Posted by JohnX2 on April 17, 2002, at 0:14:48
In reply to Re: ZOLOFT Increase, more anxiety? 3 beers » geno, posted by JohnX2 on April 16, 2002, at 19:00:05
> > 3 beers, well i just upped my dose from 25mg after 7 days, using 25mg of zoloft/.5mg of klonopin in the am. Not bad. felt pretty sleepy,or just ok. Today, was the first increase of zoloft. Dont forget i dropped the xanax .5mg in the am due to my doc 3 days ago. So today, i stayed the same on klonopin .5mg and have only .25 mg of xanax for 5pm, when the klonopin usuually wears off. (note: took zoloft/klonopin at 7am. By 3pm, im jumping out of my skin. Im panicy, muscles are really tight!!! Luckily i have more klonopin. My mood is terrible also.
> >
> > Question is, should i up the dose to 1mg of klonopin in the am. then take remaining xanax in the evening. I believe its the combonation of a few things. Zoloft is activating more at 50mg for me, kloponin dose is too low, and xanax withdrawls.
> >
> > any comments?
> >
> > I only have 1mg of klonopin a day, along with .25 xanax a day.
> >
> > OH maybe its time to ditch the desipramine 25mg????
> >
> > geno
>
> Hi Geno,
>
> 3be is still in detention , I believe.
>
> Zoloft for *many* is quite an activating drug. Some people call it the "black coffee" effect.
>
> As far as the benzos go, I really feel that you ought to be on Klonopin dosing 2x a day. Otherwise you may just be a yo-yo.
>
> I'm not sure what is behind making zoloft activating (it causes insomnia for many), maybe via some indirect mechanism the medicine increases norepinephrine conductance.. who knows. You never know. Just looking at the direct reuptake properties/binding of the medicine at hand doesn't always tell the whole story. All these SSRIs have such varied side effects, you know.
>
> So maybe not a bad idea to ditch the desipramine.
>
> Of course, you want to make the medicine maneuvers one step at a time. i.e. take it slow. (default advice).
>
> Good Luck,
> JohnHeres one study (probably could dig up more):
Sertraline, a selective serotonin reuptake inhibitor modulates extracellular noradrenaline in the rat frontal cortex.
Thomas DN, Nutt DJ, Holman RB.
University of Bristol, Psychopharmacology Unit School of Medical Sciences, UK.
The selective action of selective serotonergic reuptake inhibitors (SSRIs) on 5-hydroxytryptamine (5-HT) neurotransmission underlies the therapeutic effectiveness of this class of drugs. Yet there is increasing evidence that changes in extracellular 5-HT content may result in changes in the regulation of other neurotransmitter systems. The present study examines the effects of acute and chronic administration of the SSRI sertraline on release of endogenous noradrenaline (NA) in the frontal cortex and hippocampus of the rat using in vivo microdialysis. Acute administration of sertraline did not significantly alter NA release in either the cortex or the hippocampus. However, 24 h after chronic (14 days) administration of the drug (10 mg/kg i.p. once daily), NA release in the cortex but not hippocampus was significantly enhanced. The lack of an effect on NA release following a challenge with the alpha2-antagonist idazoxan suggests that chronic drug treatment has reduced the sensitivity of cortical pre-synaptic alpha2-adrenoceptors, activation of which would normally inhibit further NA release. The possible mechanisms underlying the regional specificity of the effect of chronic and not acute sertraline administration and the implications of these results for our understanding of depression are discussed.
PMID: 10065910 [PubMed - indexed for MEDLINE]
poster:JohnX2
thread:103249
URL: http://www.dr-bob.org/babble/20020416/msgs/103305.html