Mdh at debug.cuc.ab.ca (Mike Hamilton) writes:
> I am curious, I have been reading about the GABA inhibitory
>neurotransmitter, and how the sedatives such as alcohol and barbiturates
>are attributed to their actions on these receptors. The reasoning behind
>it is that a barbiturate would attach to the receptor would would result
>in the opening of a chloride channel, which in turn results in the
>hyperpolarization of the neuro and thus sedation? Could someone explain
>why this hyperpolarization of the neuro would result in sedation? From
>what I understand, the average potential across a neuron is approx. 90mV,
>so why would increasing this sedate a person?
A typical resting potential might be -70mv and the threshold for firing
up around -60, i.e., 10mv positive to rest. Any input that shifts the
other direction "subtracts" from excitatory inputs and makes the cell
less likely to fire.
Were this to happen in a widespread way (as from systemic drugs), a lot
fewer cortical neurons would be firing (in the usual manner, though the
number of spindles might increase). That makes movement less likely, and
probably thought as well.
If the drug affects one of the amine systems (those lawn-sprinkler-like
systems from the brainstem and basal forebrain that affect excitability
in many places at once), whole areas of cerebral cortex would be idling.
There's more in chapter six of Calvin & Ojemann, CONVERSATIONS WITH
NEIL'S BRAIN, just out from Addison-Wesley.
William H. Calvin WCalvin at U.Washington.edu
University of Washington NJ-15
Seattle, Washington 98195 FAX:1-206-720-1989