Posted by SLS on July 27, 2011, at 7:32:35
In reply to Clonazepam maintainance in bipolar, posted by linkadge on July 26, 2011, at 21:05:40
> Is there any evidence of clonazepam being effective for mood stabilization (long term) in bipolar?
>
> LinkadgeI experienced a manic reaction to Parnate + desipramine in 1988. It was pretty heavy-duty. Depakote was not available at the time. Lithium did almost nothing acutely. Adding clonazepam to lithium reduced mania, but I cannot judge the therapeutic value of the lithium. Before the advent of using anticonvuslants as mood stabilizers, adding a BZD to lithium was often employed. Lorazepam was of no help to me. Clonazepam was, for me, clinically more of an anti-manic.
One difference between clonazepam and the other BZDs is the effects it has on serotonin release. Whether or not release of serotonin is enhanced or diminished has not yet been proven conclusively. Interestingly, clonazepam does not bind to GABA-B receptors as lorazepam and diazepam. Clonazepam is of little value to reduce rigidity in serotonin syndrome. Somewhere in here might be an explanation as to why clonazepam produces depression in some individuals.
- Scott-------------------------------------------
Neuropharmacology. 1995 Oct;34(10):1327-33.
Serotonin turnover rate, [3H]paroxetine binding sites, and 5-HT1A receptors in the hippocampus of rats subchronically treated with clonazepam.
Lima L, Trejo E, Urbina M.
SourceLaboratorio de Neuroquímica, Instituto Venezolano de Investigaciones Científicas, Caracas, Venezuela.
AbstractSelective central benzodiazepine agonists, such as clonazepam, are known to modify serotonin and 5-hydroxyindoleacetic content in the brain. In order to further study the effect of this benzodiazepine on serotonin turnover rate, rats received clonazepam, 10 mg/kg for 10 days, and the concentrations of serotonin and 5-hydroxyindoleacetic acid were determined in the hippocampus after inhibition of monoamineoxidase with pargyline. The results indicate a reduction in the turnover rate of the monoamine. In addition, the systemic administration of clonazepam produced a decrease in the Bmax of [3H]DPAT binding to 5-HT1A sites in the hippocampus. By contrast, this effect was not observed if clonazepam was delivered into the dorsal raphe nucleus by osmotic minipumps. The binding of [3H]paroxetine to 5-HT reuptake sites was increased by the treatment with clonazepam. The present observations indicate that clonazepam produces a reduction of serotonin turnover rate in the hippocampus of the rat concomitant with a down-regulation of 5-HT1A binding sites, probably by an effect at the forebrain projections. There is also an up-regulation of the serotonin transporter, which might contribute to a reduction in the synaptic availability of serotonin during clonazepam treatment.
PMID:
8570030
[PubMed - indexed for MEDLINE]Some see things as they are and ask why.
I dream of things that never were and ask why not.
poster:SLS
thread:991954
URL: http://www.dr-bob.org/babble/20110714/msgs/991999.html