| During learning and development, the brain undergoes important changes in the strength and number of synaptic connections. These changes pose a stability problem for the brain: how can recurrent neural networks be both plastic and stable at the same time? In 1998, I helped identify a novel form of cortical synaptic plasticity: synaptic scaling (Turrigiano et al., 1998). Briefly, we found that cortical pyramidal neurons were able to up or down regulate the strength of all their excitatory synaptic inputs, in an activity-dependent manner, and in the direction needed to maintain stability. In addition to maintaining stable firing rates, this type of homeostatic regulation may have important implications for other forms of synaptic plasticity, such as LTP and LTD, synaptic competition, and disorders of stability such as epilepsy.; What is the activity-signal responsible for synaptic scaling? BDNF is an important activity-dependent signal that can differentially regulate excitatory and inhibitory neurons in the direction needed to achieve a balance of excitation and inhibition (Rutherford et al., 1998). Here I show that postsynaptic depolarization can also regulate quantal amplitude in a BDNF-independent manner. Together, these results suggest that synapses can be scaled by at least two independent mechanisms. |
