• Neuroscience & Pharmacology Discussion Welcome Guest
    Posting Rules Bluelight Rules
    Recent Journal Articles Chemistry Mega-Thread
    FREE Chemistry Databases! Self-Education Guide

  • N&PD Moderators: Skorpio | someguyontheinternet

Explaining Antipsychotics.

MedicinalUser247

MedicinalUser247

Music Ambassador
Joined
Aug 2, 2023
Messages
4,746
Among many antipsychotics there are many differences. First there are Atypical antipsychotics. Some have more D2 antagonism and some have more 5-HT2 antagonism. For instance Risperidone is an Atypical antipsychotic with the highest rate of D2 antagonism among the Atypicals. But Clozapine and Zyprexa have the highest rate of 5-HT2 antagonism. Seroquel also has a high rate of 5-HT2 antagonism, but also has a higher H1 antagonism to it. Second there are Typical antipsychotics with two categories. There's high potency and low potency. For instance Haldol and prolixin are both high potency Typical antipsychotics with the highest level of Extrapyramidal symptoms. Then there are low potency Typical antipsychotics such as Thorazine which is much more relaxing than Haldol with less Extrapyramidal symptoms. And unlike which most people think your more likely to get a Haldol shuffle than a Thorazine shuffle. If you have any questions about antipsychotics feel free to ask.
 
Last edited:
You make it obvious that your asking questions that you already know. Please by all means contribute to the thread.
 
Oral Haloperidol can cause terrible withdrawal symptoms upon dose reduction or full discontinutation. In my case it was worse and lasted much longer than benzo withdrawal.
 
Extrapyramidal symptoms are caused by antidopaminic action in the brains cerebral cortex. If you had strong enough 5-HT2 antagonism it could fight off 5-HT2 agonism, but that is rare.
 
The extrapyramidal symptoms come from dopamine antagonism is the striatum of the basal ganglia specifically. There are two pathways that govern voluntary initiation of movement. One that helps to initiate and one that suppresses. Both of these pathways receive dopaminergic projections from the same set of dopaminergic neurons in the substantial nigra but the direct pathway has d1 receptors which are excitatory and the indirect pathway has d2 receptors which are inhibitory. These are both GCPRs and the d1 is Gs coupled which means that it increases the possibility of an action potential and d2 is Gi coupled which decreases the possibility of an action potential.

When d2 is blocked we do not get suppression of movement from the indirect pathway when it would normally occur, leading to the extrapyramidal symptoms
 
When it comes to antagonists and agonists, if the compounds compete for the same binding site and they are in equal concentration in the target tissue, the compound with a higher affinity will win out and bind the receptor. This doesn't apply if they bind at different sites, for example if you have a noncompetitive antagonist binding at an allosteric site then the endogenous transmitter has no way of displacing the antagonist even if the transmitter is in very high concentrations
 
Last edited:
Any rules of thumb when trying to determine which antipsychotic will block which recreational drug? For example will D2 antagonist antipsychotics block amphetamine(dopamine) but not MDMA(serotonin), and will 5-HT2 antagonist antipsychotics block MDMA but not amphetamine? And what about psychedelics?
 
You must log in or register to reply here.
Top