Posted by sowhysosad on April 21, 2009, at 7:26:14
In reply to Re: Do SSRI's cause dopamine depletion, posted by sowhysosad on April 21, 2009, at 7:08:07
Due to sleep deprivation and general stupidity I just posted without even reading the research, thinking it was this old chestnut:
Résumé / Abstract
Rationale: The selective serotonin uptake inhibitor (SSRI) fluoxetine has been shown to not only increase the extracellular concentrations of serotonin, but also dopamine and norepinephrine extracellular concentrations in rat prefrontal cortex. The effect of other SSRIs on monoamine concentrations in prefrontal cortex has not been thoroughly studied. Objective: The aim of this study was to compare the ability of five systemically administered selective serotonin uptake inhibitors to increase acutely the extracellular concentrations of serotonin, norepinephrine and dopamine in rat prefrontal cortex. Methods: The extracellular concentrations of monoamines were determined in the prefrontal cortex of conscious rats using the microdialysis technique. Results: Fluoxetine, citalopram, fluvoxamine, paroxetine and sertraline similarly increased the extracellular concentrations of serotonin from 2- to 4-fold above baseline. However, only fluoxetine produced robust and sustained increases in extracellular concentrations of norepinephrine and dopamine after acute systemic administration. Fluoxetine at the same dose blocked ex vivo binding to the serotonin transporter, but not the norepinephrine transporter, suggesting that the increase of catecholamines was not due to non-selective blockade of norepinephrine uptake. Prefrontal cortex extracellular concentrations of fluoxetine at the dose that increased extracellular monoamines were 242 nM, a concentration sufficient to block 5-HT2C receptors which is a potential mechanism for the fluoxetine-induced increase in catecholamines. Conclusion: Amongst the SSRIs examined, only fluoxetine acutely increases extracellular concentrations of norepinephrine and dopamine as well as serotonin in prefrontal cortex, suggesting that fluoxetine is an atypical SSRI.I'm far too tired to get my head around that second piece of research that Amelia posted - is it contradicting other studies which say SSRI's reduce D2 receptor availability? Does the reduced binding potential mean the fluoxetine is acting as a D2 antagonist? I've also previously read that SSRI's supersensitise D2 receptors. My brain hurts...
poster:sowhysosad
thread:883495
URL: http://www.dr-bob.org/babble/neuro/20090129/msgs/891901.html