Collins D R, Korsak A, Gilbey M P
Department of Physiology, Royal Free and University College Medical School, University College London, Royal Free Campus, London NW3 2PF, UK.
Neuroscience. 2002;110(2):351-60. doi: 10.1016/s0306-4522(01)00572-3.
Neuronal population discharges within the CNS and in somatic and sympathetic motor nerves often display oscillations. Peripheral oscillations may provide a window into central mechanisms, as they often show coherence with population activity of subsets of central neurones. The reduction in heat loss through the cutaneous circulation during fever may be mediated via sympathetic premotor neurones not utilised during normal temperature regulation. Consequently, here we assessed, in anaesthetised rats, whether the frequency signature of population sympathetic discharge observed in neurones innervating the tail (thermoregulatory) circulation changed during a fever-like response induced by intracerebroventricular injection of prostaglandin E(1). We found that when core temperature was raised to 38.8-40.5 degrees C sympathetic activity was abolished. Following administration of prostaglandin (400 ng or 1 microg per rat), activity was restored to levels seen prior to heating (154+/-53.5%; n=10). Injection of vehicle had no effect (n=7). Prior to heating when most animals were in central apnoea (14/18) two peaks were observed in autospectra of sympathetic activity: one at 0.68-0.93 Hz (T-peak) and another at the frequency of ventilation (2 Hz). Central respiratory drive was recruited during hyperthermia where it was 1:2 locked to the frequency of ventilation and following prostaglandin administration, an additional peak in sympathetic autospectra was seen at this frequency. Time-evolving spectra indicated that this peak resulted from the dynamic locking of the 'T-peak' to central respiratory drive. Our data show that during a fever-like response the dominant oscillations in sympathetic activity controlling a thermoregulatory circulation and their dynamic coupling to respiratory-related inputs are similar to those seen under normal conditions. Therefore, during this fever-like response, the neural substrate(s) underlying the oscillations is not reconfigured and remains capable of sculpturing the pattern of sympathetic neuronal discharge that may be regulated by several descending pathways.
中枢神经系统以及躯体和交感运动神经内的神经元群放电常常呈现出振荡。外周振荡可能为中枢机制提供一个窗口，因为它们常常与中枢神经元子集的群体活动表现出相关性。发热期间通过皮肤循环的热量散失减少可能是由正常体温调节过程中未被利用的交感运动前神经元介导的。因此，我们在此评估了在麻醉大鼠中，脑室内注射前列腺素E(1)诱导的类似发热反应期间，支配尾部（体温调节）循环的神经元中观察到的群体交感放电的频率特征是否发生了变化。我们发现，当核心体温升至38.8 - 40.5摄氏度时，交感神经活动消失。给予前列腺素（每只大鼠400纳克或1微克）后，活动恢复到加热前的水平（154±53.5%；n = 10）。注射溶剂没有效果（n = 7）。在加热前，当大多数动物处于中枢性呼吸暂停状态时（14/18），在交感神经活动的自谱中观察到两个峰值：一个在0.68 - 0.93赫兹（T峰），另一个在通气频率（2赫兹）。在体温过高期间，中枢呼吸驱动被激活，此时它与通气频率呈1:2锁定，并且在给予前列腺素后，在这个频率上交感神经自谱中出现了一个额外的峰值。时间演变谱表明，这个峰值是由“T峰”与中枢呼吸驱动的动态锁定导致的。我们的数据表明，在类似发热反应期间，控制体温调节循环的交感神经活动中的主导振荡及其与呼吸相关输入的动态耦合与正常条件下所见相似。因此，在这种类似发热反应期间，振荡背后的神经基质没有重新配置，并且仍然能够塑造可能由几种下行通路调节的交感神经元放电模式。
