Anything immuno/cytokine related is always a bit out of my depth, so I
was wondering if anything had anything to add to this hypothesis.
I've been interested in in vitro THC-induced neurotoxicity since: Chan et
al., J Neurosci. 1998 Jul 15;18(14):5322-32. He shows that THC induced
pronouced apoptosis in hippocampal slices, and that this was PGE2
mediated.
Now whether THC induces neurotoxicity in whole animals is a point of much
contension. Its been shown that THC induces PGE2 release in animals, and
that PGE2 mediates behavioural changes due to THC, as well as the fact
that inhibiting eicosinoid synthesis inhibits some behavioural changes
normally seen in THC treated -HUMANS-.
So, although it looks likely that THC increases the level of PGE2 in
human brains, what if the trauma that a brain slice recieves, causes the
production of heaps of PGE2, and then THC just pushes it over the edge as
far as PGE2 production goes?
So, basically my question is, do you think brain slices have a much
higher PGE2 concentration or COX activity?
But then, THC is also toxic to cultured neurons. Do you think cells in
culture have a higher PGE2 concentration or COX activity?
Thanks for any input.