Faingold C L, Randall M E
Department of Pharmacology, Southern Illinois University, Springfield 62794-9230, USA.
Brain Res. 1995 Dec 18;704(2):218-26. doi: 10.1016/0006-8993(95)01116-1.
The genetically epilepsy-prone rat (GEPR-9) exhibits elevated seizure sensitivity and audiogenic seizures (AGS). The pontine reticular formation (PRF) is implicated in the neuronal network for AGS in the GEPR-9. The present study examined PRF neuronal firing and convulsive behavior simultaneously in the GEPR-9. Chronically implanted microwire electrodes in PRF allowed single neuronal responses and behavior to be examined in freely-moving rats. PRF neurons in the GEPR-9 exhibit precipitous intensity-evoked increases at a significantly lower (approx. 15 dB SPL) intensity than normal Sprague-Dawley rats. PRF neurons in the GEPR-9 also exhibit increased auditory response latencies. At the onset of AGS (wild running) the firing rate of PRF neurons increased, and the rate of PRF firing increased dramatically as the tonic phase of the seizure began. During post-ictal depression the rate of PRF neuronal firing slowed, gradually returning to normal. This pattern of PRF periseizural neuronal firing changes differ dramatically in pattern and temporal characteristics from those previously observed in inferior colliculus (IC). The IC serves as the AGS initiation site. IC neurons show extensive firing increases prior to and during the initial wild running, silence during the tonic and post-ictal phases, and gradual recovery of responses thereafter. The changes in PRF neuronal firing pattern suggest that the PRF may play a major role in the generation of the tonic phase of AGS. The premature onset of the precipitous rise in PRF neuronal firing suggests that the influence of the IC on PRF neurons may be magnified in association with AGS susceptibility. The PRF neuronal firing increases observed in the present study coupled with previous observation of AGS blockade by PRF microinjections in the GEPR-9 further support an important role of the PRF in the propagation of AGS in the GEPR-9. The mechanisms of PRF firing elevation may also be relevant in other seizure models in which the brain-stem reticular formation is implicated.
遗传性癫痫易感大鼠（GEPR - 9）表现出癫痫发作敏感性升高和听源性癫痫发作（AGS）。脑桥网状结构（PRF）参与了GEPR - 9中AGS的神经网络。本研究同时检测了GEPR - 9中PRF神经元的放电和惊厥行为。在PRF中长期植入微丝电极，可在自由活动的大鼠中检测单个神经元反应和行为。与正常的斯普拉格 - 道利大鼠相比，GEPR - 9中的PRF神经元在显著更低（约15 dB SPL）的强度下就表现出强度诱发的急剧增加。GEPR - 9中的PRF神经元还表现出听觉反应潜伏期延长。在AGS发作（狂奔）开始时，PRF神经元的放电频率增加，并且随着癫痫发作的强直期开始，PRF的放电频率急剧增加。在发作后抑郁期间，PRF神经元的放电频率减慢，逐渐恢复正常。PRF癫痫发作周围神经元放电变化的这种模式在模式和时间特征上与先前在下丘（IC）中观察到的有显著差异。IC是AGS的起始部位。IC神经元在最初的狂奔之前和期间显示出广泛的放电增加，在强直期和发作后阶段沉默，此后反应逐渐恢复。PRF神经元放电模式的变化表明，PRF可能在AGS强直期的产生中起主要作用。PRF神经元放电急剧上升的过早出现表明，IC对PRF神经元的影响可能与AGS易感性相关而被放大。本研究中观察到的PRF神经元放电增加，再加上先前在GEPR - 9中通过PRF微注射阻断AGS的观察结果，进一步支持了PRF在GEPR - 9中AGS传播中的重要作用。PRF放电升高的机制可能在其他涉及脑干网状结构的癫痫模型中也具有相关性。
