▁gl ut am ate ▁trans por ters ▁may ▁fail , ▁leading ▁to ▁to xic ▁bu il dup ▁of ▁gl ut am ate . ▁In ▁fact , ▁their ▁activity ▁may ▁also ▁actually ▁be ▁revers ed ▁due ▁to ▁in ade qu ate ▁amounts ▁of ▁ad en os ine ▁tri ph osph ate ▁to ▁power ▁ATP ase ▁p umps , ▁resulting ▁in ▁the ▁loss ▁of ▁the ▁electro chem ical ▁ion ▁gradient . ▁Since ▁the ▁direction ▁of ▁gl ut am ate ▁transport ▁depends ▁on ▁the ▁ion ▁gradient , ▁these ▁trans por ters ▁release ▁gl ut am ate ▁instead ▁of ▁removing ▁it , ▁which ▁results ▁in ▁ne uro to x icity ▁due ▁to ▁over activ ation ▁of ▁gl ut am ate ▁re cept ors . ▁ ▁L oss ▁of ▁the ▁Na + - dependent ▁gl ut am ate ▁trans porter ▁E A AT 2 ▁is ▁sus pected ▁to ▁be ▁associated ▁with ▁ne uro de gener ative ▁dise ases ▁such ▁as ▁Al z heimer ' s ▁disease , ▁Hun ting ton ' s ▁disease , ▁and ▁A LS – park inson ism ▁de ment ia ▁complex . ▁Also , ▁deg ener ation ▁of ▁motor ▁neur ons ▁in ▁the ▁disease ▁am y ot roph ic ▁later al ▁s cl eros is ▁has ▁been ▁linked ▁to ▁loss ▁of ▁E A AT 2 ▁from ▁patients ' ▁bra ins ▁and ▁sp inal ▁c ords . ▁ ▁Add iction ▁to ▁certain ▁add ict ive ▁dru gs ▁( e . g ., ▁c oca ine , ▁hero in , ▁alco hol , ▁and ▁nic ot