On Sat, 14 Feb 2004 15:20:08 -0500, "Klenow" <bakedbeans at spam.not>
} Amazingly, the Weiss paper doesn't say what kind of electrode they used
} (monopolar or bipolar or even composition). They also don't say what kind
} of DC current they were giving...only the magnitude and duration. It's kind
} of a funny paper. Their entire introduction is spent describing their
} broken stimulator and attempts to fix it. They had been giving low
} frequency (depotentiation) stimulation for 15 minutes to "quench" kindling,
} but when they had their stimulator fixed they weren't able to quench
} anymore. When they changed stimulators they still weren't able to
} demonstrate their effect. When they had an engineer look at their
} stimulators they discovered that they were pumping out low amplitude DC
} current continuously, so they decided to see how this affects kindling.
} They found that it mirrored their initial low frequency experiments.
Well, if they discovered something, it might be instructive to include
this highly abnormal "method". At least it precludes being accused of
some more common mistakes. But yes, it does sound an odd paper.
} They did silver staining for necrosis and GFAP staining for gliosis and
} found that rats treated with DC showed increases in both these stains around
} the electrode tip compared to controls. For some reason they still don't
} think there was lesioning going on. They describe some acute in vitro
} studies showing that cells survive (at least hours) after DC application.
} Why not delayed cell death then? I suppose my question is that if you can
} generate a great DC lesion with 100 uA for 10-20 seconds, then why not a
} nifty lesion with 15 uA for 15 minutes? I think I remember the original
} kindling studies by Goddard examining the effects of lesions on kindling and
} found the same results Weiss is getting.
Delayed apoptosis isn't out of the question. But alternatives would be
worth tracking down. After such a long exposure, might there not be
some deposition of the probe material? Not likely, but an interesting
question. I think there's more chance that there was some sort of
membrane disruption, fatal or no. Something reducing function from a
hyper- to a normal level. Certainly apopotosis can be instigated by a
process that doesn't become apparent for some time.