Not being too terribly educated on neurobiology, I was wondering if someone
could answer a few questions related to quinolinic acid excitotoxicity ...
First, it is my understanding that quinolinic acid's excitory effect upon
NMDA receptors is responsible for a great deal of neurotoxicity in disease
(due to induction of the conversion enzyme -- indolamine 2,3-dioxygenase?
-- which converts L-tryp to quinolinic acid). Is this well-established,
or is it just guesswork at this point?
Secondly, has quinolinic acid been found to be responsible for neurotoxicity
involved in other types of brain injury (stroke, siezure, profound
Third, have agents which block quinolinic acid's NMDA agonist activity
(either general NMDA blocks like ketamine and MK801, or specific blocks
like picolinic acid) been tested for ability to prevent neurotoxicity?
Fourth, since general blockade of NMDA receptors may be considered
undesirable, does picolinic acid (or any of its salts) cross the blood-
brain barrier effectively?
Finally, and just out of curiosity, has any evidence of neurotoxicity
been found in people who took L-tryptophan (discount EMS, since the
evidence for the effect of a contaminant is pretty strong)?
I'm just curious, since it's my hope that in the future (probably the
far future) disease or injury induced brain damage will be reduced or
eliminated. I'm not about to start dosing up on ketamine! (an example
of the cure being worse than the condition, I'm sure).
| Bill White +1-614-594-3434 | bwhite at oucsace.cs.ohiou.edu |
| 31 Curran Dr., Athens OH 45701 | bwhite at bigbird.cs.ohiou.edu (alternate) |
| SCA: Erasmus Marwick, Dernehealde Pursuivant, Dernehealde, Middle Kingdom |