Electrotonic coupling between neurones in the rat mesencephalic nucleus

Electrotonic coupling between neurones in the rat mesencephalic nucleus Electrical stimulation of the trigeminal nerve evokes a ‘short latency depolarization’ (SLD) in the first order sensory neurones of the mesencephalic nucleus (MSN) of the Vth nerve in the rat. A series of experiments suggesting ‘electrotonic coupling’ as the mechanism for this SLD is provided. 1. Electrical activity of MSN neurones was recorded intracellularly as action potentials were conducted from the periphery (somatopetally) to the masticatory nucleus. Typical sequential invasion of the initial segment and somatic region (IS—S) of the neurones was seen. The somatopetal activation of MSN neurones was characterized by the brevity, short refractoriness, high safety factor (IS—S), and short after‐hyperpolarization of the spike potential. 2. In twenty‐three (10·5%) of the penetrated neurones, stimulation at levels subthreshold for somatopetal activation uncovered a SLD with a mean latency of 180 μsec. 3. The SLDs were found to be all‐or‐none in nature, and to have constant amplitude and latency for a given cell, plus a short half decay time. 4. Hyperpolarization of a MSN neurone through the recording electrode produced a blockage of the IS—S spike and revealed M‐spikes and SLDs which could be clearly separated, in every instance, as distinct all‐or‐none components. The amplitude of the SLD was found to be insensitive to the level of membrane potential within the ranges tested. 5. In fifteen neurones the SLD generated action potentials which were conducted somatofugally as shown by their collision with somatopetally conducted action potentials in the same cell. The lack of collision between the SLD and somatopetal spikes demonstrated the independent origin of these two potentials. 6. The independence of the SLD from the somatopetal invasion of the cell was also demonstrated by collision of a somatofugal action potential following direct stimulation through the recording micro‐electrode and a somatopetal spike following trigeminal stimulation. 7. Two possible mechanisms are considered for the genesis of the SLD: chemical synaptic transmission and electrotonic coupling between neighbouring cells. The conclusion is drawn that SLDs must be generated by the latter mechanism. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Physiology Wiley

Electrotonic coupling between neurones in the rat mesencephalic nucleus

The Journal of Physiology, Volume 212 (1) – Jan 1, 1971

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Publisher
Wiley
Copyright
© 2014 The Physiological Society
ISSN
0022-3751
eISSN
1469-7793
D.O.I.
10.1113/jphysiol.1971.sp009309
Publisher site
See Article on Publisher Site

Abstract

Electrical stimulation of the trigeminal nerve evokes a ‘short latency depolarization’ (SLD) in the first order sensory neurones of the mesencephalic nucleus (MSN) of the Vth nerve in the rat. A series of experiments suggesting ‘electrotonic coupling’ as the mechanism for this SLD is provided. 1. Electrical activity of MSN neurones was recorded intracellularly as action potentials were conducted from the periphery (somatopetally) to the masticatory nucleus. Typical sequential invasion of the initial segment and somatic region (IS—S) of the neurones was seen. The somatopetal activation of MSN neurones was characterized by the brevity, short refractoriness, high safety factor (IS—S), and short after‐hyperpolarization of the spike potential. 2. In twenty‐three (10·5%) of the penetrated neurones, stimulation at levels subthreshold for somatopetal activation uncovered a SLD with a mean latency of 180 μsec. 3. The SLDs were found to be all‐or‐none in nature, and to have constant amplitude and latency for a given cell, plus a short half decay time. 4. Hyperpolarization of a MSN neurone through the recording electrode produced a blockage of the IS—S spike and revealed M‐spikes and SLDs which could be clearly separated, in every instance, as distinct all‐or‐none components. The amplitude of the SLD was found to be insensitive to the level of membrane potential within the ranges tested. 5. In fifteen neurones the SLD generated action potentials which were conducted somatofugally as shown by their collision with somatopetally conducted action potentials in the same cell. The lack of collision between the SLD and somatopetal spikes demonstrated the independent origin of these two potentials. 6. The independence of the SLD from the somatopetal invasion of the cell was also demonstrated by collision of a somatofugal action potential following direct stimulation through the recording micro‐electrode and a somatopetal spike following trigeminal stimulation. 7. Two possible mechanisms are considered for the genesis of the SLD: chemical synaptic transmission and electrotonic coupling between neighbouring cells. The conclusion is drawn that SLDs must be generated by the latter mechanism.

Journal

The Journal of PhysiologyWiley

Published: Jan 1, 1971

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