Calcium-stimulated adenylyl cyclase 1 regulates synaptic scaling in forebrain cortical neurons.
Published: 2006
Language: eng
Number of pages: 96
ISBN-13: 9780494213711
Description: Homeostatic plasticity is important to stabilize the activity level of neuronal circuits. Molecular mechanisms underlying neuronal homeostatic plasticity in response to activity deprivation are not completely understood. This study found Chat prolonged AMPA receptor blockade by CNQX resulted in larger, faster mEPSC events with enhanced frequency. Furthermore, GluR1 protein level was also increased in cultured forebrain cortical neurons. Blockade of L-type Ca2+ channels produced similar effects as AMPA receptor blockade. Genetic deletion of AC1 but not AC8 KO, a key neuronal calcium-stimulated adenylyl cyclase, significantly reduced CNQX-induced GluR1 changes. The results indicate the synthesis and possible insertion of homomeric GluR1 receptors into synapses due to synaptic inactivity in the cortex. AC1 plays a subtype selective role in this process by coupling signals from L-type Ca2+ channels to downstream signaling pathways.
Notes: Source: Masters Abstracts International, Volume: 45-03, page: 1395.

Thesis (M.Sc.)--University of Toronto, 2006.

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