The reports presented in this issue of Experimental Physiology have been provided by the speakers at the symposium Glial-neuronal interactions in central nervous cardiovascular and respiratory control which was held within the main meeting of the Physiological Society in Manchester, 30 June 2010, and was sponsored by Experimental Physiology. The idea to organize such a meeting reflects the current surge of interest in the mechanisms and functional implications of neuronal–glial interactions in the central nervous system. In contrast to the previous view, which held astrocytes as a mass of supportive cells (some sort of ‘brain glue’), we know now that glial cells can actively modulate activities of neuronal networks. When activated, astrocytes display Ca2+ responses and Ca2+ waves. Astrocytes release ‘gliotransmitters’ (ATP, glutamate and others) to signal back to neurons and neighbouring glial cells and also to control local extracellular milieu and cerebral vascular tone. The symposium concentrated on the functional role played by glia in the brain, and highlighted various aspects of glial research, from the development of new technologies to the role of astrocytes in fundamental autonomic reflexes, integral to maintenance of the respiratory and cardiovascular homeostasis. Brian MacVicar (University of British Columbia, Canada) presented an overview of the work performed in his laboratory on control of cerebral blood vessels by astrocytes (Gordon et al. 2011). This function of astrocytes puts them in a unique position as an interface between neurons and the circulatory network in the brain. The emerging view is that the astrocytes are able to change arterial diameter and thereby regulate local blood flow. Therefore, the astrocytes help to couple neural activity to blood vessels in order to co-ordinate oxygen and glucose delivery with the energy demands of the tissue. MacVicar's report published in this issue of Experimental Physiology contains an update on the complex coupling mechanism, which involves various products of arachidonic acid, nitric oxide, lactate and adenosine. Daniel Mulkey's (University of Connecticut, USA) presentation at the symposium implicated astrocytes located in the chemoreceptive area on the ventral surface of the brainstem in the detection of H+ ions (Mulkey & Wenker, 2011). His report published here looks at the evidence that purinergic signalling contributes to central chemoreception, one of the most important homeostatic signalling pathways in the brain. He presented data which suggest that pH sensitivity might involve inhibition of Kir channels and activation of a depolarizing inward current generated by the sodium–bicarbonate cotransporter. Pierre Magistretti (University of Lausanne, Switzerland) presented new data which extended his research into the role of lactate in the metabolic coupling between astrocytes and neurons (Magistretti, 2011). The main theme of his presentation and the report published here is the evidence that activation of specific neuronal networks using learning protocols in rodents leads to a set of characteristic changes in gene expression, which reflect metabolic plasticity. He also discussed the emerging evidence for altered neuron–glia metabolic coupling in neuroinflammation and neurodegeneration. Indeed, changes in brain metabolism and oxidative stress are characteristic features of neurodegenerative disorders, including Alzheimer's disease. Changes in various branches of the metabolic transformation of glucose (glycolysis, which is coupled to lactate production, tricarboxylic acid cycle, pentose phosphate pathway and incorporation into glycogen) could all be important for neurodegeneration and neuroprotection. Alexander Gourine (University College London, UK) presented an account of a large, multifaceted study, which employed a range of innovative technologies and provided one of the strongest pieces of evidence obtained so far for the active role of astrocytes in information processing in the brain (Gourine & Kasparov, 2011). He focused on central chemoreception and demonstrated that astrocytes located in the previously known chemoreceptive area in vivo respond to acidification with powerful Ca2+ waves mediated largely by ATP. Moreover, using optogenetic control of astrocytes, it was possible to trigger respiration in anaesthetized animals, an effect which again, was mediated by purinergic signalling. Astrocytes are ideally positioned to be chemodetectors because their endfeet are in direct contact with the blood vessels and also surfaces of the brain. One exciting possibility supported by several recent studies is that they do not only participate in detection of pH but also other modalities of chemoreception. We hope that the reports of the symposium published in this volume will be of interest to the readership of Experimental Physiology. The topic of glial–neuronal interactions will no doubt be a hot spot of neuroscience for years to come.
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Apr 1, 2011
Walter José Minto + 3
Open Access