Posted by Louise on September 9, 1999, at 9:27:44
In reply to Re: Examples...Is this right?, posted by JohnL on September 8, 1999, at 18:33:26
> Thanks Louise. Let me use an example to show my difficulty understanding agonist vs antagonist so maybe I can figure it out better. Naltrexone is an opiate antagonist. To me that means it blocks the effects of the body's natural opiates at the receptor sites. Does that trick the body into making more opiates because it can't sense there is enough? Same with Remeron. It antagonizes receptor sites and basically tricks the brain into stepping up production of serotonin because of the perceived lack of serotonin because it's being blocked? Is that how it works, or am I way off base? Sorry, sometimes I can understand the difficult stuff real easy, but the simple stuff confuses me. Thanks for your help.
Hi again .......
I've read that Naltrexone is used to reduce self-injurious behaviour, with the rationale that self -harm itself may trigger production of endogenous opiates in the brain, therefore providing some sort of powerful reward for the self-injurious behaviour. I would think it follows then that as an opiate antagonist, the 'reward' would be reduced. I know that the drug can also be used in other situations so I don’t know whether this applies to you.As far as the neurotransmitter action is concerned, I’m not sure exactly how this drug works, it could be by blocking opiate receptor sites or by one of the other antagonist mechanisms. I think you’re probably looking too far in wondering whether this tricks the body into producing more opiates. From my understanding it would simply reduce levels by blocking receptor sites or another antagonistic mechanism.
Remeron is a dual acting antidepressant which increases levels of both noradrenaline and serotonin .The drug stimulates norepinephrine and serotonin release while also blocking two specific serotonin receptors, (5-HT2 and 5-HT3). As far as I’m concerened, rather than diving into biochemical stuff, the levels of these nt’s are elevated, and the blocking of reuptake into the presynaptic neuron (think of this as the first one in the chain of 2 etc. etc. etc.) both have the effect of increasing the levels of these nt’s ‘floating around in the brain’. More serotonin, more happiness!
What is a bit confusing is that something which blocks receptor sites actually has an agonistic effect. This is because it can be inhibitory effects which are blocked, or because by blocking reuptake (as is SSRI's (I think!)) back into the 'no 1 neuron', the drug is preventing the nt from being broken down or taken back up into the neron and restored. (this would reduce levels available to the 'no 2 / receiving' neuron.) I think that the confusion is that when 'blockers' are discussed, it is easy to assume with little knowledge that you're talking about the receptors on the 'receiving' neuron, which sounds like reducing levels, when it can mean that it is preventing re-uptake into the transmitting (no 1) neuron and therefore increases levels.I’m a student, not an expert, and I haven’t managed 100% in anything yet (although I did manage one 97%!), so if you’re still unsure, I would call Dr. Bob!
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Am I making sense?!
(Check out Dr. Bob’s psychopharmacology tips too.)
Louise
poster:Louise
thread:11222
URL: http://www.dr-bob.org/babble/19990829/msgs/11292.html