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Felmy, F.

Publications and source records attributed to Felmy, F..

2 recordsLinked to original sources

Depolarizing afterpotentials in rodent mEC layer II neurons vary gradually across all principal cell types

Principal cells in Layer II (LII) of the rodent medial entorhinal cortex (mEC) often discharge in short burst episodes, whose biophysical mechanism and biological function are not fully understood. As shown by in vitro recordings in rats and in vivo recordings in mice, action potentials of stellate cells (SCs) and pyramidal cells (PCs) in mEC LII can trigger depolarizing afterpotentials (DAPs) that facilitate spike doublets and burst firing. In vitro recordings in mice confirm these findings for SCs and two additional cell types intermediate between SCs and PCs but suggest that mouse PCs generate minute DAPs only. To better understand the diversity and physiology of the intermediate LII mEC cell types, we performed slice experiments in Long Evans rats of both sexes and analyzed the data using clustering techniques. The analysis suggests four distinct cell clusters, reminiscent of previous observations in mice. On purpose, DAP properties were not used for the cluster analysis so that they could be studied post-hoc in an unbiased manner. Our results show that characteristic features of DAPs and other physiological markers are broadly distributed within each cell class and vary gradually from cluster to cluster, forming a continuum of biophysical properties.

neuroscience↗

GABA regulates resonance and spike rate encoding via a universal mechanism that underlies the modulation of action potential generation

Different mechanisms for action potential (AP) generation exist that shape neuronal coding and network dynamics. The neuro-transmitter GABA regulates neuronal activity but its role in modulating AP dynamics itself is unclear. Here we show that GABA indeed changes the AP mechanism: it causes regularly firing hippocampal CA3 neurons to bistably switch between spiking and quiescence, converts graded discharge-to-current relationships to have abrupt onsets, and induces resonance. Modeling reveals that A-currents enable these GABA-induced transitions. Mathematically, we prove that this transition sequence originates from a single universal principle that generically underlies the modulation of AP dynamics in any conductance-based neuron model. Conductance clamp experiments in hippocampal and brainstem neurons show the same transitions, confirming the universal theory. In simulated networks, synaptically controlled AP dynamics, permits dynamic gating of signals and targeted synchronization of neuronal sub-ensembles. These results advance the systematic understanding of AP modulation and its role in neuronal and network function.

neuroscience↗