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Re: Qs for CamW

Posted by AndrewB on October 28, 2000, at 21:55:33

In reply to Re: 3Day to 2 Week Responses. Proof, not myth. » JohnL, posted by Cam W. on October 28, 2000, at 10:53:08

> True response requires a modification of electrical flow through neurons in various brain structures. This adaptation (upregulation of some receptors and downregulation of others) takes time, as the neuronal cell membranes need to envelope and degradate some receptors and insert others into the nerve cell membranes. This is where c-Fos, the inositol pathway, etc. come into play, adjusting calcium levels to modify nerve cell excitability. Other secondary messengers shuttle proteins (receptors) from the nucleus and endoplasmic reticulum (where mRNA is making them due to these different-than-normal signals from membrane receptors created by an extracellular concentration change in one, or probably several of the numerous neurotransmitters effected by antidepressant therapy.

Thank you again for sharing your knowledge with us. I have a few questions I was hoping you could take the time to clear up for me concerning an explanation of the different ways in which neurotransmitters systems may exhibit dysfunction which can lead to depression.

Some background first so you know where I am coming from. Scott was nice enough to send me an abstract recently which indicates that SSRIs tend to be effective in people who have low dopamine post-synaptic receptor responsivity, while SSRIs tend to be ineffective in those with normal or supersensitive dopamine receptors. The study concluded that SSRIs work to ameliorate depression via increasing (upregulating) dopamine receptor sensitivity and therefore only work in those with subnormal (dysfunctional) receptor sensitivity.

Let us for the moment accept this conclusion and also note that some people with depression don’t respond to SSRIs but respond to other meds that clearly function by increasing dopamine transmission. For example, amisulpride has been shown to relieve depression in many where SSRIs have failed. Amisulpride clearly works by antagonizing dopamine pre-synaptic autoreceptors.

This seems to indicate that those helped by amisulpride like those helped by SSRIs suffer from dopaminergic hypofunction, but the specific type of the neurotransmitter dysfunction was different in the two groups. The SSRI group had low post-synaptic dopamine receptor sensitivity while the amisulpride group had some other problem (For example, maybe the amisulpride group had autoreceptors that were overactive and broke down too much dopamine and overly inhibited the release of dopamine).

Anyway, here are the questions I hope you can help me with Cam:

1) What happens specifically when an SSRI upregulates receptors. When you referred to new receptors being inserted into nerve cell membranes and calcium levels being adjusted through intermediary mechanisms to modify nerve cell excitability, does this apply to the changes that take place to create upregulation. Can you expand on this?

2) What other types of neurotransmitter system dysfunctions are you aware up (besides low post-synaptic receptor sensitivity) that could cause depression. On a related note, are you aware of what specific mechanisms would be responsible for the excess degradation (destruction) of dopamine (or serotonin if you are more familiar with that system).

With respect and gratitude,





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