Print

Print


Dear All,

Two things:

1)  I noticed someone mentioned that "Dopamine is normally stored in one
end of a nerve cell and is continuously released at a steady, gradual
rate as needed."  In actual fact, like all neurotransmitters, dopamine
is released only in response to a nerve impulse reaching the nerve
terminal.  The released dopamine from the first cell then diffuses over
to the other side of the synapse where it acts, usually to inhibit
further impulses from the second cell.  At the same time, dopamine is
actively reabsorbed into the nerve cells.  The end result is that the
dopamine concentration within a synaptic cleft is anything but constant,
and is rather pulsitile in nature.  The interesting and, at least to me,
somewhat paradoxical, thing about this is that externally applied
dopamine works at all to reduce PD symptoms.    I guess one possible
mechanism would be for the external dopamine to bind to many of the
available receptors making the neuron hypersensitive to the naturally
released dopamine.

2)  I also noticed that someone was commenting on pallidotomies and
listed tremor as one of the symptoms that is potentially reduced by the
procedure.  In fact, the ideal candidate for pallidotomy is not someone
with a great degree of tremor as it is not reliably reduced by this
surgery.  A much better candidate for pallidotomy is one who has severe
drug-induced dyskinesias, for it is this symptom (actually a
side-effect) that is most often reduced.  In most centers, the rates of
"blindness" and "paralysis" are more along the lines of 1-2% rather than
the stated 5%.  Additionally, "blindness" in most cases refers to a
blind spot that may not even be noticed by the patient (still, nothing
to take lightly).