Chiang et al. show that slow periodic activity in a horizontal hippocampal slice preparation occurs through dendritic NMDA receptor‐dependent Ca2+ spiking, which is itself self‐generating and self‐propagating, via ephaptic interactions across neurons. Consistent with purely ephaptic transmission, this activity and its active propagation across the slice were resistant to pharmacological blockers of fast ionotropic chemical neurotransmission, as well as pharmacological blockade of electrical transmission via gap junctions. What is particularly compelling is that the activity could be not only modulated, but also eliminated or even regenerated by imposed electrical fields. Most shockingly, this activity could be transmitted from one side of a surgically severed slice to the other when the two cut edges were simply placed in close proximity. These surprising findings were further supported by a computer model of hippocampal circuitry.Here are the key points listed in the Chiang et al. (open source) article:
Slow periodic activity can propagate with speeds around 0.1 m s−1 and be modulated by weak electric fields.
Slow periodic activity in the longitudinal hippocampal slice can propagate without chemical synaptic transmission or gap junctions, but can generate electric fields which in turn activate neighbouring cells.
Applying local extracellular electric fields with amplitude in the range of endogenous fields is sufficient to modulate or block the propagation of this activity both in the in silico and in the in vitro models.
Results support the hypothesis that endogenous electric fields, previously thought to be too small to trigger neural activity, play a significant role in the self‐propagation of slow periodic activity in the hippocampus.
Experiments indicate that a neural network can give rise to sustained self‐propagating waves by ephaptic coupling, suggesting a novel propagation mechanism for neural activity under normal physiological conditions.