Effect of conditioning stimulation of the limbic system on tooth pulp-driven neuron in cat's somatosensory cortex (SI).

为了确定边缘系统是否在疼痛加工中起作用，我们研究了海马、杏仁核和周围皮层的条件反射刺激对第一体感皮层（SI）牙髓驱动（TPD）神经元反应的影响。26只猫分别用2:1的n2 - o_2和1%-氟烷麻醉，用curare固定。牙髓测试刺激为单个5-15v、持续时间0.5msec的矩形脉冲，边缘系统调节刺激为33个脉冲（50-500 a）、持续时间0.5msec的序列，以330Hz传递。根据放电模式和快速（F-）、慢速（S-）和快速伴后放电（Fa）的潜伏期对TPD神经元进行分类。海马和杏仁核的条件刺激对TPD神经元的活性和自发放电无明显影响。另一方面，调节刺激位于杏仁核腹侧的杏仁核周围区（PAA）明显抑制了s型神经元的反应和fa型的后放电，尽管条件刺激对1)f型TPD神经元的放电、2)fa型的快速反应和3)三种TPD类型的自发放电几乎没有影响。抑制期300 ~ 800msec。这种抑制甚至在杏仁核的主要传出道终纹被破坏后仍然存在，而对终纹的条件反射刺激并不能模拟这种抑制效果。在一项相关研究中，用Nembutal麻醉的猫，牙髓刺激引起的二腹肌肌电活动（下颌张开反射）被100-300msec的PAA调节刺激抑制了60-100%。这些发现表明PAA在球水平上通过终纹以外的途径（可能是腹侧杏仁核纤维）调节伤害感觉的中枢机制。

In order to detemine if the limbic system has any role in pain processing, we investigated the effect of conditioning stimulation at hippocampus, amygdala and the surrpunding cortex on the response of tooth pulp-driven (TPD) neurons in the first somatosensory cortex (SI).Cats (n=26) were anesthetized with N_2O-O_2 (2:1) and 1%-halothane and immobilized by curare. The tooth pulp test stimulus was a single 5-15v rectangular pulse of 0.5msec duration and the conditioning stimuli of limbic system were trains of 33 pulses (50-500 a) having duration of 0.5msec delivered at 330Hz.TPD neurons have been classified according to their discharge patterns and latencies at fast (F-), slow (S-), and fast- accompanied by after-discharges (Fa). The conditioning stimuli of hippocampus or amygdaloid nucleus did not alter the activities of TPD neurons and their spontaneous discharges. On the other hand, the conditioning stimulation of the periamygdaloid area (PAA) that located in the ventral side to the amygdaloid nucleus markedly suppressed the response of the S-type neurons and the after-discharges of the Fa-types, although the conditioning stimulation had almost no effect on: 1) The discharge of F-type TPD neurons, 2) the fast responses of the Fa-type, and 3) the spontaneous discharge of all three TPD types. The inhibitory period was 300-800msec. This inhibition persited even after the destruction of stria terminalis that was a major efferent tract from the amygdaloid nucleus, and conditioning stimulation of the stria terminalis did not mimic the inhibitory effect. In a related study, digastric EMG activity (jaw opening reflex) induced by tooth pulp stimulation was suppressed 60-100% by the PAA conditioing stimulation for a period of 100-300msec in cats anesthetized with Nembutal. These findings indicate that the PAA modulated central mechanisms of nociception at the bulbar level via the pathway other than the stria terminalis, presumably the ventral amygdalofugal fiber.