Effects of conditioning stimulation of the central amygdaloid nucleus on tooth pulp-driven neurons in the cat somatosensory cortex (SI)

To study the limbic control of nociception, we examined the effect of condi tioning stimulation of the central amygdaloid nucleus (ACE) on tooth pulp-d riven (TPD) neurons in the first somatosensory cortex (SI). Cats were anest hetized with N2O-O-2 (2:1) and 0.5% halothane, and immobilized with tubocur arine chloride. The tooth pulp test stimulus was applied by a single rectan gular-pulse (0.5 ms in duration and 3-5 times the threshold intensity for t he jaw-opening reflex). Conditioning stimuli to the ACE consisted of trains :of 33 pulses (300 mu A) delivered at 330 Hz at intervals of 8-10 s, In 35 out of 61 of the slow (S)-type TPD neurons with latencies of more than 20 m s, conditioning stimulation in the ACE, especially in the medial division, markedly reduced the firing response to the pulpal stimulation. The inhibit ion of the firing rate in the S-type neurons was 74% of the control. In the se S-type neurons, the neurons that were inhibited had significantly longer latencies compared to the noninhibited neurons (45.0+/-17.6 ms, n=32 vs. 3 4.8+/-10.5 ms, n=26). In contrast, the ACE conditioning stimulation affecte d only one out of 18 fast-type TPD neurons with latencies of less than 20 m s. In addition, ACE stimulation had no effect on the spontaneous discharges of either S-type or F-type neurons. The ACE inhibitory effect on S-type ne urons was not diminished by naloxone administration (1 mg/kg, I.V.), while the blockade of histamine H-1-receptor by diphenhydramine hydrochloride (0. 5 mg/kg, I.V.) partially reversed the inhibitory effect. These results sugg est that the ACE inhibits ascending nociceptive information to the SI and t hat this inhibition is mediated in part by histamine (H-1) receptors. It se ems likely that the antinociceptive effect is a neurophysiological basis fo r stress-induced analgesia (SIA).