Posted by SLS on October 12, 2001, at 1:48:21
In reply to Re: Anybody tried clonidine (Catapres) for depression? » SLS, posted by JohnX on October 11, 2001, at 15:28:27
> > Drugs like Remeron that block NE alpha-2 receptors seem to make my depression worse. I'm wondering if a drug like clonidine would help. It does the opposite of Remeron. It stimulates NE alpha-2 receptors.
> >
> > Any comments are appreciated.
> What makes you believe that the alpha-2 antagonism is causing depression?It is simply an empirical observation.
Idazoxan produced a worsening of my depression for the entire 3 or 4 months I was taking it. This drug is an investigational NE alpha-2 antagonist, and is often used as a biological probe to quantitize the function of these receptors. I’ve tried Remeron twice. I tried it about 5 years ago and again this past week. My depression became markedly worse within 24 hours of taking the first dose of 15.0mg and 7.5mg. respectively. The first trial was initiated immediately following one of moclobemide, which had exacerbated my depression horribly. I was unwilling to put myself through something like that again, so I discontinued the Remeron after 2 days. This past week, I was unwilling to let it go beyond a day. It took a full 36 hours after a 7.5mg dose for my mood to return to baseline following the exacerbation.
> The alpha-2 receptor causes inhibition of norepinephrine release. Generally blocking alpha-2 is an anti-depressant.Generally, people don’t fail to respond to 40 or so antidepressants. One might entertain the idea that the properties of those drugs that are to be effective in my case will deviate substantially from – and might even be in opposition to – those that others find helpful.
> At high doses, buspar is a good alpha-2 antagonist and it is believed by some people that this explains its high dose anti-depressant activity more so that its serotonin properties.
> If anything, I may guess the anti-histamine in Remeron could make you feel tired and depressed.I am pretty sure that it is not the antihistaminergic properties of Remeron that is responsible for the worsening of my depression. This experience is quite a bit different from sedation, and nothing like the effect that Benadryl has on me. In addition, idazoxan is devoid of histaminergic receptor blockade. I felt neither sedated nor fatigued. I just felt oppressed.
> Another option would be Tenex (guanfacine), this is a clean alpha-2 agonist with a longer half-life than clonodine, but it doesnt block the post synaptic alpha-1 receptor like clonodine.
Thanks, Bob. I’ll keep guanfacine in mind.
> Anyways, clonodine and tenex have been shown to be effective adjuncts to anti-depressants in people with ADD or PTSD.
This is encouraging. When my doctors at the NIMH performed some psychometric and personality inventory examinations, they found that I tested unusually high in the “prisoner of war” category for someone suffering from bipolar disorder.
Regarding buspirone, I am guessing that its ability to act as a 5-HT1a partial agonist might be most important when used as an augmentor to antidepressants.
> Hope this helps and is not too confusing. Unfortunately, I tend to confuse people with information overload.
I do better taking small bites. Too many words on a page are overwhelming to me. Sometimes, I feel particularly piggish for placing on a page so many of my own. I might be acting under the false notion that most people find reading easier than I do.
Thanks again.
- Scott
There are probably studies that contradict this, but…
Psychoneuroendocrinology 2000 Oct;25(7):741-52Multihormonal responses to clonidine in patients with affective and psychotic symptoms.
Mokrani M, Duval F, Diep TS, Bailey PE, Macher JP.
Research Center for Applied Neuroscience in Psychiatry (FORENAP), Centre Hospitalier, 68250, Rouffach, France.
The neuroendocrine responses to the alpha(2)-adrenoreceptor agonist clonidine (CLO) (0.35 mg if body weight < 65 kg or 0.375 mg if body weight > or =65 kg, PO) were studied in a large group of subjects: 134 drug-free inpatients--with either DSM-IV schizophrenia (SCZ, n=31), schizoaffective disorder (SAD, n=16), or major depressive episode (MDE, n=87) - and 22 hospitalized controls (HCs). Comparison with a previous placebo test performed in a subgroup of 92 subjects (46 MDEs, 20 SCZs, 8 SADs, and 18 HCs) showed that CLO induced a significant increase of growth hormone, prolactin (PRL) and thyrotropin (TSH) levels but no significant change in adrenocorticotropin and cortisol release. According to diagnostic categories, we found significantly lower GH stimulation in MDEs and in SADs compared to HCs or to SCZs. In addition, we found significantly lower CLO induced PRL and TSH stimulations in paranoid SCZ patients compared to controls and disorganized SCZ patients. Taken together, these results suggest a hyposensitivity of noradrenergic alpha(2)-receptors in patients with affective symptoms.
PMID: 10938452 [PubMed - indexed for MEDLINE]
poster:SLS
thread:80969
URL: http://www.dr-bob.org/babble/20011007/msgs/81086.html