GENERALIZATION AND PLASTICITY OF SYNCHRONY DEPENDENT REGULATION OF SYNAPTIC TRANSMISSION IN CA1 ORIENS-PYRAMIDAL LAYER

Neurons integrate excitatory and inhibitory inputs to determine whether to fire an action potential(AP). This process relies on the types, density, and distribution of ion channels, which regulate AP firing.
Input Synchrony Facilitation (ISF) is a form of synaptic gain that depends on the axonal sodium channels (NaV), whose availability encodes levels of input synchrony, shapes the AP and modulate synaptic transmission (Zbili et al., 2020).
ISF has been identified at local excitatory circuits of the neocortex and the CA3 region of the hippocampus, but its contribution to other synapses remains unexplored.
We examined whether ISF is present at excitatory and inhibitory synapses within the CA1 region of the hippocampus in vitro. Pairs of monosynaptically connected neurons were recorded in organotypic slice cultures, we compared synaptic transmission evoked by synchronous and asynchronous presynaptic like action potentials; asynchronous inputs inactivate NaV channels, affecting their availability.
Data indicates that ISF is present at excitatory but rarely observed at inhibitory synapses. Its absence at inhibitory synapses reflect the high density of NaV channels in interneurons, which seems to preserve action potential amplitude and synaptic output during asynchronous inputs. Whereas pyramidal neurons exhibit greater sensitivity of excitatory transmission to input synchrony.
To investigate why ISF is absent at inhibitory synapse, we partially blocked NaV channels using (50 nM) TTX, which revealed ISF in these synapses. In contrast, lowering extracellular calcium didn’t consistently uncover ISF, suggesting that ISF absence under control conditions is likely due to the high density of sodium channels in interneurons.