Glutamate-induced transient modification of the postsynaptic density
AUTOR(ES)
Dosemeci, Ayse
FONTE
The National Academy of Sciences
RESUMO
Depolarization of rat hippocampal neurons with a high concentration of external potassium induces a thickening of postsynaptic densities (PSDs) within 1.5–3 min. After high-potassium treatment, PSDs thicken 2.1-fold in cultured neurons and 1.4-fold in hippocampal slices compared with their respective controls. Thin-section immunoelectron microscopy of hippocampal cultures indicates that at least part of the observed thickening of PSDs can be accounted for by an accumulation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) on their cytoplasmic faces. Indeed, PSD-associated gold label for CaMKII increases 5-fold after depolarization with potassium. The effects of high-potassium treatment on the composition and structure of the PSDs are mimicked by direct application of glutamate. In cultures, glutamate-induced thickening of PSDs and the accumulation of CaMKII on PSDs are reversed within 5 min of removal of glutamate and Ca2+ from the extracellular medium. These results suggest that PSDs are dynamic structures whose thickness and composition are subject to rapid and transient changes during synaptic activity.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=56977Documentos Relacionados
- Glutamate-induced uptake of proline by Streptomyces antibioticus.
- Phosphatidylcholine-specific phospholipase C regulates glutamate-induced nerve cell death
- Transduction mechanism for glutamate-induced potassium current in neurones of the mollusc Planorbarius corneus.
- Lithium activates the serine/threonine kinase Akt-1 and suppresses glutamate-induced inhibition of Akt-1 activity in neurons
- Down-regulation of protein kinase C protects cerebellar granule neurons in primary culture from glutamate-induced neuronal death.