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Zevon
medicine forum beginner
Joined: 11 Jun 2006
Posts: 8
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 Posted: Mon Jun 19, 2006 7:03 pm Post subject:
Brain-Derived Neurotrophic Factor / Ampakines
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....OR
"Where Are My Ampakines?"
Try not to flame me for being too lazy to exercise.
But where are our long awaited Ampakines?
(Any next best things - besides, you know - that exercise thing?) |
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outsor@citynet.net
medicine forum Guru
Joined: 11 Sep 2005
Posts: 569
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| Posted: Mon Jun 19, 2006 7:39 pm Post subject:
Re: Brain-Derived Neurotrophic Factor / Ampakines
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Look up the marketing blurbs, said to improve memory in rats.
Couldpossibily help you to remember that there is no substitute for
exercise in good health. |
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Zevon
medicine forum beginner
Joined: 11 Jun 2006
Posts: 8
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| Posted: Tue Jun 20, 2006 12:23 am Post subject:
Re: Brain-Derived Neurotrophic Factor / Ampakines
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out...@citynet.net wrote:
| Quote: | Look up the marketing blurbs, said to improve memory in rats.
Couldpossibily help you to remember that there is no substitute for
exercise in good health.
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No Kidding!
I simply hoped to find a safe and effective way to reverse deterioation
of Synaptic Plasticity and desterbances to long term potentiation in
the Hippocampus.
What I turned up is SCARY and from citations below.
"As LTP is associated with calpain activation and spectrin degradation,
we determined the effects of ampakine treatment of cultured hippocampal
slices on spectrin degradation. Calpain activation was evaluated by
determining the levels of the 145-150kDa degradation products of
spectrin. Our data indicated that incubation of hippocampal slices with
positive modulators of AMPA receptors resulted in enhanced spectrin
degradation, an effect that was blocked by a calpain inhibitor. In
addition, an antagonist of AMPAr but not of NMDAr blocked
ampakine-induced spectrin degradation. These results indicate that
prolonged treatment with selected ampakines leads to spectrin
degradation mediated by activation of the calcium-dependent protease
calpain."
"Prolonged exposure of cultured hippocampal slices to CX614
[2H,3H,6aH-pyrrolidino[2'',1''-3',2']1,3-oxazino[6',5'-5,4]-benzo[e]1,4-dioxan
10-one], a positive alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic
acid (AMPA) receptor (AMPAr) modulator, decreases receptor response to
synaptic stimulation, an effect that could reflect reduced receptor
expression....We conclude that CX614-induced AMPAr protein loss is
primarily mediated by AMPAr activation and involves calpain-dependent
proteolysis of SAP97 and GRIP1."
1: Jourdi H, Yanagihara T, Martinez U, Bi X, Lynch G, Baudry M.
Effects of positive AMPA receptor modulators on calpain-mediated
spectrin
degradation in cultured hippocampal slices.
Neurochem Int. 2005 Jan;46(1):31-40.
PMID: 15567513 [PubMed - indexed for MEDLINE]
2: Jourdi H, Lu X, Yanagihara T, Lauterborn JC, Bi X, Gall CM, Baudry
M.
Prolonged positive modulation of
alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)
receptors
induces calpain-mediated PSD-95/Dlg/ZO-1 protein degradation and AMPA
receptor
down-regulation in cultured hippocampal slices.
J Pharmacol Exp Ther. 2005 Jul;314(1):16-26. Epub 2005 Mar 22.
PMID: 15784649 [PubMed - indexed for MEDLINE] |
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Zevon
medicine forum beginner
Joined: 11 Jun 2006
Posts: 8
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| Posted: Tue Jun 20, 2006 4:13 pm Post subject:
Re: Brain-Derived Neurotrophic Factor / Ampakines
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OK - so exercise asside...
I am very open to suggestions.
What might be some safe and effective way to reverse deterioration
of Synaptic Plasticity and disturbances to Long Term Potentiation in
the Hippocampus? |
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Zevon
medicine forum beginner
Joined: 11 Jun 2006
Posts: 8
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| Posted: Tue Jun 20, 2006 11:18 pm Post subject:
Re: Brain-Derived Neurotrophic Factor / Ampakines
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Zevon wrote:
| Quote: |
What might be some safe and effective way to reverse deterioration
of Synaptic Plasticity and disturbances to Long Term Potentiation in
the Hippocampus?
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I ask that because it is one common problem we see in:
Age Related Dementia, PTSD, Stimulant abuse and Depression.
The basic science suggests numerous mechanisms (including promoting
glutamate receptor, cAMP, or CREB function, as three examples).
The challenge is knowing what molecules - then getting the molecules
into human brains - without doing more harm than good.
Thanks for the help - this is SO over my head! |
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timothytn@my-deja.com
medicine forum beginner
Joined: 20 Jun 2006
Posts: 1
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| Posted: Tue Jun 20, 2006 11:53 pm Post subject:
Re: Brain-Derived Neurotrophic Factor / Ampakines
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It appears that pyrrolidone derivatives fit the description like
Piracetam. |
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Zevon
medicine forum beginner
Joined: 11 Jun 2006
Posts: 8
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| Posted: Wed Jun 21, 2006 11:05 am Post subject:
Re: Brain-Derived Neurotrophic Factor / Ampakines
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timothytn@my-deja.com wrote:
| Quote: | It appears that pyrrolidone derivatives fit the description like
Piracetam.
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Yes - I came upon Aniracetam
(and a phosphodiesterase inhibitor called Rolipram)
98% of the basic science lit seems to encourage increasing cAMP
response
AND
AMPA transmission.
Sadly - 2% suggests that this is at least as neuro / excito-toxic as
benificial.
This is seriously complicated suff!
What Glutamenergic sub systems do we activate - and which do we put the
breaks on?
I am still working on it...
Warm Regards,
- Zevon |
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Zevon
medicine forum beginner
Joined: 11 Jun 2006
Posts: 8
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| Posted: Sun Jun 25, 2006 2:50 am Post subject:
Re: Brain-Derived Neurotrophic Factor / Ampakines
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The Big Question:
Simply - in abstinent, former long term substance abusers -
how might a clinician treat or reverse the 'frontal lobe' type
dysfunctions and anhedonia?
This all started by my asking a few professionals - the following -
regarding potential agents for reversing identical damage that we see
in ALL of the following:
Stimulant Abuse, PTSD, Age Related Dementia and Depression.
I asked:
What might be some safe and effective way to reverse deterioration
of Synaptic Plasticity and disturbances to Long Term
Potentiation in
the Hippocampus?
I was given 3 great examples: "Promoting glutamate receptor, cAMP, or
CREB function".
I was told that:
Both a cAMP phosphodiesterase inhibitor and
an alpha-amino-3-hydroxy-5-methylisoxazole propionate (AMPA)
potentiator were suggested to somehow
1) Enhance Neuronal plasticity and / or cellular resilience
AND / OR
2) Provide mitochondrial support / conserving growth factor receptors
It sounded good - until I came across a few articles regarding hyper
glutaminergic activity in drug addicts. Long term Cocaine abusers do
such damage to their glutaminergic system that as another researcher
put it:
"CONCLUSIONS: Cellular adaptations in prefrontal glutamatergic
innervation of the accumbens promote the compulsive character of drug
seeking in addicts by decreasing the value of natural rewards,
diminishing cognitive control (choice), and enhancing glutamatergic
drive in response to drug-associated stimuli."
Stay with me - I am getting to the question.
Forgive me,
I have now been reading too much basic science on reversing the long
term
neurological damage done by many years of substance abuse.
I have seen hopeful pharmacological treatments proposed to:
* Decrease the motivational value of the drug or
* Inhibit conditioned responses to stimuli predicting drug
availability.
I have seen nothing proposed to
* Increase the motivational value of nondrug reinforcers or to
* Improve frontal lobe dysfunction.
Simply - in abstinent, former long term substance abusers -
how might a clinician treat or reverse the 'frontal lobe' type
dysfunctions and anhedonia? (this is not only the direct result of
abuse - but further perpetuates the addiction)
What do I have to show for it?
Only one potential agent:
N-acetylcysteine.
All the AMPAkine type products stimulate drug craving.
Thank you so very much!
Warmest Regards,
- Zevon |
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TP
medicine forum beginner
Joined: 28 Jul 2005
Posts: 16
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| Posted: Sun Jun 25, 2006 4:05 pm Post subject:
Re: Brain-Derived Neurotrophic Factor / Ampakines
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"Zevon" <WarrenZevon1@aol.com> wrote in message
news:1151203822.245895.214820@u72g2000cwu.googlegroups.com...
| Quote: | What do I have to show for it?
Only one potential agent:
N-acetylcysteine.
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So, it seems reasonable. Give it a try. It can't hurt anywhere as much as
the drugs that fried you to begin with. |
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Ethereal Wolf
medicine forum beginner
Joined: 26 Jun 2006
Posts: 2
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| Posted: Mon Jun 26, 2006 8:38 pm Post subject:
Re: Brain-Derived Neurotrophic Factor / Ampakines
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Maybe try CES (cranio-electrostimulation).
Zevon wrote:
| Quote: | The Big Question:
Simply - in abstinent, former long term substance abusers -
how might a clinician treat or reverse the 'frontal lobe' type
dysfunctions and anhedonia?
This all started by my asking a few professionals - the following -
regarding potential agents for reversing identical damage that we see
in ALL of the following:
Stimulant Abuse, PTSD, Age Related Dementia and Depression.
I asked:
What might be some safe and effective way to reverse deterioration
of Synaptic Plasticity and disturbances to Long Term
Potentiation in
the Hippocampus?
I was given 3 great examples: "Promoting glutamate receptor, cAMP, or
CREB function".
I was told that:
Both a cAMP phosphodiesterase inhibitor and
an alpha-amino-3-hydroxy-5-methylisoxazole propionate (AMPA)
potentiator were suggested to somehow
1) Enhance Neuronal plasticity and / or cellular resilience
AND / OR
2) Provide mitochondrial support / conserving growth factor receptors
It sounded good - until I came across a few articles regarding hyper
glutaminergic activity in drug addicts. Long term Cocaine abusers do
such damage to their glutaminergic system that as another researcher
put it:
"CONCLUSIONS: Cellular adaptations in prefrontal glutamatergic
innervation of the accumbens promote the compulsive character of drug
seeking in addicts by decreasing the value of natural rewards,
diminishing cognitive control (choice), and enhancing glutamatergic
drive in response to drug-associated stimuli."
Stay with me - I am getting to the question.
Forgive me,
I have now been reading too much basic science on reversing the long
term
neurological damage done by many years of substance abuse.
I have seen hopeful pharmacological treatments proposed to:
* Decrease the motivational value of the drug or
* Inhibit conditioned responses to stimuli predicting drug
availability.
I have seen nothing proposed to
* Increase the motivational value of nondrug reinforcers or to
* Improve frontal lobe dysfunction.
Simply - in abstinent, former long term substance abusers -
how might a clinician treat or reverse the 'frontal lobe' type
dysfunctions and anhedonia? (this is not only the direct result of
abuse - but further perpetuates the addiction)
What do I have to show for it?
Only one potential agent:
N-acetylcysteine.
All the AMPAkine type products stimulate drug craving.
Thank you so very much!
Warmest Regards,
- Zevon |
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TP
medicine forum beginner
Joined: 28 Jul 2005
Posts: 16
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| Posted: Mon Jun 26, 2006 11:02 pm Post subject:
Re: Brain-Derived Neurotrophic Factor / Ampakines
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Heck, if you're going to follow that tact, then why not see a therapist for
EMDR?
"Ethereal Wolf" <ethereal.wolf@gmail.com> wrote in message
news:1151354285.662845.246030@b68g2000cwa.googlegroups.com...
| Quote: | Maybe try CES (cranio-electrostimulation).
Zevon wrote:
The Big Question:
Simply - in abstinent, former long term substance abusers -
how might a clinician treat or reverse the 'frontal lobe' type
dysfunctions and anhedonia?
This all started by my asking a few professionals - the following -
regarding potential agents for reversing identical damage that we see
in ALL of the following:
Stimulant Abuse, PTSD, Age Related Dementia and Depression.
I asked:
What might be some safe and effective way to reverse deterioration
of Synaptic Plasticity and disturbances to Long Term
Potentiation in
the Hippocampus?
I was given 3 great examples: "Promoting glutamate receptor, cAMP, or
CREB function".
I was told that:
Both a cAMP phosphodiesterase inhibitor and
an alpha-amino-3-hydroxy-5-methylisoxazole propionate (AMPA)
potentiator were suggested to somehow
1) Enhance Neuronal plasticity and / or cellular resilience
AND / OR
2) Provide mitochondrial support / conserving growth factor receptors
It sounded good - until I came across a few articles regarding hyper
glutaminergic activity in drug addicts. Long term Cocaine abusers do
such damage to their glutaminergic system that as another researcher
put it:
"CONCLUSIONS: Cellular adaptations in prefrontal glutamatergic
innervation of the accumbens promote the compulsive character of drug
seeking in addicts by decreasing the value of natural rewards,
diminishing cognitive control (choice), and enhancing glutamatergic
drive in response to drug-associated stimuli."
Stay with me - I am getting to the question.
Forgive me,
I have now been reading too much basic science on reversing the long
term
neurological damage done by many years of substance abuse.
I have seen hopeful pharmacological treatments proposed to:
* Decrease the motivational value of the drug or
* Inhibit conditioned responses to stimuli predicting drug
availability.
I have seen nothing proposed to
* Increase the motivational value of nondrug reinforcers or to
* Improve frontal lobe dysfunction.
Simply - in abstinent, former long term substance abusers -
how might a clinician treat or reverse the 'frontal lobe' type
dysfunctions and anhedonia? (this is not only the direct result of
abuse - but further perpetuates the addiction)
What do I have to show for it?
Only one potential agent:
N-acetylcysteine.
All the AMPAkine type products stimulate drug craving.
Thank you so very much!
Warmest Regards,
- Zevon
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Ethereal Wolf
medicine forum beginner
Joined: 26 Jun 2006
Posts: 2
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| Posted: Tue Jun 27, 2006 3:00 pm Post subject:
Re: Brain-Derived Neurotrophic Factor / Ampakines
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what is emdr.
TP wrote:
| Quote: | Heck, if you're going to follow that tact, then why not see a therapist for
EMDR?
"Ethereal Wolf" <ethereal.wolf@gmail.com> wrote in message
news:1151354285.662845.246030@b68g2000cwa.googlegroups.com...
Maybe try CES (cranio-electrostimulation).
Zevon wrote:
The Big Question:
Simply - in abstinent, former long term substance abusers -
how might a clinician treat or reverse the 'frontal lobe' type
dysfunctions and anhedonia?
This all started by my asking a few professionals - the following -
regarding potential agents for reversing identical damage that we see
in ALL of the following:
Stimulant Abuse, PTSD, Age Related Dementia and Depression.
I asked:
What might be some safe and effective way to reverse deterioration
of Synaptic Plasticity and disturbances to Long Term
Potentiation in
the Hippocampus?
I was given 3 great examples: "Promoting glutamate receptor, cAMP, or
CREB function".
I was told that:
Both a cAMP phosphodiesterase inhibitor and
an alpha-amino-3-hydroxy-5-methylisoxazole propionate (AMPA)
potentiator were suggested to somehow
1) Enhance Neuronal plasticity and / or cellular resilience
AND / OR
2) Provide mitochondrial support / conserving growth factor receptors
It sounded good - until I came across a few articles regarding hyper
glutaminergic activity in drug addicts. Long term Cocaine abusers do
such damage to their glutaminergic system that as another researcher
put it:
"CONCLUSIONS: Cellular adaptations in prefrontal glutamatergic
innervation of the accumbens promote the compulsive character of drug
seeking in addicts by decreasing the value of natural rewards,
diminishing cognitive control (choice), and enhancing glutamatergic
drive in response to drug-associated stimuli."
Stay with me - I am getting to the question.
Forgive me,
I have now been reading too much basic science on reversing the long
term
neurological damage done by many years of substance abuse.
I have seen hopeful pharmacological treatments proposed to:
* Decrease the motivational value of the drug or
* Inhibit conditioned responses to stimuli predicting drug
availability.
I have seen nothing proposed to
* Increase the motivational value of nondrug reinforcers or to
* Improve frontal lobe dysfunction.
Simply - in abstinent, former long term substance abusers -
how might a clinician treat or reverse the 'frontal lobe' type
dysfunctions and anhedonia? (this is not only the direct result of
abuse - but further perpetuates the addiction)
What do I have to show for it?
Only one potential agent:
N-acetylcysteine.
All the AMPAkine type products stimulate drug craving.
Thank you so very much!
Warmest Regards,
- Zevon
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TP
medicine forum beginner
Joined: 28 Jul 2005
Posts: 16
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| Posted: Tue Jun 27, 2006 3:33 pm Post subject:
Re: Brain-Derived Neurotrophic Factor / Ampakines
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Go visit EMDRIA.org . Eye Movement Desensitization and Reprogramming.
Basically, traumatic events are brought near the surface then the therapist
uses finger or buzzer in each of your hands and or lights (Las Vagas style)
moving from left to right, perhaps music with beats or change in volume
moving as well. The whole idea is that trauma has not been processed. When
you see a wild animal or even your pet get over a trauma, they go through a
certain pattern, which, incidently involves the tracking of the eyes and
head and shaking it off. Traumas can be resolved very quickly without
having to be relived. Or rather they are relived deep below the surface.
There are two types of traumas. The big T (I was in a car accident) and the
little t (my parents constantly told me I was no good and would never amount
to anything). I see the drug exhaustion as a little t. These take a longer
time to treat but can be treated.
"Ethereal Wolf" <ethereal.wolf@gmail.com> wrote in message
news:1151420457.041524.158290@75g2000cwc.googlegroups.com...
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TP
medicine forum beginner
Joined: 28 Jul 2005
Posts: 16
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