If NO is that important why hasn't a therapy protocol been written up for it? There are thousands of neurologists that have known about this for years and every single one has failed in that task.
http://www.frontiersin.org/Journal/10.3389/fncel.2013.00190/full?utm_source=newsletter&utm_medium=email&utm_campaign=Neuroscience-w46-2013
Neil Hardingham‡,
James Dachtler†‡ and
Kevin Fox*
- School of Biosciences, Cardiff University, Cardiff, UK
Since the observation that nitric oxide (NO) can act as an
intercellular messenger in the brain,
the past 25 years have witnessed
the steady accumulation of evidence that it acts pre-synaptically at
both glutamatergic and GABAergic synapses to alter release-probability
in synaptic plasticity. NO does so by acting on the synaptic machinery
involved in transmitter release and, in a coordinated fashion, on
vesicular recycling mechanisms. In this review, we examine the body of
evidence for NO acting as a retrograde factor at synapses, and the
evidence from
in vivo and
in vitro studies that
specifically establish NOS1 (neuronal nitric oxide synthase) as the
important isoform of NO synthase in this process. The NOS1 isoform is
found at two very different locations and at two different spatial
scales both in the cortex and hippocampus. On the one hand it is located
diffusely in the cytoplasm of a small population of GABAergic neurons
and on the other hand the alpha isoform is located discretely at the
post-synaptic density (PSD) in spines of pyramidal cells. The present
evidence is that the number of NOS1 molecules that exist at the PSD are
so low that a spine can only give rise to modest concentrations of NO
and therefore only exert a very local action. The NO receptor guanylate
cyclase is located both pre- and post-synaptically and this suggests a
role for NO in the coordination of local pre- and post-synaptic function
during plasticity at individual synapses. Recent evidence shows that
NOS1 is also located post-synaptic to GABAergic synapses and plays a
pre-synaptic role in GABAergic plasticity as well as glutamatergic
plasticity. Studies on the function of NO in plasticity at the cellular
level are corroborated by evidence that NO is also involved in
experience-dependent plasticity in the cerebral cortex.
No comments:
Post a Comment