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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 3 of 3. This is the beginning of the thread.
Posted by JohnX2 on November 28, 2001, at 9:32:32
hello out there,I've talked myself into the fact that an a2a drug
will improve my headaches and depression symptoms.Accordingly an a2a medication such as clonodine
and guanfacine will help to alleviate nmda receptor
hypoactivity according to dr. Olney's research
articles on the nmda hypofunction hypothesis on
schizophrenia. While I do not believe I have
schizophrenia, I would not be surprised if I had
dysfunctional a2a noradrenergic receptor regulation
as a result of repeated trauma. Repeated trauma
will reduce the density of a2a receptors and chronically
downregulate the receptors due to *uck up in the
affinity states (high vs. low) for the receptor.
People theorize that a partial agonist at the a2a site
may "buffer" the problem.Supposedly guanfacine (tenex) is less sedating.
I was also refered to tizanidine (zanaflex)
by a neurologist. Tizanidine is a dirivative of
clonodine with fewer anti-hypertensive side effects
but a crummy 1/2 life. I think there may be a sustained
release version of tizanidine in europe...anyone?Seeing as how all these meds may have side effects
consistent with anti-cholinergics (dry mouth,dizziness,
somnolence) that is consistent with my research
indicating that alpha-2 heteroreceptors modulate
acetylcholine transmission. I haven't quite narrowed
down if this is mainly for the centrally acting
a2a meds (in the locus coerulus) or if it is a
peripheral effect.Anyways, I find that a high dose of the anti-muscarinic
chlorpheniramine maleate *comepletely* alleviates my
depression and difficulties sitting still. I have
been experimenting with this for quite some time and
have found the necessary references indicating that
the anti-histamine has a strong anti-muscarinic
effect at the m2 recognition site. This is thought
to inhibit eps like symptoms (where a anti-cholinergic
would be more direct).Any thoughts on tizanidine? The dr. bob facts on
the use of guanfacine vs. clonodine seem to favor
guanfacine due to reduced sedation. I would prefer
to try guanfacine since it has a nice 1/2 life and
I don't want to be groggy. I think tizanidine is less
likely to have orthostatic side effects than clonodine.
I also "think" tizanidine is a partial a2a agonist
like clonodine which is actually a little more interesting
with regards to "buffering" noradrenergic activity.Any thoughts?
thanks,
john
Posted by Cam W. on November 29, 2001, at 0:34:47
In reply to a2a agonists - CAM,SLS,ETC, posted by JohnX2 on November 28, 2001, at 9:32:32
John - Aren't A2A receptors adenosine receptors? I know that it is thought that blocking adenosine-A2A receptors is a proposed mechanism of action for Elavil™'s (amitriptyline's) ability to decrease neuropathic pain and for migraine prophyllaxis.
Just a thought - Cam
Posted by JohnX2 on November 29, 2001, at 6:34:47
In reply to Re: a2a agonists - CAM,SLS,ETC » JohnX2, posted by Cam W. on November 29, 2001, at 0:34:47
Ooops, sorry if I using a misleading acronym.I was simplifying:
alpha-2 noradrenaline agonist = A2AThere are alpha-2 noradrenaline heteroreceptors
located on acetylcholine cell bodies. An
alpha-2 agonist like Clonidine reduces the firing
of the acetylcholine. Generally the noradrenaline
comes from activation of the locus coerulus.
In a state of nmda hypofunctioning
a pathological activation of acetycholine can
cause neurodegeneration. Another way to treat this
is with a muscarinic3 antagonist, as the
acetylcholine hits this receptor in the
extrapyramidal tract.The simplist adenosine antagonist is our
favorite friend caffeine.regards,
john> John - Aren't A2A receptors adenosine receptors? I know that it is thought that blocking adenosine-A2A receptors is a proposed mechanism of action for Elavil™'s (amitriptyline's) ability to decrease neuropathic pain and for migraine prophyllaxis.
>
> Just a thought - Cam
This is the end of the thread.
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