Psycho-Babble Medication Thread 400390

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Buspar as antidepressant.

Posted by Ted Brosnan on October 8, 2004, at 11:50:02

Hello.

I suffer from a rather mild depression. It's some lack of energy, motivation etc.. I already started taking Reboxetine (a norepinephrine reuptake inhibitor), and it's promising.

I been on Lexapro for a while but I think my mild depression doesn't justify the awful side effects of a SSRI.

Instead of targeting Serotonin with a SSRI I started taking Buspar (buspirone) which acts as an agonist at the serotonins 5HTA1 receptor. I read that some studies have found it effective as an antidepressant at doses ranging fom 45 to 60 or 90 mg a day.

I am planning to start taking it at 45mgs a day.

Has anyone found it effective as an antidepressaqnt at these doses?!

Thanks

 

Re: Buspar as antidepressant.

Posted by griswald on October 8, 2004, at 19:50:52

In reply to Buspar as antidepressant., posted by Ted Brosnan on October 8, 2004, at 11:50:02

I have had some antidepresant effects at lower doses. It took about three weeks to work.

 

Re: Buspar as antidepressant. ยป Ted Brosnan

Posted by zeugma on October 8, 2004, at 20:46:22

In reply to Buspar as antidepressant., posted by Ted Brosnan on October 8, 2004, at 11:50:02

I would think it makes sense to add buspar to reboxetine. Buspar's metabolite, 1-PP, is an alpha-2 antagonist and this can actually boost the effect of an NRI:

Locus coeruleus neuronal activity and noradrenaline availability in the frontal cortex of rats chronically treated with imipramine: effect of alpha 2-adrenoceptor blockade
by
Linner L, Arborelius L, Nomikos GG, Bertilsson L, Svensson TH
Department of Physiology and Pharmacology,
Karolinska Institutet, Stockholm, Sweden
Biol Psychiatry 1999 Sep 15; 46(6):766-74

ABSTRACT
BACKGROUND: Previous studies indicate a reduced feedback inhibition of brain noradrenaline (NA) neurons in the locus coeruleus (LC) during chronic administration of antidepressants which inhibit the NA reuptake mechanism due to functional downregulation of somatodendritic alpha 2-adrenoceptors in the LC. Therefore, we have here studied the LC neuronal responsiveness to administration of the alpha 2-adrenoceptor antagonist idazoxan (IDA) after both short-term and long-term imipramine (IMI) administration. METHODS: Rats were treated for different periods with systemic IMI. In these rats, basal activity of central noradrenergic function and the effect of IDA was assessed by means of extracellular single-cell recording from LC neurons and in vivo microdialysis of extracellular NA levels in the frontal cortex (FC). RESULTS: The average firing rate of LC neurons was significantly reduced in rats by short-term IMI treatment compared with long-term treatment. The output of NA in the FC of all IMI-treated animals was significantly increased compared with saline-treated rats. Moreover, the enhancing effect of IDA on both the firing rate of LC neurons and the cortical NA output was larger in rats after long-term treatment with IMI than after short-term administration. CONCLUSIONS: Our results clearly support the notion of development of functional downregulation of alpha 2-autoreceptors on LC neurons during chronic administration of NA reuptake inhibiting antidepressants. Moreover, the data suggest that addition of alpha 2-adrenoceptor antagonists may augment the clinical effect of such drugs in major depression.


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