Neurons are the principal transducing cells of both the central and peripheral nervous systems. Though they exhibit great structural variation, they all serve the same purpose: to receive, process, and transmit information via bioelectric signals (Kreutzberg et al. 1997). Neurons are characterized by their excitability and ability to conduct impulses, i.e., if sufficiently stimulated they release a brief electrical discharge, termed an action potential, which is conducted along the axon. The action potential is a major constituent
of communication among nerve cells and between nerve cells and the body; it is an indispensable link between the central nervous system (CNS) and the world around us.
An action potential is created by the movement of ions through the cell membrane, which requires an electrical potential between the interior and exterior of the cell, the membrane potential. The electrical current is transformed at the synaptic level into a chemical signal: the released transmitters bind briefly to receptors on the postsynaptic membrane.
The action potential is based on the presence of voltage-gated Na+ channels that open when the membrane is depolarized. Depolarization can result from electrical stimulation or opening of transmitter-gated Na+ channels. The latter induces a flow of Na+ into the cell driven by the concentration gradient and membrane potential. The inflow of Na+ ions ceases once the membrane depolarizes to +55 mV.
The action potential is the result of an invariable all-or-nothing phenomenon. Messages can only be varied by a variation in the rate of action potentials, which in turn depends on the degree of depolarization. Some neurons are capable of a maximum frequency of action potentials exceeding 100 per second (100 Hz).
The velocity at which an impulse is conducted depends on the axon's diameter and myelin thickness and in meters per second is roughly 6 times the axo-nal diameter in microns. An action potential is generated when positive charges penetrate to the proximal part of the axon, which at that point becomes positive relative to more distal parts along its length. A corresponding current of positive charges moves in the opposite direction outside the axon, thus establishing an electrical circuit. The action potential in myelinated axons spreads passively (electronically) to the first node of Ranvier and is regenerated at each further node, where the axon membrane lacks a myelin sheath. The action potential moves by "jumping" from one node of Ranvier to the next.
Several authors have studied the role of neurons in the immune response process (Sedgwick and Hickey 1997). It is thought that healthy neurons probably do not respond even to cytokines, such as interferon-y (IFN-y), which are associated with the major histocompatibility complex (MHC). On the other hand, following infection, MHC expression has been found in neurons in vivo.
In the healthy CNS, MHC class I and II molecules are virtually absent. Under pathological conditions, however, MHC molecules are known to be upregu-
lated by various cells within the CNS (see below). Under normal circumstances neurons are able to prevent and/or limit inflammatory responses (for review see Neumann 2000, 2001). Under pathological conditions such as mechanical brain injury, genes are turned on, inducing a proinflammatory milieu with upregulation of MHC molecules, local production of proinflammatory cytokines, and recruitment of inflammatory cells (Streit et al. 1989; Olsson et al. 1992).
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