Posted by AMenz on July 7, 2001, at 10:43:11
In reply to Re: Modafinil Paul B, posted by PaulB on July 6, 2001, at 18:18:56
Thanx for response, but have more questions, if you will bear with me.
Please explain what precisely are the receptors you are speaking of. Are these in the dendrites. I am having trouble keeping track of what does what to what receptor because of lack of familiarity.
Otherwise, If the general idea is that serotonin is fired through the synapse goes to the next cell (receptors come in here?) and then float back to the previous cell to be reabsorbed, what does the mimicking reaction result in? The spurious seratonin is then converted to some electrical response?
I hope I don't sound hopelessly naive. Which I am in biochemistry. But I would like to know what the hell these guys are doing with my brain.
BTW, cessation of Buspar immediately resulted in the abatement of all these symptoms.
Buspar was prescribed to substitute for Lorezapam. The idea was to have Buspar kick in and then withdraw from Lorezapam. Which in itself seems now stupid since I've read that Buspar will not help with the withdrawal symptoms from Lorezapam. I don't think this guy thinks his biochemistry through.
You are lucky to have such an understanding of biochemistry, which is completely lacking in my educational background.
> > What is the action of Buspar. REcently I had to go off it because it created anxiety, racing thoughts, etc.
> >
> > Does it affect sertonin levels at all like the Zoloft I am taking. Would the combination of the two cause these symptoms?
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> > > Although Modafinil is the newer version of Adrafinil and more expensive generally I read that the latter is the more popular. One of the things that didnt seem to be clear was whether Modafinil was like a classical stimulant such as ritalin and blocked the re-uptake of dopamine or whether it was an alpha1-adrenergic agonist. There seems to be overriding opinion that it is the latter although has some properties of DA re-uptake.
> > >
> > > The interesting thing is that there could be further speculation as to how it exerts it alpha1 adrenergic agonist activity. A lot of agonists mimic the neurotrnamsitter to exert their therapeutic effects such as Buspirone and many newer drugs in development i.e. pagoclone, however it is so often written in webpages on these drugs that 'the basis of their UNIQUENESS lies in their ability to only stimulate when stimulation is required' This may explain why there tolerance potential is so low because they may just fill the receptor if no neurotranmsitter was present overwise there would be no point in taking them? This may also explain why you dont notice the alertness until the evening after norepinephrine usually decline. Any views??????
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> In response to Buspar ?
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> There are A LOT of drugs being developed at the moment that are designed to 'mimic' the neurotransmitters in the brain and they tend to be very selective. Buspirone is one and is the only agonist of 'this' type available at this time that I am aware of. It 'mimics' the neurotrnasmitter serotonin at the 5-HT1a receptors. 5-HT1a is indicated in Generalised Anxiety Disorder but doesnt seem to help much with social anxiety, panic or obsessive compulsive disorder. The combination of Zoloft and Buspirone may well cause drug-drug interactions and problems such as those you cited. The SSRI's all have significant affinity for the 5-HT1 receptors and 5-HT2 receptors particulalarly 5-HT1a and 5-HT2a. Other then than that Buspirone is known to have a serotonin metabolite as well so be warned.
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> If Zoloft had stopped working for you it would not have been unreasoinable to augment with Buspirone to potentiate its activity overwise if Zoloft hadnt stopped working the co-medication is somewhat risky I think and your symptoms may be charactteristic of a mild serotonin syndrome.
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poster:AMenz
thread:68842
URL: http://www.dr-bob.org/babble/20010701/msgs/69275.html