ACTIVE-SLEEP-RELATED SUPPRESSION OF FELINE TRIGEMINAL SENSORY NEURONS- EVIDENCE IMPLICATING PRESYNAPTIC INHIBITION VIA A PROCESS OF PRIMARY AFFERENT DEPOLARIZATION

1. Changes in the excitability of lumbar and trigeminal primary affere nt terminals have long been used as an index of primary afferent depol arization (PAD). PAD has been linked in part to the presynaptic inhibi tion of neurotransmission. During the behavioral state of active sleep , synaptic transmission through the rostral tri-geminal sensory nuclea r complex (TSNC) is suppressed when compared with other states such as wakefulness or quiet sleep. The mechanism underlying the suppression of neuronal activity in the rostral TSNC during active sleep is not kn own. Accordingly, experiments were conducted to determine, by examinin g the excitability of tooth pulp afferent terminals in cat during slee p and wakefulness, whether PAD processes might contribute in part to t he suppression of rostral TSNC neuron activity. 2. Unitary potentials recorded in the maxillary canine tooth pulp were evoked by low-intensi ty stimuli applied to the rostral TSNC. Unitary potentials were identi fied by their ''all-or-nothing'' response, their invariant amplitude a nd latency, and their ability to follow a short train of high-frequenc y (333 Hz) stimuli. 3. The firing index (FI), a measure of the probabi lity of evoking a unitary potential, was used to assess the changes in excitability of tooth pulp primary afferents. The proximity of stimul ating electrodes to the terminal segment rather than a nonterminal seg ment of a tooth pulp afferent was demonstrated by observing an increas e in the Fl as a consequence of conditioning stimuli applied to ipsila teral branches of the trigeminal nerves. Increases in the Fl over base line were obtained for conditioning test intervals ranging from 20 to 80 ms, with the peak effect of conditioning occurring at 30 ms. 4. A t otal of 25 tooth pulp afferent terminals were identified and changes i n their FI were examined during wakefulness, quiet sleep, and active s leep. The FI for all 25 terminals during wakefulness (FIW: 0.29 +/- 0. 04, mean +/- SE) did not differ from that during quiet sleep (0.32 +/- 0.04). However, when compared with wakefulness, the FI during active sleep (FIAS:0.52 +/- 0.07) was increased. The mean ratio of change in the FI (FIAS/FIW) was 3.5 +/- 0.9. These findings indicate that, as a population, tooth pulp afferent terminals are depolarized during the s tate of active sleep and that PAD processes may partly underlie the su ppression of synaptic transmission through the rostral TSNC during thi s state. 5. To explore whether presynaptic excitability changes underl ie the modulation of rostral TSNC neuron activity during active sleep, additional experiments were performed in which tooth-pulp-evoked resp onses of individual rostral TSNC neurons and the FIs of adjacent indiv idual tooth pulp afferent terminals were analyzed as a function of sle ep and wakefulness. The results indicated that active-sleep-related PA D was associated with active-sleep-related suppression of tooth-pulp-e voked activity of rostral TSNC neurons. 6. The conclusion is reached t hat PAD processes contribute to the mechanism whereby synaptic activit y through the rostral TSNC is suppressed during the behavioral state o f active sleep.