Search Results

Spiking neural P systems are the subject of this chapter. They were inspired by a very specific kind of cell: neurons, and their method of operation mimics the functioning of these cells. Despite the fact that this model is relatively recent compared to the other ones considered in this book, the number of results concerning it is considerable.

This chapter focuses on the receptors expressed by different types of glial cells for neurotransmitters and hormones. Topics discussed include astrocytes (e.g., ionotropic glutamate receptors, metabotropic glutamate receptors, gamma-aminobutyric acidA receptors), oligodendrodcytes (e.g., glutamate receptors, ionotropic gamma-aminobutyric acid receptors, purinergic receptors), and Schwann cells.

This chapter focuses on astrocytes. In the last fifteen years, the status of astrocytes has changed profoundly from a cell scaffold and metabolic-trophic reservoir offering neurons a necessary, yet only passive, support to a full actor, working in collaboration with other glial cells and with the surrounding neurons by the continuous exchange of chemical messengers including glutamate, a classical neurotransmitter. Astrocytes as neurosecretory cells, stimulus-secretion coupling in astrocytes, and the role of regulated secretion from astrocytes in brain physiology are discussed.

This chapter describes the structure and function of the blood-brain barrier (BBB) represented by brain capillary endothelial cells. Special attention is given to the influence of astrocytes and astrocytic factors. Ontogenetic development and pathological aspects of the BBB are considered.

This chapter focuses on signaling and homeostasis. Electrical signaling in nervous systems involves considerable fluxes of ions across the neuronal membranes to carry electrical charge in and out. These ion fluxes tend to change the ion concentrations inside and outside cells, and these concentration changes, if sufficiently large, would change the functioning of cells and hence of the tissue as a whole. Changes in ion concentrations are usually opposed by homeostatic processes and, in general, are not large enough to have radical effects on function. However, modest changes in ion concentrations during physiological activity are often observed, and some of these can be regarded as signals passing through the extracellular spaces (ECS). Ions participating in major fluxes across cell membranes include those responsible for electrical signaling (mainly Na⁺, K⁺, and Cl^-), and also HCO3^-, H⁺, and NH4⁺, which are linked to metabolism.

The action of neurotransmitters can be terminated by cleavage, diffusion, binding, or cellular uptake. In some cases, uptake is accomplished by glial cells localized at or near the synapse. Glial cells express a variety of neurotransmitter uptake systems, and these systems play a fundamental role in both normal brain function and disease states. All types of glial cells—astrocytes, oligodendrocytes, and microglia—can express transporters for neurotransmitter uptake. This chapter focuses on astrocyte glutamate uptake, which is the most fully characterized of the astrocyte neurotransmitter uptake systems.

Neuronal survival and functions require bidirectional communication between neurons and glia that involves a large variety of growth factors. Neurotrophic factors are operationally defined as proteins that regulate neuron survival and differentiation. They can be synthesized by nonneuronal target cells, neurons, and glial cells. This chapter focuses on neurotrophic factors secreted from macroglial cells, that is, astrocytes, oligodendrocytes, and Schwann cells, and their effects on neuronal differentiation and survival in the intact and lesioned brain and peripheral nervous system.

A general perception has emerged over the past two decades of research that astrocytes are relatively resistant to insults such as those caused by ischemia [oxygen/glucose deprivation (OGD)], and oxidative stress [e.g., reactive oxygen species (ROS)] damage. Recent work, however, points to significant astrocyte dysfunction in response to these injuries. This chapter focuses on the responses of astrocytes to hypoxia/ischemia and trauma. It argues that given the importance of astrocyte functioning to the microenvironment of the central nervous system (CNS), it is apparent that alterations in their physiology during pathological states (such as ischemia and traumatic brain injury) could have profound implications for the progression of these insults.

This chapter discusses the response of microglia to brain injuries. Microglia are activated to induce various cellular changes, including morphology, immunohistochemical properties, proliferative activity, chemotactic mobility, biochemical change, secretion, and phagocytosis, in response to the signal(s) produced in the extracellular milieu of the pathological brain. Some putative or plausible signals from injured neurons or activated astrocytes have been predicted based on an acute injury model. In response to these candidate molecules, the microglia produce a specific combination of secretory molecules through a specific signal transduction cascade. Thus, the activated microglia might play different roles according to the type of pathology.

This chapter shows the disease-specific, individual, and finely tuned reaction pattern of astrocytes and microglia during central nervous system (CNS) infections and their contribution to the intracerebral immune response. While both soluble mediators and the induction and/or upregulation of immunologically relevant cell surface molecules contribute to elimination of offending pathogens, microglia also serve an immunoregulatory function in order to minimize damage and destruction of vulnerable brain tissue. However, while these various components of the immune reaction serve a protective function, it is also evident that, depending on the underlying pathology, reactions of microglia and astrocytes may also be detrimental, as antibacterial effector molecules may also be neurotoxic and thereby contribute to neuronal damage, apoptosis, and, ultimately, long-term neurological sequelae.

This chapter provides a historical perspective that highlights the early period of glial research. Topics covered include Virchow's invention of the term neuroglia in 1856, Heinrich Müller' picture of a glial cell, stellate cells in white and gray matter, and Camillo Golgi's description of cells with characteristic features of astrocytes and oligodendrocytes.

Glia are recognized as active partners with neurons as participants in neurotransmission and they play essential roles in axonal conduction, synaptic plasticity, and information processing. In the adult human brain, glia outnumber neurons by one order of magnitude. There are two classes of glia: microglia (which mediate inflammatory responses in the central nervous system) and macroglia. Macroglia are oligodendrocytes and astrocytes. This chapter focuses on astrocytes, which are the most paradigmatic glia.

. This chapter emphasizes the general principles of brain metabolism and the haemodynamic response to neuronal activity. The precise mechanisms responsible for the links between brain energy metabolism and brain work are not well defined. The chapter gives a detailed description of the nature of the metabolic work for information transfer in the brain, which provides an understanding of the link between changes in energy metabolism affecting physiological parameters such as blood flow and neuronal activity. It proceeds with a discussion of biochemical pathways that provide energy for brain work and also discusses the role of astrocytes in the regulation of the metabolic response to neuronal excitation. The chapter attempts to identify an alternative regulator that changes in response to work and influences the rate of energy metabolism.

This chapter on estrogenic regulation of glia and neuroinflammation reviews the role of glial cells in the modulation of synaptic function under physiological conditions and in the regulation of the neuroinflammatory response under pathological conditions. The anti-inflammatory actions of estradiol on astrocytes, oligodendrocytes, and microglia and the implication of these actions for the neuroprotective and tissue repair effects of the hormone are also discussed. Finally, the therapeutic potential of synthetic and natural estrogenic compounds for the control of neuroinflammation is examined. Because reducing neuroinflammation prevents the progressive loss of neural structure and function that leads to functional and mental impairments, regulation of glial cell activation via estradiol is a promising therapeutic approach.