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Originally published at
https://thingsididntknowinpsychiatry.wordpress.com/
I thought I’d share some of the teaching I’ve been doing with junior doctors.
The way I tend to teach, is to canvass for questions over the preceding few
days. I then pick one of the questions. I record myself answering it with voice-
to-text software, then on any places I seem to have stumbled I annotate. The
next step is error checking. After that, I put together a series of slides
(powerpoint) and it’s essentially ready to present.
This is a portion of material where I was explaining the basics of dopamine-
related side effects of schizophrenia.
“However. To solve this problem, we needed to know how the heck this
medication worked.
Now, the old theories were very hit and miss. There was the reticular
depression theory. There were NMDA and glutamate theories. These were
respectable attempts, some of which has descendants today. But that wasn’t
the theory that allowed an unpacking of the effects and side effects of this
antipsychotic. We’re going to talk about the dopamine theory, which is still
the basic-level knowledge you’d be expected to know today.
A chap called Arvid Carlsson did a lot of the work. He identified that
dopamine was a neurotransmitter. Then he identified that if you deplete
dopamine in the brain, you get some antipsychotic-like effects, along with a
few parkinsonian symptoms. This was the basis of the hypothesis. He argued
too much dopamine causes psychosis. Antipsychotics reduce it- somehow.
As to how they did it? Another scientist, Peter Seeman, identifies this. He
identifies that the antipsychotic operates at the membrane, binding
somewhere there. It’s only a few short hops until it’s identified it is binding
to the dopamine receptors, and blocking them. Antipsychotics block the
dopamine receptor.