Cerebral Cortex: Further Aspects of Cortical Function, by George G. Somjen (auth.), Edward G. Jones, Alan Peters

By George G. Somjen (auth.), Edward G. Jones, Alan Peters (eds.)

Volume 6 of Cerebral Cortex is in a few respects a continuation of quantity 2, which handled the useful features of cortical neurons from the physiological and pharmacological issues of view. within the present quantity, chapters are dedicated to the catecholamines, which for a few purposes weren't represented within the past quantity, and to acetylcholine and the neuropeptides, approximately which a lot new details has lately seemed. quantity 6 bargains partly with the constitution and serve as of cholinergic and catecholaminergic neuronal structures within the cerebral cortex and with new features of the cortical peptidergic neurons, particularly the virtually common propensity of the recognized cortical peptides for being colocalized with classical transmitters and with each other. It hence completes our assurance of the foremost cortical neuro­ transmitter and neuromodulatory platforms. different chapters during this quantity care for information bearing on the proportions of other varieties of cells and synapses within the neocortex and the body structure of the cortical neuroglial cells. those latter are themes that hardly obtain separate therapy and the present chapters serve back to proceed discussions of topics that have been brought in quantity 2. the former volumes have all been dedicated to the neocortex however the current one introduces the topic of the archicortex. To this finish, separate chapters are dedicated to the body structure and anatomy of the hippocampal formation.

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1986). Transport of K + ions from CNS into blood plasma may take care of the overall long-term regulation of [K +]0 in brain, but each time a neuron is activated it releases some K + into the restricted volume of the interstitial fluid. Neuronal activity can thus perturb [K +]0> on a time scale of milliseconds to seconds, and such transient fluctuations of [K +]0 probably cannot be compensated by transport of K + between CNS and blood. K + ions that have been lost from neurons must, in time, be restored to the cells that lost them, or the brain could not continue to function for very long.

1980) obtained negative effects: uptake blockers did not alter the effectiveness of applied GABA. In central gray matter this type of experimental approach is complicated by the fact that GABAergic neurons mingle with glial cells, and both accumulate GABA actively. To distinguish between the two systems in the olfactory cortex, Brown et at. (1980) used several selective blockers. They found that only those that selectively blocked neuronal uptake had any effect; those working mainly on glial cells had none.

This experiment shows that even without preloading there is enough GABA in satellite cells to influence neuronal function, if the 25 FUNCTIONS OF GLIAL CELLS IN CEREBRAL CORTEX 26 CHAPTER 1 cells are provoked to discharge their content. Not answered by any of the foregoing experiments is the question whether in normal tissue physiologic stimuli ever act to cause such release. It is thus a well-documented fact that glial elements can make GABA, they can take it up from their environment, and they also can release it.

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