Topic: neurotransmitter receptors

Microglia-synapse interactions have been examined in a variety of contexts, in vitro and in vivo, which revealed an important role for microglia in synaptic pruning and loss. Nevertheless, it remains to be determined whether and how microglia are involved in the process of synapse formation under physiologic conditions. We hypothesize that microglia serve as a link between pre- and post-synapse by sensing neurotransmitter release at highly active pre-synaptic sites and actively modulate the formation of new dendritic spines.To examine this relationship, we target microglia-synapse communicatio

Astrocytes play an active role in shaping and maintaining neuronal circuits and the blood-brain barrier. In addition to their long-established role in extracellular potassium buffering and glutamate uptake, these cells can also regulate the activity of local synaptic circuits through secretion and clearance of neurotransmitters. Whilst the molecular signal exchange between astroglia and synapses occurs in a highly heterogeneous microenvironment on the nanoscale, the spatial subcellular distribution of the underlying molecular machineries remains poorly understood. Similarly, in addition to clo

Astrocytes were seen for a long time as supportive cells in the central nervous system. However, evidence points to the pivotal role of these cells in brain function, including the modulation of synaptic transmission. Astrocytes express neurotransmitter receptors at the cellular membrane, whose activation may cause somatic calcium elevations and consequently release signaling molecules in the synaptic cleft. The impact of astrocytic signaling in the modulation of neuronal circuits and behavior is still poorly understood. Social behavior results from a complex interaction between brain regions.

Angelman Syndrome (AS) is a neurodevelopmental disorder with complex symptomatology caused by the loss of maternal allele expression of one single gene in the brain, the ubiquitin E3 ligase UBE3A. Even if the underlying genetic basis of AS has previously been extensively described, the molecular mechanisms regulated by UBE3A ubiquitination in the brain remain highly elusive. Here we provide the first proteomic report of UBE3A-mediated ubiquitination events in a mammalian brain. In order to identify Ube3a substrates, we have combined our previously described bioUb mouse with a new mouse strain