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Extracellular Environment of CNS Neurons - A.R. Gardner-Medwin
Refs: From Neuron to Brain (Nicholls, Martin & Wallace) Chapters on glia and (in
earlier editions) on extracellular environment. Sections on csf and blood-brain barrier
in most textbooks.
Learning Objectives:
Understand mechanisms by which the composition of the micro-environment in the
CNS is :(a) regulated in the long term by the blood-brain barrier
(b) altered by neural activity in both normal and pathological situations
(c) buffered in special circumstances by diffusion and glial function
Understand how the size of the extracellular space has been measured experimentally,
why it often comes to appear abnormally small in histological and EM pictures, and
how it is altered by neurological and osmotic disturbances.
Understand the relation between the cerebrospinal fluid (csf) and the microenvironment of the brain: parallel regulating mechanisms, bulk flow of fluid out of the
brain (cf. lymphatic drainage in other systems), free but very slow diffusional
equilibration.
Understand the principal functions of the csf: reduced gravitational effects on the
brain, lubrication, limited volume adjustment to cope with swelling, limited
homeostasis.
Understand why glial physiology was first studied in invertebrates, what special
physiological membrane properties have been identified in glial cells (in vertebrates,
particularly in astrocytes) and how these may play a role in short term homeostasis
countering neurally induced disturbances of the micro-environment.
Understand how the ionic composition of the micro-environment can be measured
experimentally with ion-selective microelectrodes and how both these measurements
and glial membrane potentials change during disturbances such as epilepsy, or even
during normal physiological activity.
Understand how positive feedback processes (such as K+ induced K+ release) can
lead to severe dysfunction of neural tissue, as for example in the transient neural
disorder called Spreading Cortical Depression (probably contributing to migraine),
and how these effects may be countered by homeostatic buffering mechanisms, such
as the K+ spatial buffer mechanism in glial cells.
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