Models for PD (4)

["Ronald F. Vetter" <rfvetter@xxxxxxxxxxxxxxxx>]

Phil Gesotti <ermin@xxxxxxxxxxxxx> wrote:

<<Where is the summing node, is also a question. Is this a chemical
reaction between two neurotransmitters as Duvoisin's book would have you
believe? Is it the interaction of different types of receptors in the
same pathway as might be suggested by STEPHAN SCHWARTZ's post?>>

The five gigabillion neurons are vastly interconnected with much
redundancy and alternatives in many parts of the neural networks.

every square inch of skin has millions of sensors and connections. every
muscle has many connections. the favorite transmitter of some synapses
is dominant for some connections apparently, but scarcity of some is
changed by releases of large amounts of one or a substitute chemical
under certain conditions. Being startled may ascend to fright or flight
adrenaline (epenephrine) overload; &c.

Duvoisin argues that dopamine receptor cells in some neurons receive
signals that reduce the output from that cell - that output being
acetylcholine.  There are mostly acetylcholine-as-neurotransmitter
synapse junctions in the brain. "It is believed that dopamine acts to
restrain the acetylcholine nerve cells, and that in parkinsonism the
acetylcholine nerve cells are released from this restraining
influence.": page 59 third edition. Parkinson's Disease.

The control circuit in the model is not functional when the "static" is
dominant over the dopamine-ion-transmitters are too few to make the
control circuit function.  This is a model of the "symptoms".

The model of the disease etiology is a whole different ballgame!
--
ron      1936, dz PD 1984  Ridgecrest, California
Ronald F. Vetter <rfvetter@xxxxxxxxxxxxxxxx>