Psycho-Babble Medication | about biological treatments | Framed
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Re: In PLAIN English, can someone please explain... » SLS

Posted by v on September 22, 2001, at 7:44:15

In reply to Re: In PLAIN English, can someone please explain..., posted by SLS on September 22, 2001, at 1:46:44

scott..
i just want to thank you for your information. it is quite frustrating not having at least a decent rudimentary understanding, hence the original post by janelle... and BTW, thanks janelle for asking the question!

and it was a great follow-up to "making the three tenors sing" (i love that phrase!) which gave just the basic info

thanks again,
v

> Hello one and all.
>
> I'll give it a shot. I know it looks like a lot of words. You asked for specific details and a simple way of describing them. Hopefully, you'll find both. I had nothing else better to do after Bruce, so it's no big deal if I've failed. I just like to waste bandwidth.
>
> The most important thing to remember is that trying to break down these illnesses into a simple recipe of the known chemicals has not worked very well. To a great degree, calculated trial-and-error is still necessary when trying to figure out which drugs will work for each individual. Even though two people's depressions look exactly alike, they can be very different chemically (and psychologically).
>
> You can skip the next paragraph if you like and move on to the one succeeding it.
>
> Using various methods, scientists have tentatively mapped out which brain regions and their associated chemical messengers (neurotransmitters) are involved with specific functions: locomotor (movement), thought, mood, drive, sleep, sensory, hormonal, control of organs, and other such stuff. Many of these regions use the same neurotransmitters. For instance, regions known to be composed predominantly of dopaminergic (using the neurotransmitter dopamine) neurons include those that participate in locomotion, drive, reward, organization of thought, and the perception of emotion. Areas rich in norepinephrine neurons include those that initiate movement, direct thought, and increase mental energy and level of alertness. Areas containing serotonergic (serotonin) neurons can regulate and influence the activity of those listed above. It seems that OCD might involve an imbalance in the relationship between norepinephrine and serotonin pathways. Glutamate neurons activate dopamine neurons if stimulated by norepinephrine neurons and not inhibited by GABA neurons.
>
> Now, if this stuff seems to be getting more complex as we continue to try figuring out the way the brain works, you are looking at but the tip of the ice-berg. There are literally hundreds of different chemical messengers both inside and outside the neuron. And this doesn't take into consideration enzyme systems and control of gene activity.
>
> So, what causes depression? How do antidepressants work?
>
> Cruz has pretty much captured the flavor.
>
> Neuroscience has positioned us closer to unlocking some doors. Psychiatry is beginning to find the information evolving from neuroscience useful in constructing associations between what drugs do chemically and what they do clinically.
>
> Example: Antipsychotics reduce dopamine activity in the frontal cortex by blocking the dopamine receptors (neurotransmitter = key; receptor = keyhole; ion-channel = door). The frontal cortex, high in dopamine neurons, is responsible for organizing thought. Disorganized thinking is a feature of schizophrenia. The frontal cortex of schizophrenics and siblings of schizophrenics have abnormally high numbers of dopamine type-1 receptors in the frontal cortex. This yields a hypothesis that certain features of schizophrenia are produced by excessive or erratic dopaminergic neuronal activity.
>
> Psychiatrists can also use their experience with people and drugs to witness trends in the associations between specific illnesses and their subtypes (symptom clusters), the drugs that work for them, and the biological activities of these drugs. Some drugs increase the number of neurotransmitter molecules available to stimulate neuron_2 by preventing them from being absorbed and recycled by neuron_1 after it has released them to send its message to neuron_2 - reuptake inhibition. Other drugs increase the stimulation of neuron_2 receptors by acting as a fake neurotransmitter. Still other drugs reduce the stimulation of neuron_2 by blocking or hiding these receptors from the real neurotransmitter. Some drugs allow for a build up of neurotransmitter levels in neuron_1 by preventing it from getting rid of the excess normally accomplished by a disassembly enzyme - MAO-inhibition. Anticonvulsant mood stabilizers block ion-channels and/or increase GABA activity, which usually results in reducing the excitability of norepinephrine and dopamine neurons and influencing the overall balance of activity. Lithium? Well, it does so many different things that are relevant to neuronal function, that it's hard to know where to start. It pretty much acts inside neuron_2 to produce changes on its outside.
>
> So, now we finally arrive at the point where we started. (You can now reread the first paragraph if you like).
>
> How's that?
>
> Please don't ask me to do it again. My brain hurts. Besides, I'm sure there are plenty of factual errors for others to correct. Please forgive me for not proof-reading. I'll let that be your job. :-)
>
> I had fun.
>
> :-)
>
> Silly.
>
> See ya'...
>
>
> - Scott


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poster:v thread:79238
URL: http://www.dr-bob.org/babble/20010917/msgs/79290.html