Topic: brevican

Major depressive disorder is a debilitating neurodegenerative disorder which afflicts approximately 14-20% of the general population; of those individuals, approximately 30% are treatment resistant to antidepressant medications. Recently, the FDA has approved a novel antidepressant, Zuranolone for use in individuals who suffer from postpartum depression and, this drug has shown very promising results. Using 488uM thick hippocampal brain slices, local field potential (LFP) recordings were conducted and analyzed for changes in sharp wave ripple (SWR) complexes. In order to assess in-vivo changes

Learning and memory formation require activity-dependent rearrangements of neuronal networks driven by structural plasticity. The brain's perineuronal extracellular matrix (ECM), composed mainly of chondroitin sulfate proteoglycans from the lectican family, suppresses structural plasticity in the mature brain. Several members of this family, such as aggrecan and brevican, undergo proteolytic cleavage by proteases from the ADAMTS family, which may loosen the ECM structure. Therefore, we hypothesize that activity-dependent extracellular proteolysis weakens the ECM, supporting neuronal plasticity

Synaptic homeostatic plasticity maintains firing of neuronal networks within physiological range, by adjusting synaptic strength via molecular and morphological changes in the synapse. The perineuronal extracellular matrix (ECM), which is mainly composed of chondroitin sulfate proteoglycans such as brevican, stabilizes synapses and reduces their plasticity. Previous data indicated that brevican is cleaved during homeostatic plasticity, which may facilitate synapse remodeling. The proteases ADAMTS4, -5 and the closely related ADAMTS8 and -15 may share brevican as substrate for ECM regulation. T