GABA as the obstacle to non-structural neuroplasticity

[[aw...]]

I've been suspecting this is the case.  Anxiety responses seem to be a major foundation of learning (particularly learning through negative stimuli, i.e. negative reinforcement).  New thought patterns, nerve configurations, etc.. all  come about more easily during benzo withdrawal.  Therefore, protracted withdrawal can be discouraged by (a) slow taper, (b) the brain not running wild during the recovery process. 

 

Thoughts?

[[ri...]]

Hi awave, your post's title caught my attention, because I started a somewhat similar thread, looking for answers to protracted w/d anxiety. You may have seen it: "Is Robert DuPont's "lifetime steady dose of benzos" total nonsense?"

 

So I'm curious about your concepts here, but not totally understanding what your proposing. It sounds like what you're saying is that the more anxiety responses we have, the more negative reinforcement our brain's learn, so if we can dial down the number of anxiety responses during w/d through a slow taper, or the brain not running wild during the recovery process, we could shorten the withdrawal...is that correct?

 

Of course, this begs other questions, like, how do we keep the brain from running wild during the recovery process...it is a very brain-frightening recovery after all? And how, in your post title, is GABA an obstacle to non-structural neuroplasticity? Can you translate "non-structural neuroplasticity" for us non-scientists & nerds? 

 

I think you may have some good information here, but your wording is pretty clinical; you may need to put it in lay terms for us high-school biology flunk-outs to respond 

[[be...]]

Hi awave, your post's title caught my attention, because I started a somewhat similar thread, looking for answers to protracted w/d anxiety. You may have seen it: "Is Robert DuPont's "lifetime steady dose of benzos" total nonsense?"

 

So I'm curious about your concepts here, but not totally understanding what your proposing. It sounds like what you're saying is that the more anxiety responses we have, the more negative reinforcement our brain's learn, so if we can dial down the number of anxiety responses during w/d through a slow taper, or the brain not running wild during the recovery process, we could shorten the withdrawal...is that correct?

 

Of course, this begs other questions, like, how do we keep the brain from running wild during the recovery process...it is a very brain-frightening recovery after all? And how, in your post title, is GABA an obstacle to non-structural neuroplasticity? Can you translate "non-structural neuroplasticity" for us non-scientists & nerds? 

 

I think you may have some good information here, but your wording is pretty clinical; you may need to put it in lay terms for us high-school biology flunk-outs to respond 

 

:laugh:

[[aw...]]

Hi awave, your post's title caught my attention, because I started a somewhat similar thread, looking for answers to protracted w/d anxiety. You may have seen it: "Is Robert DuPont's "lifetime steady dose of benzos" total nonsense?"

 

So I'm curious about your concepts here, but not totally understanding what your proposing. It sounds like what you're saying is that the more anxiety responses we have, the more negative reinforcement our brain's learn, so if we can dial down the number of anxiety responses during w/d through a slow taper, or the brain not running wild during the recovery process, we could shorten the withdrawal...is that correct?

 

Of course, this begs other questions, like, how do we keep the brain from running wild during the recovery process...it is a very brain-frightening recovery after all? And how, in your post title, is GABA an obstacle to non-structural neuroplasticity? Can you translate "non-structural neuroplasticity" for us non-scientists & nerds? 

 

I think you may have some good information here, but your wording is pretty clinical; you may need to put it in lay terms for us high-school biology flunk-outs to respond 

 

Hi riddim,

 

Yes, the idea would be that slow withdrawals prevent escalations of stress/anxiety responses, thus minimizing the net impact of withdrawal.  This would also suggest that some therapeutic approaches designed to minimize anxious thoughts, and to educate the precise nature (and eventual success) of withdrawal, would physiologically hasten its course. 

 

"Non-structural neuroplasticity" is a sort of simplistic way to describe what I was thinking of - neuroplasticity (neural changing), including neuroplasticity that means the changing of neurotransmitter/receptor configuration, but not the  broader linking of neurons themselves.  As I understand this is the primary type of neuroplasticity in effect during withdrawal (and for adulthood in general).   

 

GABA - the "red traffic light" of neurotransmitters - minimizes anxious responses, and hence negative reinforcements, etc., and hence, changes in individuals resulting from negative reinforcements.  But the severity of the withdrawal experience is mediated both by GABA reception, and that of other neurotransmitters, such as the stress response. 

 

So a severe withdrawal  generates a "feedback loop" - stress triggers worse withdrawal triggers stress.  In effect, the quickness of withdrawal is correlated to the net amount of trauma experienced.

[[be...]]

Hi awave, your post's title caught my attention, because I started a somewhat similar thread, looking for answers to protracted w/d anxiety. You may have seen it: "Is Robert DuPont's "lifetime steady dose of benzos" total nonsense?"

 

So I'm curious about your concepts here, but not totally understanding what your proposing. It sounds like what you're saying is that the more anxiety responses we have, the more negative reinforcement our brain's learn, so if we can dial down the number of anxiety responses during w/d through a slow taper, or the brain not running wild during the recovery process, we could shorten the withdrawal...is that correct?

 

Of course, this begs other questions, like, how do we keep the brain from running wild during the recovery process...it is a very brain-frightening recovery after all? And how, in your post title, is GABA an obstacle to non-structural neuroplasticity? Can you translate "non-structural neuroplasticity" for us non-scientists & nerds? 

 

I think you may have some good information here, but your wording is pretty clinical; you may need to put it in lay terms for us high-school biology flunk-outs to respond 

 

Hi riddim,

 

Yes, the idea would be that slow withdrawals prevent escalations of stress/anxiety responses, thus minimizing the net impact of withdrawal.  This would also suggest that some therapeutic approaches designed to minimize anxious thoughts, and to educate the precise nature (and eventual success) of withdrawal, would physiologically hasten its course. 

 

"Non-structural neuroplasticity" is a sort of simplistic way to describe what I was thinking of - neuroplasticity (neural changing), including neuroplasticity that means the changing of neurotransmitter/receptor configuration, but not the  broader linking of neurons themselves.  As I understand this is the primary type of neuroplasticity in effect during withdrawal (and for adulthood in general).   

 

GABA - the "red traffic light" of neurotransmitters - minimizes anxious responses, and hence negative reinforcements, etc., and hence, changes in individuals resulting from negative reinforcements.  But the severity of the withdrawal experience is mediated both by GABA reception, and that of other neurotransmitters, such as the stress response. 

 

So a severe withdrawal  generates a "feedback loop" - stress triggers worse withdrawal triggers stress.  In effect, the quickness of withdrawal is correlated to the net amount of trauma experienced.

 

Wow. You should be in Mensa, not me. ~~ Bets