Due to other time-constraints I have not been keeping up with the ASA list,
so the following comment goes back to a thread from last month. A t the risk
of splitting the hairs of already split hairs I would like to respond to the
following post from Stephen Matheson in response to my post of Oct. 28
>Judy Toronchuk wrote :
>>Although I am in neuroscience I have never read anything
>>about individuals responding to pink light, but I can tell
>>you that norepinephrine (also called noradrenalin) is
>>hardly a tranquilizer. It is structurally nearly
>>identical to adrenalin and affects the body and brain in
>>an almost identical manner.
Stephen Matheson wrote: "But the statements above regarding norepinephrine
and
epinephrine are inaccurate. Norepi is, in fact, a
powerful sedative if applied to the right cells
in the brain. (For aficionados, this would be the
locus coeruleus, the area of the brain that actually
makes and secretes norepi. It turns out that
an autofeedback loop activates alpha-2
receptors on the same neurons and can shut
down LC activity.) The structural similarity to
epi is irrelevant: the effects of interest are
controlled by the receptors, not by the
chemical messengers themselves. The above
statements suggest that norepi should be
considered a stimulant just because it
looks like epi, which is considered a
stimulant. All these generalizations are
flawed by attributing activity (in the
brain especially) to the nature of the
chemical messenger. Big mistake.
Baugh makes it too, though he's so
pervasively ignorant that it's hard to even
attribute specific errors to his claims."
My response to Stephen:
I was trying to give a fast, simple reply, but of course nothing is truly
simple. I know the effect of a transmitter is due to structure of the
receptor not that of the transmitter, but in fact epinephrine and
norepinephrine (NE) not only have similar structure but will bind to the
same alpha and beta adrenergic receptor sites. So in this case the structure
is not irrelevant. While the locus coeruleus alpha 2 autoreceptor, when
stimulated, does have a sedative effect, it does so because of negative
feedback which turns down the levels of NE sent out to the rest of the
brain. In other words the sedation is due to decreased NE transmission
everywhere else. In _general_ the effects of NE on the rest of the brain
and body have an arousing effect e.g. hence the stimulant amphetamine
increases levels of NE; the sympathetic nervous system uses NE to arouse the
"fight and flight" mechanism; resperpine which blocks reuptake of NE was
used to treat hypertension etc.
I suspect the line of reasoning behind Baugh's original statement _might_
have had someting to do with the fact that broad spectrum light is effective
in treating seasonal affective disorder and sometimes depression, and many
anti-depressants increase NE levels as well as serotonin levels. But an
antidepressant is not the same thing as a tranquilizer.
Judy Toronchuk
Psychology & Biology
Trinity Western University
Langely, BC
This archive was generated by hypermail 2b29 : Fri Nov 30 2001 - 20:26:40 EST