The small molecule NMDA-receptor antagonist MK801 has been genetically targeted to specific cell types in brain tissue to examine the role of NMDA receptors in cocaine-induced synaptic plasticity.
Fly protein families Dprs and DIPs can create a multitude of complementary interfaces for homo- and heterophilic adhesion complexes, resulting in instructive roles for connectivity in the motor neuron circuitry.
Vascular endothelial cells in the brain, heart and lung exhibit tissue-specific heterogeneity and plasticity, expressing genes that were traditionally thought to be only expressed by the surrounding parenchymal tissue cells.
The substrate for evolutionary divergence does not lie in changes in neuronal cell number or targeting, but rather in sensory perception and synaptic partner choice within invariant, prepatterned neuronal processes.
Auxiliary subunits Neto1 and Neto2 regulate the GluK1 receptor targeting to excitatory silent synapses through different molecular mechanisms and also modify receptor biophysics through distinct mechanisms.
Single molecule subunit counting, FRET and electrophysiology experiments reveal that metabotropic glutamate receptor subunits interact and rearrange at the level of the transmembrane domains in response to allosteric modulators.
Parabrachial neurons expressing CGRP relay affective components of ascending pain information via distinct thalamic and amygdalar pathways, which together contribute to complementary aspects of adaptive threat responses.
