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Titolo:
Effects of conditioning stimulation of the central amygdaloid nucleus on tooth pulp-driven neurons in the cat somatosensory cortex (SI)
Autore:
Kawarada, K; Kamata, K; Matsumoto, N;
Indirizzi:
Iwate Med Univ, Sch Dent, Dept Oral Physiol, Morioka, Iwate 0208505, JapanIwate Med Univ Morioka Iwate Japan 0208505 Morioka, Iwate 0208505, Japan
Titolo Testata:
JAPANESE JOURNAL OF PHYSIOLOGY
fascicolo: 6, volume: 49, anno: 1999,
pagine: 485 - 497
SICI:
0021-521X(199912)49:6<485:EOCSOT>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
PHYSIOLOGICAL-PROPERTIES; ELECTRICAL-STIMULATION; NOCICEPTIVE NEURONS; INDUCED ANALGESIA; BLOOD-PRESSURE; STRESS-ULCERS; C-FOS; RATS; ANTINOCICEPTION; PROJECTIONS;
Keywords:
central amygdaloid nucleus; stress-induced antinociception; somatosensory cortex; tooth pulp-driven neuron; H-1 receptor;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Matsumoto, N Iwate Med Univ, Sch Dent, Dept Oral Physiol, 1-3-27 Chuo Dori, Morioka, Iwate 0208505, Japan Iwate Med Univ 1-3-27 Chuo Dori Morioka Iwate Japan 0208505 n
Citazione:
K. Kawarada et al., "Effects of conditioning stimulation of the central amygdaloid nucleus on tooth pulp-driven neurons in the cat somatosensory cortex (SI)", JPN J PHYSL, 49(6), 1999, pp. 485-497

Abstract

To study the limbic control of nociception, we examined the effect of conditioning stimulation of the central amygdaloid nucleus (ACE) on tooth pulp-driven (TPD) neurons in the first somatosensory cortex (SI). Cats were anesthetized with N2O-O-2 (2:1) and 0.5% halothane, and immobilized with tubocurarine chloride. The tooth pulp test stimulus was applied by a single rectangular-pulse (0.5 ms in duration and 3-5 times the threshold intensity for the 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 35out of 61 of the slow (S)-type TPD neurons with latencies of more than 20 ms, conditioning stimulation in the ACE, especially in the medial division,markedly reduced the firing response to the pulpal stimulation. The inhibition of the firing rate in the S-type neurons was 74% of the control. In these 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. 34.8+/-10.5 ms, n=26). In contrast, the ACE conditioning stimulation affected only one out of 18 fast-type TPD neurons with latencies of less than 20 ms. 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 neurons was not diminished by naloxone administration (1 mg/kg, I.V.), whilethe blockade of histamine H-1-receptor by diphenhydramine hydrochloride (0.5 mg/kg, I.V.) partially reversed the inhibitory effect. These results suggest that the ACE inhibits ascending nociceptive information to the SI and that this inhibition is mediated in part by histamine (H-1) receptors. It seems likely that the antinociceptive effect is a neurophysiological basis for stress-induced analgesia (SIA).

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Documento generato il 25/11/20 alle ore 01:15:33