Persistent negative potential provoked by a single wave of cortical spreading depression in different brain structures of a rat

Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, Moscow.
Zhurnal vysshei nervnoi deiatelnosti imeni I P Pavlova (Impact Factor: 0.11). 07/1998; 48(4):654-63.
Source: PubMed


The persistent negative potential (PNP) developed after a single wave of cortical spreading depression (SD) in the cortex, hippocampus, thalamus, and caudate nucleus. The PNP lasted for about 3-4 hours, its amplitude was 6-7 mV in the ipsilateral and 3-4 mV in the contralateral structures. After development of bilateral primary cortical SD waves the amplitudes of the respective PNP were summed up and reached 9-11 mV. However, after the repeated waves of cortical SD produced with 15-30-min intervals, the PNP level remained unchanged. We think that the PNP is an electrographic manifestation of the well known persistent vasoconstriction after a single wave of cortical SD. It seems to be related with reticular activation due to functional decortication.

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    ABSTRACT: Die Arbeit thematisiert den Einfluss von Somatostatin auf die experimentell herbeigeführten elektrophysiologischen Phänomene spreading depression, sowie die long-term potentiation in somatosensorischen, neokortikalen Schnitten des adulten Rattenhirns. Die elektrophysiologischen Aufzeichnungen, die in der dritten und fünften Schicht des somatosensorischen Neokortex aufgenommen wurden, zeigten nach der Gabe von Somatostatin, sowohl bei der durch KCl- Induktion in der sechsten Schicht herbeigeführten SD, als auch bei der Herbeiführung einer long- term potentation deutliche Veränderungen. Somatostatin führte zu einer dosisabhängigen Verringerung der SD-Amplitude, die Stärke und Dauer hingegen wurden nicht signifikant verändert. Bei der Untersuchung der LTP zeigte sich bei allen Versuchsdurchgängen eine Unterdrückung derselben. Der therapeutische Effekt von Somatostatin ist eventuell durch die modulierenden Aktionen auf die neokortikalen SD zu erklären.
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    ABSTRACT: The functional consequences of spreading depression (SD) during the evolution of ischemic damage was studied in two models: focal cortical ischemia induced by photothrombosis of the middle cerebral artery (MCA) and systemic hypoxia induced by 0.8% carbon monoxide (CO). These studies showed that cortical waves of SD, arising spontaneously during MCA thrombosis and after arterial occlusion delayed thrombus formation and promoted the establishment of a collateral blood supply in the perifocal zone of ischemic lesions. The underlying mechanism consisted of episodes of intense vasodilation at the decay phase of every wave of SD. Respiration of 0.8% CO increased the blood carboxyhemoglobin level to 50-60%. In lightly anesthetized rats (pentobarbital 20 mg/kg), cortical and subcortical spontaneous waves of SD were transformed into stable hypoxic depolarization, leading to death of 60% of the animals or severe lesions of the central nervous system, in 20% of animals. Increases in the level of anesthesia (50 mg/kg anesthetic) prevented the spontaneous appearance of SD during long-lasting exposure to CO. In these conditions, experimentally induced waves of SD demonstrated that the hippocampus has a high sensitivity to moderate levels of hypoxia. The duration of hypoxic depolarization of the hippocampus, provoking a single SD wave, reached 30-60 min. Selective neuron damage in field CA1 was seen 30 days after hypoxia. Additionally, the left hippocampus of rats frequently showed profound morphological lesions in the form of "granules." Cerebrolysine (2.5 ml/kg daily for 10 days) completely prevented the formation of these lesions.
    No preview · Article · Sep 1999 · Neuroscience and Behavioral Physiology