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Thread: Is there any proof that Chrlopromazine (Thorazine) DOESN'T have any effect on GABA?

  1. #1

    Capsule Is there any proof that Chrlopromazine (Thorazine) DOESN'T have any effect on GABA?

    I'd say it was equally as effective as Diazepam for anxiety. It is also the only drug that isn't a benzo or barbiturate that has had any effect at all on my anxiety. I feel like it has at least a weak affinity for GABA receptors.
    I haven't found any proof that it DOES, but is there any proof that it DOESN'T?

  2. #2
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    Jekyl Anhydride's Avatar
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    I would look to it's Serotonin antagonism to explain the anxiety relief more so than GABA. If you need proof though it's most likely going to be behind a $ pay wall.

    like this:

    Annals of the New York Academy of Sciences-
    CHLORPROMAZINE AND GABA
    https://nyaspubs.onlinelibrary.wiley...1969.tb54273.x

  3. #3
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    kleinerkiffer's Avatar
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    ^ I've skimmed through the paper Jekyl posted ( just a tip, a hub in the Sci helps with the pay wall ) and the paper is really old and imo hasn't much value, but it's pretty much the only paper talking about cpz and Gaba (or better free amino acids in general iirc)

    As Jekyl said, Serotonin receptor antagonism explains the anxiolytic effects, plus it's simply a dirty drug and interacts with a lot of receptors (it might even have some affinity to Gaba receptors, but at concentrations you'll never reach)

  4. #4
    Chlorpromazine is a "typical" antipsychotic, i.e. one with significant activity as a dopamine antagonist (in addition to the serotonergic and antihistaminergic effects you find in 2nd-generation-antipsychotics).

    The problem with typical antipsychotics is that once you exceed a certain threshold (when a significant portion of dopamine receptors have been blocked) you start developing unpleasant side-effects, most notably parkinsonism (i.e. temporary shaking similar to a patient with Parkinson's disease. "Real" PD results from the death of dopaminergic neurons; therefore, reversibly blocking dopamine receptors with antipsychotics temporarily produces similar effects). If high doses are taken for extended amounts of time, some side-effects may become persistent.

    Thus, they have mostly been supplanted by 2nd-generation antipsychotics.

    Re: GABAergic activity, chlorpromazine was invented almost 70 years ago, and has seen widespread use in clinical practice since atleast 60 years. Its pharmacology has been studied extensively, and if it had any significant affinity for binding sites on the GABA receptor, it probably would have been noticed by now. Remember, there was *a lot* of commercial interest in exploring the structure-activity-relationship of the phenothiazine class of drugs in order to find more well-tolerated antihistamines, antiemetics, antipsychotics and sedatives.
    Last edited by Hodor; 18-01-2019 at 18:04.

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