ACTIVE SLEEP-RELATED SUPPRESSION OF FELINE TRIGEMINAL SENSORY NEURONS:
EVIDENCE IMPLICATING PRESYNAPTIC INHIBITION VIA A PROCESS OF PRIMARY AFFERENT
Cairns, Brian E., Miguel C. Fragoso, and Peter J. Soja.
Division of Pharmacology and Toxicology, Faculty of Pharmaceutical
Sciences, The University of British Columbia, Vancouver, BC V6T 1Z3
APStracts 3:0028N, 1996.
SUMMARY AND CONCLUSIONS
1) Changes in the excitability of lumbar and trigeminal primary afferent
terminals have long been used as an index of primary afferent depolarization
(PAD). PAD has been linked in part to the presynaptic inhibition of
neurotransmission. During the behavioral state of active sleep, synaptic
transmission through the rostral trigeminal sensory nuclear complex (TSNC) is
suppressed when compared to other states such as wakefulness or quiet sleep
(Cairns et al. 1995). The mechanism underlying the suppression of neuronal
activity in the rostral TSNC during active sleep is not known. Accordingly,
experiments were conducted to determine whether PAD processes might contribute
in part to the suppression of rostral TSNC neuron activity by examining the
excitability of tooth pulp afferent terminals in cat during sleep and
wakefulness. 2) Unitary potentials recorded in the maxillary canine tooth pulp
were evoked by low intensity stimuli applied to the rostral TSNC. Unitary
potentials were identified by their "all or nothing" response, invariant
amplitude and latency, and their ability to follow a short train of high
frequency (333 Hz) stimuli. 3) The firing index (FI), a measure of the
probability of evoking a unitary potential, was used to assess the changes in
excitability of tooth pulp primary afferents. The proximity of stimulating
electrodes to the terminal rather than a non-terminal segment of a tooth pulp
afferent was demonstrated by observing an increase in the firing index as a
consequence of conditioning stimuli applied to ipsilateral branches of the
trigeminal nerves (Curtis and Lodge 1982). Increases in the FI over baseline
were obtained for CT intervals ranging from 20 to 80 ms with the peak effect
of conditioning occurring at 30 ms. 4) A total of 25 tooth pulp afferent
terminals were identified and changes in their firing index were examined
during wakefulness, quiet sleep and active sleep. The firing index for all 25
terminals during wakefulness (FIW = 0.29 0.04) did not differ from that during
quiet sleep (FIQS = 0.32 0.04). However, when compared to wakefulness, the FI
during active sleep (FIAS = 0.52 0.07) was increased. The mean ratio of change
in the firing index (FIAS/ FIW) was 3.5 0.9. These findings indicate that, as
a population, tooth pulp afferent terminals are depolarized during the state
of active sleep and that PAD processes may partly underlie the suppression of
synaptic transmission through the rostral TSNC during this state (Cairns et
al., 1995). 5) To explore whether presynaptic excitability changes underlie
the modulation of rostral TSNC neuron activity during active sleep (Cairns et
al., 1995), additional experiments were performed where tooth pulp evoked
responses of individual rostral TSNC neurons and the FI of adjacent individual
tooth pulp afferent terminals were analyzed as a function of sleep and
wakefulness. The results indicated that active-sleep-related PAD was
associated with active-sleep-related suppression of tooth pulp-evoked activity
of rostral TSNC neurons. 6) The conclusion is reached that PAD processes
contribute to the mechanism whereby synaptic activity through the rostral TSNC
is suppressed during the behavioral state of active sleep.
Received 6 April 1995; accepted in final form 29 September 1995.
APS Manuscript Number J229-5.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 29 January 96