Excitotoxicity

major neurotransmitter in excitotoxicity

permeability of glutamate?

where is glutamate synthesized?

glutamate synthesis process

VGLUT

glutamine synthetase

glutaminase

EAAT

EAA receptor category comparison

ionotropic EAA receptor subtypes

metabotropic EAA receptor subtypes

NMDA receptor characteristics

excitotoxins

endogenous excitotoxin examples

exogenous excitotoxin examples

Neuroendocrinopathies; glutamate & MSG
counter mechanisms, target locations, symptoms, other

neurolathyrism; BOAA
counter mechanisms, target locations, symptoms, other

APD complex; BMAA
counter mechanisms, target locations, symptoms, other

Domoic acid (seafood poisoning)

1. misfolding: changes in protein structure (i.e. harsh conditions, genetic mutation) prevent proper alpha helix/beta sheets OR change structure/decrease activity
2. oligomerization: chemical process that converts monomers to macromolecular complexes via polymerization, rearranges/changes structure
3. fibrilization: changes in quaternary protein structure, proteins acquire distinct physical properties - cross-beta structure, decreased solubility, increased stability against proteases
4. inclusion formation and deposition: aggregation and sequestration of fibrils, incorporation of other proteins and molecules, post-translational modifications (e.g. methylation) increases stability against degradation/proteases