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Re: Mirtazapine with Tianeptine » cybercafe

Posted by Shawn. T. on September 13, 2002, at 3:01:12

In reply to Re: Mirtazapine with Tianeptine » Shawn. T., posted by cybercafe on September 12, 2002, at 22:00:06

>four articles that contradict
>
> 1. 5HT2A increases firing in Naccumbens
> 2. 5HT2A decreases firing in Naccumbens
> 3. increased # of 5HT2A receptors found in >suicide victims
> 4. decreased # of 5HT2A receptors found in >suicide victims

1. that seems to be the case

2. where did you read that?

3. this data could possibly be interpreted as suicides that were caused by major depression

4. this data could possibly be interpreted as suicides that were caused by an anxiety disorder or bipolar disorder (where did you read this?)

I'll have to expand upon the Remeron(mirtazapine)/atypical antipsychotic connection sometime. 5-HT2 receptor antagonism combined with 5-HT1A activation seems to be a mechanism of efficacy in treating schizophrenia (check out the link at the bottom of the message). This implies that low dose Remeron wouldn't cut it for schizophrenia treatment; 30-45mg would likely be needed to see benefits (alpha-2 antagonism kicks in at higher doses). One link between 5-HT1A activation and 5-HT2A antagonism is that both actions cause K+ channels to close. That causes an increase in tyrosine hydroxylase, which is the rate limiting enzyme in the production of dopamine and noradrenaline (more tyrosine hydroxylase = more dopamine). It is interesting to note that Remeron has been shown to increase dopamine in the prefrontal cortex, which adds some clout to my claim. I'm beginning to realize that 5-HT2A antagonism without 5-HT2C antagonism results in some undesirable consequences. With regards to the nucleus accumbens, if 5-HT2A receptors are antagonized without 5-HT2C antagonism, dopamine is decreased in the nucleus accumbens. This is because 5-HT2C receptors in the ventral tegmental area exert a tonic inhibitory control upon dopamine release in the accumbens. The big downfall of M 100907 is that it is an inverse agonist at 5-HT2C receptors, which means that it activates the PLA-2-AA signalling cascade ... 5-HT2A receptors do the same thing. Regular agonists at 5-HT2A receptors normally activated the PLC beta2 signalling cascade (PLC beta2 -> IP3/DAG). See my pages on 5-HT2A and 5-HT2C for verification of these claims (I'm working on a Remeron page).


Ichikawa, Junji, Ishii, Hideo, Bonaccorso, Stefania, Fowler, Wiley L., O'Laughlin, Ian A., Meltzer, Herbert Y.
5-HT2A and D2 receptor blockade increases cortical DA release via 5-HT1A receptor activation: a possible mechanism of atypical antipsychotic-induced cortical dopamine release
J Neurochem 2001 76: 1521-1531
"These results suggest that the atypical APDs via 5-HT2A and D2 receptor blockade, regardless of intrinsic 5-HT1A affinity, may promote the ability of 5-HT1A receptor stimulation to increase mPFC DA release, and provide additional evidence that coadministration of 5-HT2A antagonists and typical APDs, which are D2 antagonists, may facilitate 5-HT1A agonist activity." http://www.jneurochem.org/cgi/content/abstract/76/5/1521


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URL: http://www.dr-bob.org/babble/20020906/msgs/119710.html