In article <3v0i6i$l1n at portal.gmu.edu> HARRY R. ERWIN,
herwin at osf1.gmu.edu writes:
>channels reopen. Meanwhile the membrane is a bit depolarized and
>in sensitivity. During this period, if a GABA receptor is activated, it
>produces arachnoic acid, which can bind to the PKC, stabilizing it. The
These are interesting ideas. Is any of this work available in published
form? Is any of it electrophysiological data? What is the evidence that
LTP is *not* involved in memory?
I've never heard of GABA receptors producing arachnoic (arachidonic?)
acid. Is there any independent confirmation of this phenomenon?
It seems to me that the long-term shut down of potassium channels would
be interpreted as LTP in a current clamp or extracellular recording. But
LTP is defined as a synaptic phenomenon. Do any of the studies you
describe specifically address synaptic phenomena?
Rather than "rapid convergence to a common model", these data seem a bit
more like splitting off into an alternate paradigm than the one most
studies are currently pursuing.