Cortical spreading depression (CSD) plays a role in migraine with aura. However, studies of the neuronal effects of CSD in human cortex are scarce. Therefore, in the present study, the effects of CSD on the field excitatory postsynaptic potentials (fEPSP) and the induction of long-term potentiation (LTP) were investigated in human neocortical slices obtained during epilepsy surgery. CSD significantly enhanced the amplitude of fEPSP following a transient suppressive period and increased the induction of LTP in the third layer of neocortical tissues. These results indicate that CSD facilitates synaptic excitability and efficacy in human neocortical tissues, which can be assumed to contribute to hyperexcitability of neocortical tissues in patients suffering from migraine.

SUMMARY The present study on rats and cats aimed to clarify the role played by hypoxia, hypercapnia and acidosis in spontaneous arrest of seizures. In most experiments cortical pO2 declined during seizure activity, whereas pCO2 increased. Occasionally, however, reverse reactions occurred. Since the increase in cortical blood flow varied over a wide range, it could account for the fact that gas tension did not always change in the same direction or to the same degree during a seizure. Cessation of seizure activity was independent of the degree and direction of the changes in gas tension. When seizures were arrested by experimentally produced hypoxia, cortical and spinal neurons always showed a distinct depolarization. When convulsive discharges were suppressed by artificial increase in PCO2 most units were concomitantly hyperpolarized. When seizures ceased spontaneously, both cortical and spinal neurons showed a steep re‐ and hyperpolarization, independent of concomitant fluctuations in local gas tension. The findings lead to the conclusion that the degree of hypoxia and hypercapnia usually encountered during prolonged seizure activity does not reach the critical level sufficient to depress seizure activity. It must be assumed that spontaneous seizure termination is based, primarily, on neuronal processes. RESUME Cette étude se propose de préciser, chez les rats et les chats, le rôle de l'hypoxie, de l'hypercapnie et de l'acidose dans l'arrêt des crises spontanées. Dans la majorité des expériences, Ia pO2 au niveau cortical diminue pendant la crise, tandis que la pCO2 augmente, quoique occasionnellement, on ait observé le contraire. La très grande variabilité de l'augmentation de la circulation sanguine cérébrale pouvait rendre compte du fait que pendant une crise, la tension des gaz ne changeait pas toujours dans le même sens ou dans les mêmes limites. L'arrêt de la crise était indépendant du degré et du type des modifications de la tension des gaz. Lorsque les crises étaient arrêtées à la suite d'une anoxie provoquée expérimentalement, on a toujours observé une dépolarisation des neurones corticaux spinaux. Lorsque les décharges convulsives étaient supprimées par une augmentation artificielle de la pCO2, la majorité des neurones était parallèlement hyperpolarisée. Lorsque les crises s'arrêtaient spontanément, les neurones du cortex et de la moelle montraient une rapide repolarisation et ensuite une hyperpolarisation indépendamment des fluctuations concomitantes de la tension des gaz. Ces données amènent à la conclusion que le degré d'hypoxie et d'hypercapnie qu'on observe habituellement pendant des crises prolongées n'atteint pas un niveau suffisant pour déprimer l'activité paroxystique. On doit en tirer la conclusion que l'arrêt spontané d'une crise est dûà des processus nerveux.

The serum- and glucocorticoid-dependent kinase SGK1 is regulated by alterations of cell volume, whereby cell shrinkage increases and cell swelling decreases the transcription, expression and activity of SGK1. The kinase is expressed in all human tissues studied including the brain. The present study was performed to localize the sites of SGK1 transcription in the brain, to elucidate the influence of the hydration status on SGK1 transcription and to explore the functional significance of altered SGK1 expression. Northern blot analysis of human brain showed SGK1 to be expressed in all cerebral structures examined: amygdala, caudate nucleus, corpus callosum, hippocampus, substantia nigra, subthalamic nucleus and thalamus. In situ hybridization and immunohistochemistry in the rat revealed increased expression of SGK1 in neurons of the hippocampal area CA3 after dehydration, compared with similar slices from brains of euvolaemic rats. Additionally, several oligodendrocytes, a few microglial cells, but no astrocytes, were positive for SGK1. The abundance of SGK1 mRNA in the temporal lobe, including hippocampus, was increased by dehydration and SGK1 transcription in neuroblastoma cells was stimulated by an increase of extracellular osmolarity. Co-expression studies in Xenopus laevis oocytes revealed that SGK1 markedly increased the activity of the neuronal K+ channel Kv1.3. As activation of K+ channels modifies excitation of neuronal cells, SGK1 may participate in the regulation of neuronal excitability.

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