[John Anderson (960118.0745)]
It seems to me that finding the various components of control systems in real
nervous systems is tricky business, even in very simple ones. For example,
consider the gill withdrawal circuit of the marine snail Aplysia, studied by
Kandel and Schwartz, and discussed on pages 113-115 of _Introduction to Modern
Psychology_ (1990) by Robertson and Powers (IMP), on pages 1010-1011 of
_Principles of Neural Science_ (1991) by Kandel, Schwartz, and Jessell, and in
chapter 11 of _Neurons and Networks_ (1992) by Dowling. If you touch the
animal on the skin near its gill (the mantle), it quickly pulls the gill
inside its body. Touch it over and over, and withdrawal becomes less and less
vigorous. This is called "habituation". If you give the animal a shock on
its head or tail, and _then_ touch the mantle, the gill is withdrawn more
vigorously than it would have been without the shock. This is called
"sensitization".
Here is a crude diagram of the neural circuit responsible for all this (see
Fig. 8.1 of IMP for a better illustration):
head---<(FI)>---tail
>
>
---------- ----- ------
mantle | | |
\ | ^ |
>-------(SN)--------<(IN)--------|--
/ | | | |
> > > >
---------- | ^ ^
----------------<(MN)
>
>
___^___
> gill |
Only one of each type of neuron in the circuit is shown. The skin near the
gill is innervated by a total of 24 sensory neurons (SN). The SN's contact 6
motor neurons (MN) innervating the gill muscle. The SN's also contact 1
inhibitory and 2 excitatory interneurons (IN), which in turn contact the MN's.
The mechanism of habituation seems to involve inactivation of a
depolarization-sensitive calcium channel in the presynapses of the SN's
innervating the mantle. This reduces the flow of calcium ions (Ca++) into the
synapses during the depolarization caused by each sensory action potential.
Ca++ influx is required for neurotransmitter release from the presynaptic
membrane, so reducing the Ca++ current into the terminal reduces the amount of
neurotransmitter released onto the motor neurons responsible for withdrawing
the gill. Habituation also involves a reduction in the ability of transmitter
vesicles to be readied for release.
Sensitization, on the other hand, involves an _increase_ in the Ca++ current
into the SN terminals, resulting in _more_ neurotransmitter being released
with each sensory action potential. This is accomplished in the following
way: Shocking the head or tail excites "facilitating interneurons" (FI), which
release serotonin onto the axon terminals of the SN. This activates the
enzyme (adenylate cyclase) responsible for synthesizing cyclic AMP (cAMP) in
the axon terminals, leading to an increase in the concentration of cAMP in the
terminals. The elevated cAMP activates an enzyme (A kinase) that attaches a
phosphate group to a certain type of potassium (K+) channel, reducing its K+
conductance. Ordinarily, K+ efflux out of the axon terminal during an action
potential helps restore the resting potential of the terminal's membrane.
Reducing K+ efflux prolongs the depolarization due to an action potential,
thus allowing Ca++ to flow through voltage-activated Ca-channels for a longer
time, leading to a larger buildup of internal Ca++, which leads to more
transmitter being released.
There is a control theory explanation for gill withdrawal presented in section
8.3 of IMP, but I find it muddled and confusing. It would be instructive for
me, and maybe for others too, if some veteran PCTer(s) would render the gill
withdrawal phenomena into control theory terms here on CSGNET.
Thanks for your help.
John