This agerelated deficit is specific to certain bra in regions and end productinh ibit ion by GLU and GLU analogues appears in tact. Ca lc ium activation and phospha te activationof PAG are also dimin ished in the aged nervous system. In general, ammonia levels increase in the bra in as a functionof age, whereas GLU contenttendsto decrease in cortical areas has proposed th atabno rmalammonia detoxifica erative diseases.Ca lc ium dependentGLU release appears no rmalor elevated in aged rats depend ingon the bra in region and intensityof depolarization condit ions. Ifthe aged bra in is less responsiveto feedback inhi, then agents thatpertu rb release may be more effective in sustaining prolonged periodsof excessive GLU releaseor delayed G LU inactivation.A numberof neuro tox ican ts are known to influence GLU. By contrast, metabolic extremes like hypoxia and ischemiaproduce severe but acute elevationsof GLU efflux and neuronaldea th. Mofezolac Neurodegenerative processes are more insidious in na tu re and are mo re likely related to modest butsustained elevationof extracellular EAA concen tra tions.Trime thylt in produces substantial damage to thehippocampus and related limbic and cortical areas. Theseaged an im als also showed agrea ter fall inhr a in GLU andASP contenthr after ka in ic ac id trea tm ent also found KA to induce a significantlygrea ter inc rease in ASP releasefromhra in slicesof aged rats.Thesestud iessuggest th ataged an im als arc comp romis ed in re sponseto excessive act iv ationof KA recep tors. Oln ey and co wo rke rs havereport edsimil arfindings andthese datatendtosubst anti atethehum andata on domoic acid tox icity. The aged ne rvousMofezolac system is also kn ownto havecomp ro. Itis a lso known th atc onditionsth atc om promisen eu ron alene rgymetaboli sm greatly exace rba te the tox icityof exog enousEAA cemia is knownto inc rease thest imulated releaseof ASP and GLU cemia on potass ium st imulated GLU and ASP release in aged rats haveprev ious lybe en ex am in ed andfound to he augm entedtothes amelevel as th atofadultcontrols. S ubsequentau thors will also add ress thep ivo talroleof energymetaboli sm andmitochondrial funct ion in agere la tedneu rod eg ener ativcprocesses.N cu ro tox ins th at inh ibitelectron tr an sport inmi to chondri aor inh ibit theproductionof high energy pho sph ate compoundslead to energy failure and bo th enh anced GLU release and inc reased vu lne rabilityto extracellu larGLU mo re. GLU act iv ationofNMDA recep tors enh ancesnitric ox ide fo rm ationwh ich can contr ibute to free rad icalmedi icalmed ia ted ox idativedam agecan result in a lossofg luta andcan also lead to inc reased levelsofhr a in GLU. N cu ro toxic ants with diverse specificme ch anismsofactionmayultima te ly trig ger an excito tox ic ca scade in theaged ne rvoussys tem. Themodel ingof neu ro log icaldiseases using selected tox ic chem icals descr ibed in th is art ic le reveals th at interact ionsbe tween these two modalitiesa rc likelyto play a role in ho th agere la ted and envi ro nm entallycaused changesin ne rve function.

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