> I forgot to mention that I have personally experienced a clonidine-induced exacerbation of depression.
>
> Most salient, though, is that clonidine is capable of producing significant depression in people who have no history of depression.
>
> 1. Clonidine = (norepinephrine) NE alpha-2 presynaptic autoreceptor agonist (stimulatior).
>
> 2. NE alpha-2 receptors control the manufacture and release of NE via a negative feedback loop.
>
> 3. When NE presynaptic autoreceptors are antagonized (blocked), the presynaptic neuron increases the manufacture and release of NE. This is because the presynaptic neuron "sees" less synaptic NE than there actually is by blocking its "eyes" (autoreceptors) from accurately measuring synaptic NE levels. It sees less than there really is. The neuron is thus fooled into manufacturing and releasing more NE.
>
> 4. When NE autoreceptors are agonized (stimulated), the presynaptic neuron "sees" more synaptic NE than there really is. The presynaptic neuron thus reduces its manufacture and release of NE to compensate.
>
> 5. Clonidine thus reduces the synaptic concentration of NE by stimulating presynaptic autoreceptors.
>
> 6. Reduced synaptic concentrations of NE are associated with depression.
>
>
> * I hope I got that right.
>
>
> - Scott
I am sure your mechanisms are right, Scott...but the bottom line, clonidine is a very powerful drug, given 0.1mg's lower almost anyone's blood pressure. Clonidine was used quite a bit in the 70's and 80's to help many rock stars and celebrities kick heroin. I have had that experience of sub-low blood pressure, and it is not a nice feeling.
So, I think, tiny amounts are the key. I don't think, for psychiatric use, there is any need to go above 0.1mg b.i.d. Your body does adjust, once on a regular schedule. It was *magic* for my PTSD nightmares. But, I tried raising the dose. Not good for mental health.
Jay
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