matthew john baggott
bagg at ellis.uchicago.edu
Sat Oct 10 02:37:41 EST 1992
In article <1992Oct9.085725.26902 at u.washington.edu> lamontg at carson.u.washington.edu (Lamont Granquist) writes:
>alves at calvin.usc.edu (William Alves) writes:
>>First, this whole neurotransmitter business. As I see it, there are only
>>two possible effects a neurotransmitter can have on a neuron - it can
>>inhibit or excite the cell. Then doesn't it seem logical that there would
>>be only two types of neurotransmitters, instead of the pharmacopeia that
>>has been discovered? What is the difference between inhibition from one
>>neurotransmitter and another?
>Well, in a nutshell, your body is more complex than that. Like what would
>happen if your body dumped some adrenalin into your system and every nerve
>in your body responded to it? -- thats probably the simplest thing to consider.
Having different neurotransmitter systems lets the body have separate
"circuits" close together without having neurotransitters from one
interfere with another circuit.
>>Second, the non-technical sources I have read have made a big deal out of
>>the chemical similarities between certain hallucinogens (LSD for example)
>>and certain neurotransmitters (serotonin for example). Yet is simple
>>mimickry behind all of the drug's effects? If that is so, why do different
>>serotonin-like drugs have wildly different effects, and others have none
>Cuz, for example, you can mimic 5-HT at 5-HT1A, 5-HT1B, 5-HT1C, 5-HT1D, 5-HT2A
>and 5-HT2B (*) receptor sites in addition to "mimicing 5-HT" via blocking the
>reuptake 5-HT at the reuptake transporter. Oh, and you can also enter the
>neuron and release a neurotransmitter directly like amphetamines do to DA.
>And then there is also potential effects to second messangers and effects on
>calcium channels and probably other shit that I'm forgetting or haven't yet
>learned about.. (oh and then there's chronic effects like the receptor
>down/up regulation which is thought to be responsible for antidepressant
>responce and also things like heroin resonance -- but this might be due to
>more complicated factors like second messagers or axonal arborization --
>blah, blah, blah...)
There are drugs which imitate 5-HT (for ex.) at its various receptors
and transporters. There are drugs which attach to its receptors a/o
transporters by which don't do anything other than get in the way.
These are agonists and antagonists respectively. And there are drugs
which affect the functioning of the serotonergic system in some other
way and don't directly "imitate" serotonin in any way.
There are a number of ways of measuring the strength with which a
drug attaches to a receptor and the degree to which its presence
causes some further event in the receptor-bearing neuron. So a
serotonergic drug doesn't just imitate serotonin, it imitates it to
various degrees in various situations.
Futhermore, it is rare for a drug to just affect one neurotransmitter
system. Many "imitate" several (such as both dopamine and serotonin).
In addition, a drug might affect the neuron's behavior without imitating
a neurotransmitter. Lamont names some of these ways above.
>Lamont Granquist lamontg at u.washington.edu
> "'Tis an ill wind that blows no minds."
> -- Principia Discordia
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