Main description:

Stability of the internal environment in which neuronal elements are situated is unquestionably an important prerequisite for the effective transmission of information in the nervous system. During the past decade our knowledge on the microenvironment of nerve cells has expanded. The conception that the microenvironment of neurones comprises a fluid with a relatively simple and stable composition is no longer accepted; the microenvironment is now envisaged as a dynamic structure whose composition, shape, and volume changes, thereby significantly influencing neuronal function and the trans mission of information in the nervous system. The modern conception of the neuronal microenvironment is based on the results of research over the last 20 years. The extracellular space (ECS) is comprehended not only as a relatively stable microenvironment containing neurones and glial cells (Bernard 1878), but also as a channel for communica tion between them. The close proximity of the neuronal elements in the CNS and the narrowness of the intercellular spaces provides a basis not only for interaction between the elements themselves, but also between the elements and their microenvironment. Substances which can cross the cell membranes can easily find their way through the microenvironment to adjacent cellular elements. In this way the microenvironment can assure non-synaptic com munication between the relevant neurones. Signalization can be coded by modulation of the chemical composition of the ECS in the vicinity of the cell membrane and does not require classic connection by axones, dendrites, and synapses.

Contents:

1 Introduction.- 2 Ion-Selective Microelectrodes.- 3 K+ Homeostasis in the ECS.- 3.1 Stability of K+ in the Extracellular Fluid.- 3.2 Sources of [K+]e Increases.- 3.3 Redistribution of Extracellularly Accumulated K+.- 3.3.1 Role of Active Transport.- 3.3.2 Role of Glial Cells in K+ Homeostasis.- 3.3.2.1 The Spatial Buffer Mechanism.- 3.3.2.2 Active K+ Transport.- 3.3.2.3 Channel-Mediated KCl Uptake.- 3.3.3 K+ Diffusion in the ECS.- 3.3.4 K+ Exchange Between Extracellular Fluid and Blood.- 4 Dynamic [K+]e Changes.- 4.1 Dynamic [K+]e Changes in the Spinal Cord...- 4.1.1 [K+]e Changes Induced by Electrical Stimulation of Peripheral Nerves.- 4.1.2 Depth Profile of [K+]e Changes in the Spinal Cord.- 4.1.3 Electrical Stimulation of Descending Pathways.- 4.1.4 [K+]e Changes Induced by Adequate Stimulation.- 4.1.4.1 Acute Nociceptive and Non-Nociceptive Stimuli.- 4.1.4.2 Chronic Nociceptive Stimuli.- 4.1.5 [K+]e Changes Associated with Spontaneous Activity in the Dorsal Horns of the Spinal Cord.- 4.1.6 [K+]e Changes Induced by Systemic Administration of Drugs, Transmitters, and Neuropeptides.- 4.2 Dynamic [K+]e Changes in the Brain.- 4.2.1 Dynamic [K+]e Changes in the Cerebral Cortex and Striatum.- 4.2.2 Dynamic [K+]e Changes in the Mesencephalic Reticular Formation.- 4.2.3 Dynamic [K+]e Changes in the Cerebellum and Hippocampus.- 4.3 Functional Significance of [K+]e Changes in the CNS.- 4.3.1 Role of K+ in Presynaptic Inhibition.- 4.3.1.1 Depolarization of Primary Afferents.- 4.3.1.2 Effect of Picrotoxin and Bicuculline.- 4.3.2 Effect of K+ Accumulation on Synaptic Transmission.- 4.3.2.1 Effect of K+ on Neuronal Membrane Potential.- 4.3.2.2 Effect of K+ on Synaptic Potentials and Spontaneous Activity.- 4.3.2.3 Effect of K+ on Flexor Reflex.- 4.3.3 K+ Accumulation and Glial Cell Function.- 4.3.4 K+ Accumulation and the Therapeutic Effect of Electrostimulation.- 4.3.5 Other Functional Correlates of a [K+]e Increase.- 4.3.6 K+ Accumulation and Its Functional Significance in Pathological Processes.- 4.3.6.1 [K+]e Changes During Ischaemia and Hypoxia.- 4.3.6.2 K+, Epilepsy, and Epileptiform Activity.- 4.3.6.3 [K+]e and Spreading Depression.- 4.4 Dynamic K+ Changes in the Organ of Corti.- 4.4.1 Resting K+ Concentration in the Inner Ear.- 4.4.2 Dynamic Changes in K+ Concentration in the Organ of Corti Evoked by Acoustic Stimuli.- 4.4.3 Functional Significance of Dynamic [K+]e Changes in the Organ of Corti.- 4.5 Changes in K+ Concentration in the Retina.- 4.5.1 Regulation of [K+]e by Glial Cells in the Retina.- 5 Dynamic Changes in Extracellular Na+, Cl-, and Ca2+ Concentration.- 5.1 Changes Induced in Resting [Ca2+]e During Stimulation of Afferent Input.- 5.2 [Ca2+]e Changes in Pathological States.- 5.3 Functional Significance of Dynamic [Ca2+]e Changes.- 6 Dynamic pHe Changes.- 6.1 Extracellular Buffering Power.- 6.2 Activity-Related Dynamic pHe Changes in Nervous Tissue.- 6.2.1 Resting pHe.- 6.2.2 pHe Changes Evoked by Stimulation of Afferent Input.- 6.2.2.1 pHe Changes Evoked by Adequate Stimulation of Skin Nociceptors.- 6.2.3 Effect of Block of Synaptic Transmission on pHe Changes.- 6.2.4 pHe Changes Induced by K+ Depolarization.- 6.3 Mechanisms of pHe Changes in the CNS.- 6.3.1 Effect of Sodium Fluoride.- 6.2.3 Effect of Ouabain.- 6.3.3 Effect of Amiloride.- 6.3.4 Effect of SITS and DIDS.- 6.3.5 Effect of Acetazolamide.- 6.3.6 Effect of Furosemide.- 6.3.7 Effect of Block of H+ Channels.- 6.4 Role of Glial Cells in pHe Homeostasis.- 6.5 pHe Changes in the Retina.- 6.6 pHe Changes During Anoxia, Ischaemia, Epilepsy, and SD.- 6.7 Functional Significance of pHe Changes.- 7 Dynamic Changes in Size of the ECS.- 7.1 Measurement of Changes in Size of the ECS by Means of K+-ISMs.- 7.2 Changes Induced in Size of the ECS by Electrical Stimulation.- 7.3 Changes Induced in Size of the ECS by Adequate Stimulation.- 7.4 Mechanisms of Dynamic Changes in Size of the ECS.- 7.4.1 Volume Changes Induced by Changes in Extracellular Osmolarity.- 7.4.2 Volume Changes During Neuronal Activity.- 7.4.3 Transport Systems of Glial Cells and Regulation of Their Volume.- 7.4.4 Changes in Cell Volume Induced by Inhibition of Na+/K+ ATPase.- 7.5 Functional Significance of Dynamic Volume Changes in the Microenvironment of Nerve Cells.- 8 Conclusion.- References.