Posted by SLS on November 26, 2004, at 8:32:37
In reply to Re: Scott ,another thing to add., posted by denise1904 on November 26, 2004, at 6:39:53
Hi Denise.
It's too bad that lithium didn't do the trick. It would have been a nice, simple fix. Lithium actually makes me feel significantly worse. If it hadn't, I would like to have remained on it, even if only to act to preserve hippocampal and cerebral tissue. As far as to why lithium acts to augment antidepressants, the simple explanation invariably involves a pro-serotonergic mechanism. That it acts so quickly, usually within 3-7 days, might argue against an effect on second messenger events. Many investigators speculate that lithium promotes an increase in the levels of extracellular serotonin. I wonder if it might act directly upon the G-protein coupled receptors, changing their sensitivity. Lithium does so many things, though, it is difficult to isolate its mechanism of action for augmentation.
I decided to discontinue Cymbalta two days ago. I had taken it for at least 12 weeks. I received a significant improvement during the second and third weeks, but nothing thereafter. Unfortunately, this is exactly the same pattern of response to antidepressants that I have experienced since beginning this odyssey 22 years ago.
RU-486 (mifepristone) might be the very next thing I try. I have to bug my doctor to do the paperwork necessary to get it. In the meantime, I will have allowed enough of a washout period from Cymbalta that I could start a MAOI. I have not decided which one I will go with yet. Probably Parnate.
I guess the logical question to ask you - and I apologize if you have already answered it - have you yet tried a tricyclic or MAOI? What are your primary symptoms?
- Scott
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Effect of subchronic lithium treatment on citalopram-induced increases in extracellular concentrations of serotonin in the medial prefrontal cortex.Muraki I, Inoue T, Hashimoto S, Izumi T, Ito K, Koyama T.
Department of Psychiatry, Hokkaido University School of Medicine, Sapporo, Japan. smuraki@mtj.biglobe.ne.jp
We investigated the effect of citalopram [a selective serotonin (5-HT) reuptake inhibitor; SSRI] and MKC-242 (a selective 5-HT1A agonist), following treatment with subchronic lithium (p.o., 1 week) on extracellular 5-HT concentrations in the medial prefrontal cortex (mPFC). Acute treatment with citalopram (3 and 30 mg/kg) led to significant increases in extracellular 5-HT concentrations. The subchronic lithium group showed significantly higher basal levels of extracellular 5-HT than normal diet controls. Acute citalopram (3 and 30 mg/kg) treatment together with subchronic lithium treatment showed significant increases in the extracellular 5-HT concentrations, compared with citalopram treatment alone. Acute MKC-242 (1 mg/kg) treatment showed significant decreases in extracellular 5-HT concentrations, in both the normal diet and lithium diet groups to the same extent. The addition of lithium did not change the effect of the 5-HT1A agonist on extracellular 5-HT concentrations. This study suggests that lithium augmentation of the antidepressant effect of SSRI is mediated by the additional increases in extracellular 5-HT concentrations following the co-administrations of lithium and SSRI.
PMID: 11208912 [PubMed - indexed for MEDLINE]
poster:SLS
thread:419276
URL: http://www.dr-bob.org/babble/20041123/msgs/420449.html