Genetic contribution has been consistently implicated in several neurological disorders, however only a fraction of candidate genes can be directly linked to these disorders. Many known risk factors for psychiatric diseases are related to the enzymatic regulatory machinery of the actin based cytoskeleton of neuronal cells. Synaptic plasticity - which is fundamental for neuronal function - heavily relies on actin-polymerization. To gain insight into the neuronal architecture during actinrelated pathologic conditions, using quantitative electron-microscopy, the authors investigated a conditional knock-out mice breed, in which they studied the result of the postnatal loss of ArpC3 subunit of the Arp2/3 complex - an evolutionary conserved final output of actin signalling pathways that orchestrates de novo actin polymerization. They found, that in the hippocampus - which is a particularly favourable model for synaptic plasticity and believed to play a key role in learning and memory - and neocortex, synaptic architecture is significantly altered compared to the wild-type. Their results suggest that dysregulation of the actin cytoskeleton results in pathologic neuronal architecture which may contribute to the ethiology of complex neurological disorders.
|Number of pages||7|
|Journal||Magyar Allatorvosok Lapja|
|Publication status||Published - Jan 1 2014|
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