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Abstract: Glutamate receptors of the kainate subtype are ionotropic receptors that play a key role in the modulation of neuronal network activity. The role of kainate receptors depends on their precise membrane and subcellular localization in presynaptic, extrasynaptic and postsynaptic domains. These receptors are composed of the combination of five subunits, three of them having several splice variants. The subunits and splice variants show great divergence in their C-terminal cytoplasmic tail domains, which have been implicated in intracellular trafficking of homomeric and heteromeric receptors. Differential trafficking of kainate receptors to specific neuronal compartments likely relies on interactions between the different kainate receptor subunits with distinct subsets of protein partners that interact with C-terminal domains. These C-terminal domains have also been implicated in the degradation of kainate receptors. Finally, the phosphorylation of the C-terminal domain regulates receptor trafficking and function. This review summarizes our knowledge on the regulation of membrane delivery and trafficking of kainate receptors implicating C-terminal domains of the different isoforms and focuses on the identification and characterization of the function of interacting partners. [Copyright &y& Elsevier]

Reports the isolation and sequence of complementary DNA's that encode an adenylyl cyclase amino acid, from a bovine brain library. The sequence divided into two alternating sets of hydrophobic and hydrophilic domains, and an unexpected topographical resemblance between adenylyl cyclase and various plasma membrane channels and transporters was observed.

The plasticity of excitatory synapses is an essential brain process involved in cognitive functions, and dysfunctions of such adaptations have been linked to psychiatric disorders such as depression. Although the intracellular cascades that are altered in models of depression and stress-related disorders have been under considerable scrutiny, the molecular interplay between antidepressants and glutamatergic signaling remains elusive. Using a combination of electrophysiological and single nanoparticle tracking approaches, we here report that the cognitive enhancer and antidepressant tianeptine (S 1574, [3-chloro-6-methyl-5,5-dioxo-6,11-dihydro-(c,f)-dibenzo-(1,2-thiazepine)-11-yl) amino]-7 heptanoic acid, sodium salt) favors synaptic plasticity in hippocampal neurons both under basal conditions and after acute stress. Strikingly, tianeptine rapidly reduces the surface diffusion of AMPA receptor (AMPAR) through a Ca2+/calmodulin-dependent protein kinase II (CaMKII)-dependent mechanism that enhances the binding of AMPAR auxiliary subunit stargazin with PSD-95. This prevents corticosterone-induced AMPAR surface dispersal and restores long-term potentiation of acutely stressed mice. Collectively, these data provide the first evidence that a therapeutically used drug targets the surface diffusion of AMPAR through a CaMKII-stargazin-PSD-95 pathway, to promote long-term synaptic plasticity. [ABSTRACT FROM AUTHOR]