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How do High dose benzo binges affect the brain?


[Dr...]

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When I was on benzos I had a different kind of "Addiction". I didn't take benzos daily too much but when things got out of control I would take a massive amount of benzos in one day.

 

My last binge I took over 100mg of alprazolam in a single day. Do any of you know what that would do to your brain? I suppose it might start binding to different sub unit gaba receptors but there's gotta be more that's happening. You guys have any idea how high doses for a small amount of time affect the brain?

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You might take a look at this...

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2453238/

 

Thanks for posting.  I pulled some quotes for those who want a summary of sorts.

 

The original poster, doing 100mg of xanax.  Not sure if it’s a real post, but if it is, you are using a very fast onset Benzodiazaphine, with a very short half life, and binging on it.  This is a very dangerous combination.  I’m not sure how many times you’ve done this, but you do not want to push it and transition into a neuro-kindled state.  It will take  a very long time to restabilize.  It’s not worth it.  You are messing around with the worst drug class to binge on.

 

See below from the reference cited above.

 

 

Quotes

 

Another key factor that deserves consideration in explanations of the differences in reinforcing effectiveness among the compounds in Table 1 is pharmacokinetics. While little has been published regarding the pharmacokinetic parameters of TPA023 and L-838,417 following intravenous administration in monkeys, L-838,417 is purported to have a relatively short half- life similar to that of midazolam (153; J.R. Atack, personal communication). In contrast, TPA023’s duration of receptor occupancy in rodents suggests that this compound may be relatively long-acting (6). These findings suggest that TPA023 might not maintain self-administration behavior due to its long duration of action. However, other compounds with a long duration of action (e.g. diazepam) clearly are self-administered under the procedures used by both Ator ( 8 ) and Rowlett et al. (153).

 

In fact, onset of action may be the most important pharmacokinetic factor that determines the degree of reinforcing effects of abused drugs (70), but empirical information regarding the onset of action for TPA023 and L-838,417 is not yet available.

 

 

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As discussed previously, there are a number of adaptations that occur at the level of the GABAA receptor (i.e., downregulation, allosteric uncoupling, subsensitivity, etc.) following administration of benzodiazepines. However, they do not appear to make an impact significant enough to account entirely for such complex behaviors as those associated with abuse potential (141). Instead, non-GABAergic mechanisms must also contribute to the abuse and dependence liability of benzodiazepine-type drugs; accordingly, glutamatergic mechanisms are involved. For instance, the acquisition of a diazepam-induced conditioned place preference was attenuated by pretreatment with a glutamate receptor antagonist (63), suggesting that glutamate contributes to the rewarding or reinforcing effects of benzodiazepines.

 

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Interestingly, the contribution of AMPA and NMDA receptor mechanisms may be regulated temporally such that each is involved at specific time points during the expression of withdrawal and development of tolerance, respectively (89).

 

Similar findings have been observed in long-term potentiation and kindling, which like the neuroadaptive processes associated with the consumption of drugs of abuse, are forms of synaptic plasticity (15). However, whether or not the involvement of glutamate in the abuse and dependence liability of benzodiazepine-type drugs is similar to that observed with other drugs of abuse (e.g. psychostimulants), remains relatively unexplored.

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Indeed, both CamKIIα (e.g., 104,131) and BDNF (e.g., 25,35) have been demonstrated to play prominent roles in the plasticity believed to underlie the addictive potential of drugs of abuse. Together, these results are just some examples of how intracellular events may function as the liaison between allosteric modulation of GABAA receptors by benzodiazepines and behavior—again, a relatively unexplored area of research.

 

End quotes

 

 

 

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