The electrophysiological characteristics and behavioral manifestations of hippocampal and thalamic spreading depression]

Behavioral manifestations of spreading depression (SD) were compared with SD electrophysiological characteristics in these structures. Carbon electrodes were suitable for recording DC slow potential changes in freely moving animal. It was shown that short (0.1 s) high-frequency (200 Hz) electrical stimulation of thalamus and hippocampus with intensity 50-300 microA easily triggered SD wave in these structures in narcotized and awake rats. The threshold of SD occurrence in dorsal hippocampus was the same or sometimes lower than that of the primary afterdischarge. Penetrating SD into ventral hippocampus provoked long latency seizure discharge and wet-dog shakings in awake rats. Intensity of locomotor activity accompanying bilateral hippocampal SD exceeded orienting response significantly. Contrary to hippocampus, thalamic SD was usually subseizure and unilateral phenomenon and had a clear tranquil effect on the rat locomotor activity. It was found that the rats didn't change the compartment preference after 20-45 SD waves in the thalamus or in the hippocampus.     

Properties of spreading depression during different phases of cyclic excitation of the rat neocortex

Properties of cortical spreading depression were studied during different phases of cyclic excitation developing in the neocortex of rats under the influence of low-frequency electrical stimulation. Waves of spreading depression appeared in the cortex spontaneously or after microinjection of potassium chloride. During each excitation cycle a state preventing the passage and appearance of these waves developed in the region of electrical stimulation. The degree of blocking in other areas of the cortex outside the region of stimulation depended on the distance from the site of electrical stimulation and on generalization of excitatation over the cortex. After the end of the excitation phase, while the current continued to act, the ability of the cortex to conduct the depression wave was restored. In intervals of cyclic excitation the duration of the waves of spreading depression remained on average only half its duration in the absence of stimulation. The time course of development and the character of recovery of depression during the intervals confirm the hypothesis that activation of the potassium-sodium pump may have a role in the blocking mechanism and enable the temporal parameters of this process to be estimated.