Laurent Fagni

TL;DR: In neurons, the constitutive activity of these receptors is controlled by Homer proteins, which bind directly to the receptors' carboxy-terminal intracellular domains, which show that these glutamate GPCRs can be directly activated by intraceocytes as well as by agonists.

TL;DR: The data indicate that in hippocampal neurons N-cadherin and GluR2 form a synaptic complex that stimulates presynaptic development and function as well as promoting dendritic spine formation.

TL;DR: A tight functional coupling between ryanodine receptors and L-type Ca2+ channel in neurons is demonstrated and is demonstrated to be a novel mechanism for Ca2-channel modulation in neurons.

TL;DR: These mGluR-mediated effects often result from mobilization of Ca2+ from ryanodine-sensitive, rather than Ins(1,4, 5)P3- sensitive,Ca2+ stores, suggesting that close functional interactions exist between mGLURs, intracellular Ca2+, stores and Ca2-sensitive ion channels in the membrane.

TL;DR: It is reported that knock-down of Shank3/prolinerich synapse-associated protein-2 by RNA interference reduces spine density in hippocampal neurons and transgene expression of Shank 3 is sufficient to induce functional dendritic spines in aspiny cerebellar neurons, which strongly suggest that Shank proteins and the associated glutamate receptors participate in a concerted manner to form spines and functional synapses.