title: Balancing feed-forward excitation and inhibition via Hebbian inhibitory synaptic plasticity.
abstract: It has been suggested that excitatory and inhibitory inputs to cortical cells are balanced, and that this balance is important for the highly irregular firing observed in the cortex. There are two hypotheses as to the origin of this balance. One assumes that it results from a stable solution of the recurrent neuronal dynamics. This model can account for a balance of steady state excitation and inhibition without fine tuning of parameters, but not for transient inputs. The second hypothesis suggests that the feed forward excitatory and inhibitory inputs to a postsynaptic cell are already balanced. This latter hypothesis thus does account for the balance of transient inputs. However, it remains unclear what mechanism underlies the fine tuning required for balancing feed forward excitatory and inhibitory inputs. Here we investigated whether inhibitory synaptic plasticity is responsible for the balance of transient feed forward excitation and inhibition. We address this issue in the framework of a model characterizing the stochastic dynamics of temporally anti-symmetric Hebbian spike timing dependent plasticity of feed forward excitatory and inhibitory synaptic inputs to a single post-synaptic cell. Our analysis shows that inhibitory Hebbian plasticity generates 'negative feedback' that balances excitation and inhibition, which contrasts with the 'positive feedback' of excitatory Hebbian synaptic plasticity. As a result, this balance may increase the sensitivity of the learning dynamics to the correlation structure of the excitatory inputs.
authors.affiliation: Department of Physiology and Neurobiology, Ben-Gurion University of the Negev, Beer-Sheva, Israel.
authors.forename: Yotam
authors.initials: Y
authors.lastname: Luz
authors.forename: Maoz
authors.initials: M
authors.lastname: Shamir
mesh_terms: D019706:Excitatory Postsynaptic Potentials; D008959:Models, Neurological; D009473:Neuronal Plasticity / Q000502:physiology*; D009474:Neurons / Q000502:physiology*; D009435:Synaptic Transmission / Q000502:physiology*