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Re: RLS, Akathisia + Dopamine D-2 receptors? cache-monkey

Posted by Larry Hoover on April 12, 2007, at 9:04:13

In reply to RLS, Akathisia + Dopamine D-2 receptors?, posted by cache-monkey on April 9, 2007, at 15:13:14

I've been cogitating on this for a while, and my response is pure speculation.....two of your posts together include:

> The common link seem to be the D-2 receptor. I recently discovered that Celexa (and also SSRIs) increases the expression of the D-2 receptor (http://tinyurl.com/2bs2ub). Further, BuSpar and neuroleptics block it, which can lead to actue and chronic akathisia when a certain percentage of receptors are blocked (e.g. http://tinyurl.com/2v2o7z).
>
> The trouble is, I'm not sure what to make of this. Besides the null that the D-2 system is totally uninvolved, there are two hypothesis that I have:
>
> A) My receptors are down-regulated
> * This would be consistent with the acute akathisia from low concentrations of D-2 blockers. I.e. a large percentage of receptors get blocked because there are relatively few of them
> * It would also be consistent with my medium term (after start-up, before discontinuation) success with Celexa: I felt better once the D-2 receptors began to proliferate
>
> B) My receptors are up-regulated
> * This tends to be the effect of mid- to long-term treatment with D-2 blockers
> * This is possibly consistent with ongoing akathisia-like issues -- under the assumption that tardive akathisia is like other TD

What about both occurring simultaneously? It's often little appreciated that auto-receptors (i.e. pre-synaptic receptors) also influence responsivity of the neural network. Auto-receptors are often inhibitory, serving as an internal signal feedback mechanism. There are also generally external feedback mechanisms, downstream from the neuron across the synapse. Genetic up-regulation could explain both observations, as activation of the higher receptor numbers on both sides of the synapse would lead to behavioural inhibition and excitation at the same time. Or, simply concluding that pre-synaptic and post-synaptic effects might differ, without characterizing them further.

> I would think that they then get hyper-stimulated. I would suspect that in most people there ends up being down-regulation and homeostasis is achieved once again. But, I'm wondering if in some susceptible individuals the receptors get stuck being super-sensitive, like in TD. I'm wondering if that would lead to anxiety and an alternative type of akathisia-like experience.

I think we often discount the biochemical changes that occur from experience, including that from exogenous substances. Neurons have learned responses, whatever they might be. So, prior experience can colour future opportunity. Once activated, genes are (frequently) more easily activated any time thereafter.

Lar

 

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poster:Larry Hoover thread:747867
URL: http://www.dr-bob.org/babble/20070407/msgs/749269.html