WELL EVER attempt to cold turkey from GABAergics. The seizure risk, and not to mention just the withdrawal symptoms are in and of themselves, without suffering a seizure, absolutely brutal. Benzo, and other GABAergic drug withdrawal makes opiate withdrawal even from severe opiate habits look like a wonderful treat by comparison.
As far as librium tapers go (librium is chlordiazepoxide), actually, having done it once, didn't find it much use at all really. Chlordiazepoxide has one useful trait and one only, its long duration of action. Which is far from unique amongst the benzos. Otherwise its not worth a streak of cat piss. For a true emergency to prevent seizure, or chlordiazepoxide is the ONLY option, then go for it. otherwise pretty much any benzo is better than that one.
of the prescribed benzos, nitrazepam would be the one that Tsath would personally recommend, due to its combination of very respectable potency, long duration of action, and strongly hypnotic and anxiolytic, and as well as doing a very effective job at preventing seizures, its long lasting enough for it not to result in any nasty surprises on waking up.
And its got enough of a hypnotic and anxiolytic effect to it to help make things pretty painless if the taper is done slowly enough as it should bee.
You should make sure to IGNORE the dangerous, ignorant garbage ofifered up as advice by scarecrow with respect to dose reduction.
Scarecrow-you shouldn't go making suggestions to people that have a large benzo physical dependency follow a detox schedule you yourself used to taper from a mere few fuckin days for cunt-cancer's bloody sake, especially when you knew it wasn't enough, because even then, YOU still felt rough.
By a quarter every 2 days? thats going from the level the subject requires detoxing from to zero in a mere week and a day.
That would be stupid and dangerous, not to mention bloody uncomfortable and generally equating to much misery and torment for the person having to endure it.
1/4 every 2 days would be suitable for only the ABSOLUTE mildest, most farty insignificant levels of habituation physically possible, I.e a week or two's light dose regime of benzos, longer w/ the Z-drugs Tsath would think because they are so much weaker, and less prone to proconvulsant effects of WD, especially in the case of zaleplon, as its so pissweak as to be barely active in the first place
![Tongue :P](https://thevespiary.org/talk/Smileys/default/tongue.gif)
For grey market benzos, do make sure that you STICK to your taper plan. Get enough to permit following the taper from initiation through to end point and being benzo-free, to make sure that one cannot be forcibly dropped in it at the deep end by means of the chosen taper agent by the government filth infesting your country.