In the neocortex, the coexistence of temporally locked excitation and inhibition governs complex network activity underlying cognitive functions, and is believed to be altered in several brain diseases. We recently showed that this equilibrium can be unlocked by increased activity of layer 5 pyramidal neurons that triggers long-term potentiation of GABAergic synapses (LTPi).
Conversely, in cortical layer 2/3, activity of pyramidal neurons induce a powerful long-term depression of synaptic inhibition (LTDi). LTPi relies on retrograde signaling of nitric oxide, which persistently alters presynaptic GABA release from parvalbumin basket cells, leaving dendritic inhibition and glutamatergic excitation intact.
Conversely, LTDi depends on the activation of the endocannabinoid system and likely relies on a different basket cell type.
I will discuss how this bi-directional persistent change of perisomatic inhibition onto single pyramidal neurons can effectively alter their spiking dynamics, ultimately affecting the computational properties the local cortical networks.
The neuronal identity bias behind neocortical GABAergic plasticity.
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Non-associative potentiation of perisomatic inhibition alters the temporal coding of neocortical layer 5 pyramidal neurons. Lourenço J, Pacioni S, Rebola N, van Woerden GM, Marinelli S, DiGregorio D, Bacci A. PLoS Biol. 2014 Jul 8;12(7):e1001903. doi: 10.1371/journal.pbio.1001903. eCollection 2014 Jul.
Autaptic self-inhibition of cortical GABAergic neurons: synaptic narcissism or useful introspection? Deleuze C, Pazienti A, Bacci A. Curr Opin Neurobiol. 2014 Jun;26:64-71. doi: 10.1016/j.conb.2013.12.009. Epub 2014 Jan 14. Review.