Registration for a live webinar on 'Immunoregulation in avascular regions of the eye: A role for the lens' is now open.More details
Physiology and Pathophysiology of NeurogliaRoles in health and disease
University of Manchester, UK
University of Alabama at Birmingham, USA
Glial cells are the most numerous cells in the human brain and outnumber neurones by 10 to 1. Yet, until very recently glia were considered as purely supportive elements of the brain, so that the attention of neuroscientists was concentrated almost exclusively on neurones and neuronal networks, which were considered... read moreas the only substrate for the highest brain functions.
The last two decades have brought upon us an incredible increase in knowledge about the appearance, physiological properties and functions of neuroglia. We have learned that these cells are as diverse as neurones; they shape the micro-architecture of the brain matter; they are capable of expressing the same receptors and channels as neurones do; they receive synaptic inputs; they are organized as communicating networks; they are able to release “glio” transmitters and produce long-range information exchange; and finally they act as pluripotent neural precursors and some of them are, most likely, neural stem cells, which provide for adult neurogenesis. These advances in gliology constitute a tremendous challenge to the neuronal doctrine, calling for a fundamental reshaping of our perception of the brain organization, which undeniably will lead to an appearance of a more inclusive theory of brain function.
Similarly, our perception of brain pathology, which, for a long time was revolving around neuronal reactions, their survival or death, has now turned into investigations which very much emphasize the role of glia in the progression and handling of the insults to the nervous system. The brain pathology, is, to a very great extent, a pathology of glia, which, when failing to function properly, determines the degree of neuronal death, the outcome and the scale of neurological deficit.