Abstract
Excitatory synaptic transmission takes place at actin-rich protrusions called dendritic spines. Strong synaptic input activates NMDA-type glutamate receptors and induces calcium flux into these structures, initiating a program of cytoskeletal rearrangement that results in larger spines with stronger synapses. These changes in synaptic strength are thought to be the primary cellular mechanism underlying learning and memory. We recently reported that the dual Ras/Rac1 guanine nucleotide exchange factor (GEF) RasGRF2 links calcium flux to both spine enlargement and synaptic strengthening through its Rac-GEF activity. Additionally, we demonstrated that acute Rac1 activation is sufficient to enhance synaptic transmission. Since Rac1 is a major regulator of the actin cytoskeleton, these results suggest that the cytoskeleton itself regulates synaptic strengthening. Here we discuss models for how cytoskeletal modifications may enhance synaptic AMPA-type glutamate receptor abundance during long-term potentiation.
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