Psycho-Babble Medication Thread 11222

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Anhedonia, Agonist, Antagonist....???

Posted by JohnL on September 8, 1999, at 3:53:42

I am hoping someone might explain some terms so I might understand them better. First, how is "anhedonia" pronounced? My general practioner didn't even know what this word meant. After that, I didn't even venture trying to ask him my next question, which was to explain to me what is meant by "agonist" and "antagonist". Dictionary meanings didn't clarify this much to me. Can you share with me examples of these words in action? For example, Remeron I believe is an antagonist...what does that mean? Does it hamper something or enhance something? What is the end result of an agonist? What is the end result of an antagonist? I hope this doesn't sound too silly, it's probably psych 101, but I read these words all the time and never really understand what they mean or how they work. Thanks in advance for your help.

 

Re: Anhedonia, Agonist, Antagonist....???

Posted by Louise on September 8, 1999, at 4:56:14

In reply to Anhedonia, Agonist, Antagonist....???, posted by JohnL on September 8, 1999, at 3:53:42

> I am hoping someone might explain some terms so I might understand them better. First, how is "anhedonia" pronounced? My general practioner didn't even know what this word meant. After that, I didn't even venture trying to ask him my next question, which was to explain to me what is meant by "agonist" and "antagonist". Dictionary meanings didn't clarify this much to me. Can you share with me examples of these words in action? For example, Remeron I believe is an antagonist...what does that mean? Does it hamper something or enhance something? What is the end result of an agonist? What is the end result of an antagonist? I hope this doesn't sound too silly, it's probably psych 101, but I read these words all the time and never really understand what they mean or how they work. Thanks in advance for your help.

Hi John

Psychotropic drugs (or any substance affecting brain chemistry) may be described as agonist or antagonist according to how they effect neurotransmitter action in the brain. When a neuron fires, neurotransmitters are released from the cell via the synapse and one mechanism that takes place is binding to receptors on a subsequent neuron. Think of it like a chain reaction running between cells through the brain, with the neurotransmitters which have been released passing the link / message on from one neuron to another. A further mechanism is the re-uptake of neurotransmitters which are 'floating around' after release. Although some bind to another cell (post synaptic receptors) to carry on the 'chain', some are taken back (called re-uptake) into the neuron which released them. Remaining neurotransmitters are broken down by enzymes.

Drugs can interfere with these (and other) processes of neurotransmitter action. Drugs which facilitate the effect of a specific neurotransmitter action are called agonists. They 'heighten' the effect of the neurotransmitter (you could think of it as allowing this neurotransmitter to flow more freely around the brain). The agonistic drugs work e.g. by destroying the enzymes which break the target neurotransmitter down; blocking deactivation by blocking reuptake.

Antagonistic drugs do the opposite; they inhibit the effects of a the target neurotransmitter e.g by blocking a receptor site on the (2nd / receiving) cell so that the neurotransmitters can't permeate the cell.

Different drugs / chemicals can act as agonists / antagonists for different types of receptors in the brain. e.g. an anti-psychotic drug such as chlorpromazine can inhibit / block dopamine action. Drugs such as LSD stimulate seratonin receptors, producing a 'high', this is therefore an agonist.

I hope this helps. If it's still unclear, post another message and I'll try again!

Louise

P.S. I haven't got a clue how you pronounce anhedonia!

 

Re: A A A..?? - Neuroscience info site

Posted by Louise on September 8, 1999, at 5:00:25

In reply to Anhedonia, Agonist, Antagonist....???, posted by JohnL on September 8, 1999, at 3:53:42

Hello again,

One of the best web sites I know (and much used by psychology undergraduates!) is The Neuroscience for Kids website run by Dr Eric Chudler. If you're really interested, you can sign up to receive the newsletter by email. I have done this since last Sept and I'm pretty impressed.

http://faculty.washington.edu/chudler/neurok.html

 

Re: Examples...Is this right?

Posted by JohnL on September 8, 1999, at 18:33:26

In reply to Re: A A A..?? - Neuroscience info site, posted by Louise on September 8, 1999, at 5:00:25

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.

 

Re: Examples...Is this right?

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!

Did this help?

Am I making sense?!

(Check out Dr. Bob’s psychopharmacology tips too.)

Louise


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