Hemidactylus at my-dejanews.com wrote in message
<7bev7d$5oh$1 at nnrp1.dejanews.com>...
>In article <7be3iu$cg4$2 at denws02.mw.mediaone.net>,
> "Richard Norman" <rsnorman at mw.mediaone.net> wrote:
>>It is interesting when looking at individuals of given species to note the
>variety of transmitters, but it is also interesting that a certain degree
>conservation exists across phyla. From Shepherd's text _Neurobiology_ (p.
>537-8): (begin quote) "With regard to neurotransmitters, it should already
>apparent that there is a strong tendency toward conservation across the
>phyla. Thus, we have seen that glutamate is an excitatory transmitter and
>GABA is an inhibitory transmitter...; indeed the earliest evidence for the
>identification of these substances as transmitters was obtained in
>invertebrates. Similarly, ACh is widespread as a neurotransmitter in many
>invertebrate species; in fact, many insecticides have as their primary mode
>of action a blocking of cholinergic synapses. Finally, we have noted the
>of 5HT in modulating behavioral states of some invertebrates... One can
>conclude that there is a limited set of small molecules that have similar
>functions across many phyla." (end quote)
>>This is yet another theme of evolution (i.e.- conservation). This does not
>contradict your quote above, but complements it. There is diversity in
>transmitters when looking at, lets say, a human brain, but when comparing
>humans to other species one can appreciate that the same basic ideas are
>continually re-used, perhaps in slightly different contexts(?).
>>I got a little too broad on the "evo, devo, and neuro" post wrt
>Hopefully the conservation subtheme is more appropriate in this context.
>get it right one of these days :-)
>>Shepherd GM. 1994. Neurobiology (3rd ed.). Oxford University Press. New
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A behavioural-functional categorisation of some neurochemicals relevant to
the "AEVASIVE" system (don't worry about what I mean by this system, at
least for now, other than I have used the entire variety of endo-opiates as
a major point of reference):
Although there are usually not a simple relationship between behavioural
effects and the concerted release of different neuromodulators, a few of
these can be characterised according to their function as adaptations to
broadly classified environmental challenges:
Noradrenaline: mediates stress, including stress-related alertness and
increased perceptual resolution or 'sharpening of the senses'. Endoopiates
counterbalance its actions in these respects; But also - a balanced mixture
of the "two" modulators (opioids and norepinephrine) may give rise to forms
of eustress such as different kinds of thrills.
'Substance P' is thought to specifically contribute to pain transmission
(ie. response, experience or actention), at least in the spinal cord. It and
other, vaguely categorisable as similar, signal substances (eg.
prostaglandins, histamine), can be seen as Behaviourally opposed to opioids
(except perhaps for when opioid-action gives rise to feelings of nausea;
since nausea may EPTly be considered a mild form of pain).
Serotonin, on the other hand, can be seen as a modulator that 'sides' with
Endorphins; It is opposed to mediators of distress, and has a prototypal
regulatory action in the direction of parasympathetic and/or opportune
(prototypically, feeding) Behaviour [ ref: 'The Neurobiology of Feeding in
Leeches', Scientific American June 1988].
Dopamine can also be considered an add-on to the Opportunity-side of
AEVASIVE coping and 'the AEVASIVE trend of adaptations'. It
reinforces ---i.e. it promotes by being positively rewarding of--- among
else, AEVASIVE "actentions" [or any ditto *type* of "focuses of
activity/attention"] and lowers thresholds to firing in emotional, cognitive
and motor areas of the brain. In the difference between busy and 'too busy'
dopaminergic activity, apparently lies the commonly noted relation between
creativity and 'its unhealthy extremes', ie madness. In general, "mental
madness" (eg symptoms of disordered cognition covered by the umbrella label
"Schizophrenia") involve actentions with spasmodically manic
motor-behavioural activities and a lot of mental activity.
When the stimulating (or thresholds-lowering) function of Dopamine in the
motor division of the brain is deficient it shows up as symptoms of
'Parkinson's disease' --- that is symptoms such as a greater or lesser
difficulty to 'get going' with certain Behaviour. Meanwhile, on the 'mental
side to the role of Dopamine in the brain, some not very apparent
Behavioural effects of damaged and depleted dopaminergic neural tissues and
pathways is presumably making the thus afflicted mind less flexible and
creative than normal. This effect may however be too subtle and not
ostentatious enough to bee easily recognised and investigated.