3880769
Descripción
Fichas por Sophie Obayashi, actualizado hace más de 1 año
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Creado por Sophie Obayashi
hace alrededor de 9 años
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| Pregunta | Respuesta |
| major neurotransmitter in excitotoxicity | glutamate (non-essential amino acid) |
| permeability of glutamate? | not readily cross BBB |
| where is glutamate synthesized? | presynaptic terminal |
| glutamate synthesis process | |
| VGLUT | vesicular glutamate transporters: energetically favorable |
| glutamine synthetase | astrocytes: glutamate --> glutamine manganese dependent enzyme |
| glutaminase | presynaptic terminal: glutamine --> glutamate e.g. pyruvate activated glutaminase (PAG) |
| EAAT | excitatory amino acid transporter glutamate --> glutamine energetically UNfavorable |
| EAA receptor category comparison | 1. Ionotropic receptors: FAST mediated, shorter lasting 2. Metabotropic receptors: SLOW mediated, longer lasting |
| ionotropic EAA receptor subtypes | NMDA AMPA KA |
| metabotropic EAA receptor subtypes | g-protein coupled |
| NMDA receptor characteristics | only receptor that allows calcium through allows Ca2+, K+, Na+ glutamate & GLYCINE are coagonists Mg block |
| excitotoxins | chemicals that at as excitatory amino acids (EAA)exc |
| endogenous excitotoxin examples | glutamate aspartate quinolinate |
| exogenous excitotoxin examples | kainic acid domoic acid |
| Neuroendocrinopathies; glutamate & MSG counter mechanisms, target locations, symptoms, other | counter: ? target: hypothalamic neurons & arcuate nucleus symptoms: retinal nerve layer, pituitary system, short stature, obesity other: effects children more |
| neurolathyrism; BOAA counter mechanisms, target locations, symptoms, other | counter: EAA antagonists block effects target: spinal cord, myelin loss, neurofibrillary tanges in hippocampusAPD complex symptoms: lumbar pain, weakness, leg spasticity, seizures, gait disturbances |
| APD complex; BMAA counter mechanisms, target locations, symptoms, other | counter: NMDA antagonists block effects target: ? symptoms: ? other: exposure to BMAA via bats who ate cycad plant |
| Domoic acid (seafood poisoning) | counter: ? target: selectively reacts w/kainate receptor (KA) symptoms: persistent seizures |
| 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 | d |
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