Abstract
Synaptic inputs from different brain areas are often targeted to distinct regions of neuronal dendritic arbors. Inputs to proximal dendrites usually produce large somatic EPSPs that efficiently trigger action potential (AP) output, whereas inputs to distal dendrites are greatly attenuated and may largely modulate AP output. In contrast to most other cortical and hippocampal neurons, hippocampal CA2 pyramidal neurons show unusually strong excitation by their distal dendritic inputs from entorhinal cortex (EC). In this study, we demonstrate that the ability of these EC inputs to drive CA2 AP output requires the firing of local dendritic Na+ spikes. Furthermore, we find that CA2 dendritic geometry contributes to the efficient coupling of dendritic Na+ spikes to AP output. These results provide a striking example of how dendritic spikes enable direct cortical inputs to overcome unfavorable distal synaptic locale to trigger axonal AP output and thereby enable efficient cortico-hippocampal information flow.
Highlights
The active properties of neuronal dendrites are important for integrating and processing excitatory and inhibitory synaptic inputs (Johnston et al, 1996; London and Hausser, 2005; Johnston and Narayanan, 2008; Major et al, 2013)
We report that dendritic Na+ spikes play an important role in the ability of hippocampal CA2 pyramidal neurons (PNs) to generate axonal action potential (AP) output in response to synaptic input from the direct entorhinal cortical (EC) projections that terminate on CA2 PN distal dendrites
Through computational modeling based on morphological reconstructions of CA2 and CA1 PNs, we find that the distinct dendritic geometry of CA2 PNs contributes to the ability of CA2 neurons to efficiently couple dendritic Na+ spikes to AP output
Summary
The active properties of neuronal dendrites are important for integrating and processing excitatory and inhibitory synaptic inputs (Johnston et al, 1996; London and Hausser, 2005; Johnston and Narayanan, 2008; Major et al, 2013). In most instances, dendritic Na+ spikes propagate poorly to the soma and so fail to act as reliable triggers of somatic APs (Stuart and Sakmann, 1994; Stuart et al, 1997a; Golding and Spruston, 1998). Under physiological conditions, the APs in most principal neurons, including neocortical layer 5 and hippocampal CA1 pyramidal neurons (PNs), are usually initiated at the axonal initial segment (AIS) before back-propagating to the dendrites (Stuart and Sakmann, 1994; Stuart et al, 1997a, 1997b; Golding and Spruston, 1998). We report that dendritic Na+ spikes play an important role in the ability of hippocampal CA2 PNs to generate axonal AP output in response to synaptic input from the direct entorhinal cortical (EC) projections that terminate on CA2 PN distal dendrites
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