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Introducción a la Neurología Dr. Edgar Avalos Herrera Neurólogo Internista
El Cerebro Humano ,[object Object]
El Cerebro Humano ,[object Object]
El Cerebro Humano ,[object Object]
El Cerebro Humano ,[object Object],[object Object]
Divisiones ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Divisiones ,[object Object],[object Object],[object Object]
Divisiones ,[object Object],[object Object],[object Object]
Divisiones ,[object Object],[object Object]
Divisiones ,[object Object],[object Object]
Divisiones ,[object Object],[object Object]
Divisiones ,[object Object],[object Object]
Información ,[object Object],[object Object],[object Object],[object Object],[object Object]
Información ,[object Object],[object Object],[object Object]
Información ,[object Object]
Información ,[object Object]
Información ,[object Object]
Información ,[object Object]
Información ,[object Object]
Orientación ,[object Object]
Orientación
Orientación
Terminología
Organización ,[object Object],[object Object],[object Object],[object Object],[object Object]
Terminología ,[object Object],[object Object]
Terminología ,[object Object],[object Object]
Terminología ,[object Object],[object Object]
Terminología ,[object Object],[object Object]
Terminología ,[object Object],[object Object]
 
La Neurona ,[object Object],[object Object],[object Object]
La Neurona ,[object Object],[object Object],[object Object],[object Object]
La Neurona
La Neurona
La Neurona
 
 
 
 
 
 
Núcleo ,[object Object],[object Object],[object Object]
Núcleo ,[object Object]
Núcleo ,[object Object],[object Object],[object Object]
Núcleo ,[object Object],[object Object],[object Object]
Núcleo ,[object Object],[object Object],[object Object]
Nucléolo ,[object Object],[object Object],[object Object],[object Object]
Nucléolo ,[object Object],[object Object],[object Object],[object Object]
Núcleo
Membrana Plasmática ,[object Object],[object Object],[object Object]
Membrana Plasmática ,[object Object],[object Object]
Membrana Plasmática ,[object Object],[object Object],[object Object]
Membrana Plasmática ,[object Object],[object Object],[object Object]
Membrana Plasmática ,[object Object],[object Object],[object Object],[object Object]
Membrana Plasmática ,[object Object],[object Object],[object Object],[object Object],[object Object]
Membrana Plasmática ,[object Object],[object Object],[object Object],[object Object]
Membrana Plasmática ,[object Object],[object Object],[object Object],[object Object]
Membrana Plasmática ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Membrana Plasmática ,[object Object],[object Object],[object Object],[object Object],[object Object]
Membrana Plasmática ,[object Object],[object Object],[object Object]
Membrana Plasmática ,[object Object],[object Object],[object Object]
Membrana Plasmática ,[object Object],[object Object],[object Object],[object Object],[object Object]
Membrana Plasmática ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Membrana Plasmática ,[object Object],[object Object],[object Object]
Membrana Plasmática ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Membrana Plasmática ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Membrana Plasmática ,[object Object],[object Object],[object Object],[object Object],[object Object]
Membrana Plasmática ,[object Object],[object Object]
Membrana Plasmática
Cuerpos de Nissl ,[object Object],[object Object],[object Object]
Cuerpos de Nissl
Cuerpos de Nissl ,[object Object],[object Object],[object Object]
Ribosomas ,[object Object],[object Object],[object Object]
ARN - ADN
Tipos de ARN ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Codones ,[object Object],[object Object]
RER ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
REL ,[object Object],[object Object],[object Object]
Mitocondrias ,[object Object],[object Object]
Mitocondrias ,[object Object]
Mitocondrias ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Mitocondrias ,[object Object],[object Object],[object Object]
Mitocondrias ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Mitocondrias ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Mitocondrias ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Mitocondrias ,[object Object],[object Object],[object Object],[object Object]
Mitocondrias ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Mitocondrias ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Mitocondrias ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Mitocondrias ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Mitocondrias ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Mitocondrias ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Mitocondrias ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Mitocondrias ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Mitocondrias ,[object Object],[object Object],[object Object],[object Object],[object Object]
Peroxisomas ,[object Object],[object Object]
Peroxisomas ,[object Object],[object Object],[object Object],[object Object]
Lisosomas ,[object Object],[object Object],[object Object]
Lisosomas ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Lisosomas ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Lisosomas ,[object Object],[object Object],[object Object],[object Object]
Lisosomas ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Lisosomas ,[object Object],[object Object]
Aparato de Golgi ,[object Object],[object Object],[object Object]
Aparato de Golgi ,[object Object],[object Object],[object Object]
Citoesqueleto ,[object Object],[object Object],[object Object]
Neurotúbulos ,[object Object],[object Object],[object Object]
Neurofilamentos ,[object Object],[object Object],[object Object],[object Object],[object Object]
Citoesqueleto ,[object Object],[object Object],[object Object],[object Object],[object Object]
Transporte Axoplásmico ,[object Object],[object Object],[object Object],[object Object]
Transporte Axoplásmico ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Transporte Axoplásmico ,[object Object],[object Object],[object Object],[object Object],[object Object]
Transporte Axoplásmico ,[object Object],[object Object],[object Object],[object Object]
Transporte Axoplásmico ,[object Object],[object Object],[object Object],[object Object],[object Object]
Transporte Axoplásmico
Transporte Axoplásmico ,[object Object],[object Object],[object Object],[object Object]
Transporte Axoplásmico ,[object Object],[object Object],[object Object],[object Object],[object Object]
Dendritas ,[object Object],[object Object],[object Object]
Axón ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Tipos de Terminaciones
Neurópilo ,[object Object],[object Object],[object Object],[object Object],[object Object]
 
 
 
 
 
 
 
 
Sinapsis ,[object Object],[object Object],[object Object],[object Object],[object Object]
Sinapsis ,[object Object],[object Object],[object Object],[object Object]
Sinapsis ,[object Object],[object Object],[object Object]
Sinapsis
Sinapsis ,[object Object],[object Object],[object Object],[object Object],[object Object]
 
 
 
 
 
Sinapsis Químicas ,[object Object],[object Object]
Sinapsis Químicas ,[object Object],[object Object]
Neurotransmisor ,[object Object],[object Object],[object Object]
Neurotransmisor
Neuroglia ,[object Object],[object Object],[object Object],[object Object],[object Object]
Neuroglia
Astrocitos ,[object Object],[object Object],[object Object],[object Object]
Astrocitos ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Astrocitos ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Astrocitos ,[object Object],[object Object],[object Object],[object Object]
Astrocitos ,[object Object],[object Object],[object Object]
Astrocitos
Oligodendrocitos ,[object Object],[object Object]
Oligodendrocitos ,[object Object],[object Object]
Oligodendrocitos
Oligodendrocitos ,[object Object],[object Object],[object Object]
Microglia ,[object Object],[object Object],[object Object]
Microglia ,[object Object],[object Object],[object Object],[object Object],[object Object]
Microglia ,[object Object],[object Object],[object Object],[object Object]
Microglia ,[object Object],[object Object]
Epéndimo ,[object Object],[object Object],[object Object],[object Object],[object Object]

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Introducción a la Neurología

Notas del editor

  1. The release of neuroactive substances is linked to the arrival of an action potential at the presynaptic terminal, which elicits the opening of voltage-dependent Ca2+ channels (so-called L-type channels). Following diffusion through the intersynaptic cleft, the neurotransmitter binds to the postsynaptic receptor complex. This leads by confor- mational changes or allosteric mechanisms to the opening of ion channels followed by voltage change at the postsynaptic site.
  2. Gracias a los glicolípidos y glicoproteínas
  3. Evitar difusión de moléculas hidrosolubles Permeabilidad selectiva a ciertas moléculas a través de poros o canales (ionóforos) Transducción de información a través de proteínas receptoras que responden a distintos estímulos físicos o químicos; por neurotransmisores, hormonas, luz, vibraciones, presión
  4. Tráfico contínuo de estos elementos
  5. Transporte Pasivo no requiere energía, utiliza la energía del gradiente de concentración Difusión facilitada gracias a proteínas transportadoras Transporte Activo, Endocitosis, Exocitosis ocurren para el transporte de un gradiente menor a uno mayor ATP powers the active transport by transferring its terminal phosphate group directly to the transport ion.
  6. Transporte Pasivo no requiere energía, utiliza la energía del gradiente de concentración Difusión facilitada gracias a proteínas transportadoras Transporte Activo, Endocitosis, Exocitosis ocurren para el transporte de un gradiente menor a uno mayor ATP powers the active transport by transferring its terminal phosphate group directly to the transport ion.
  7. Prior to phosphorylation, the binding sites face the cytoplasm and only the Na+ sites are receptive. Sodium binding induces phosphate transfer from ATP to the pump, triggering the conformational change. In its new conformation, the pump’s binding sites face the extracellular side of the plasma membrane, and the protein now has a greater affinity for K+ than it does for Na+. Because the pump also acts as an enzyme that removes phosphate from ATP, it is also called ATPase.
  8. Prior to phosphorylation, the binding sites face the cytoplasm and only the Na+ sites are receptive. Sodium binding induces phosphate transfer from ATP to the pump, triggering the conformational change. In its new conformation, the pump’s binding sites face the extracellular side of the plasma membrane, and the protein now has a greater affinity for K+ than it does for Na+. Because the pump also acts as an enzyme that removes phosphate from ATP, it is also called ATPase.
  9. Permite el paso de ciertos iones Na+, K+, Cl– and Ca2+ Glycoproteins surrounding continuous pores through the membrane (transmembrane) that allow some ions to flow at rates as high as 100 million ions per second per channel. Some channels are permanently open; others only transiently open. The latter are said to be “gated.”
  10. Transport certain ions or metabolic precursors of macromolecules. Pumps work against an ionic gradient and thus extrude Na+ from the neuron. Energy for this activity is obtained from the hydrolysis of ATP.
  11. Recognition of neurotransmitters and hormones. They act as binding sites for these substances on the outer surface of the plasma membrane. The sites initiate the responses of the neuron, muscle fiber, or gland cell to specific stimuli (chemical or mechanical).
  12. Neurons, unlike most cells, lack the ability to store glycogen as an energy source. As a consequence, they are dependent for their energy on circulating glucose and oxygen. Glucose is the substrate utilized by mitochondrial enzyme systems of neurons for the aerobic generation of ATP. (Neurons do not utilize fat as a substrate for the process of anaerobic generation of ATP.) This explains why we lose consciousness if the blood supply to the brain is interrupted for a short time.
  13. Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  14. Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  15. Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  16. Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  17. Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  18. Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  19. Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  20. Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  21. Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  22. Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  23. Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  24. Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  25. Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  26. Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  27. Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  28. Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  29. Detoxify, with the enzyme catalase, by hydrolyzing hydrogen peroxide
  30. The GA is a complex organelle composed of stacks of flattened cisternal sacs, vesicles, and membranous tubules Newly Ersynthesized protein molecules move through the ER tubules and then bud off into vesicles that are transported to the GA and sequentially through several cisternal compartments. While passing through, the proteins are modified and sorted out before finally emerging from the GA
  31. Each membranous vesicle budded from the GA apparently has external molecules that recognize “docking sites” on the surface of the specific organelle to which they are destined to join.
  32. Adaptation to various shapes (and to carry out coordinated and directed movements) is dependent on complex internal scaffolds of protein filaments and tubules and their associated proteins called the cytoskeleton. The cytoskeletal network extends throughout the cell body, dendrites, and axon. The cytoskeleton is not a fixed structure but undergoes changes during development and growth and after injury. The cytoskeleton consists of numerous fibrillar organelles called (1) neurotubules (microtubules), each roughly 20–25 nm in diameter, (2) neurofilaments (microfilaments), roughly 10 nm in diameter, and (3) actin microfilaments, about 5 nm in diameter. The tubules and filaments comprise about 25% of the total protein of a neuron. Neurotubules and neurofilaments are found throughout the cytoplasm. As molecular motors, they mediate movement of organelles by transport. These tubules and filaments are of variable length with no single element extending the entire length of an axon or dendrite. The tubules are polar structures. Within an axon, the so-called plus end of each tubule is oriented toward the axon terminus and the minus end is oriented toward the cell body In a dendrite, the polarities of the tubules are mixed, with about half having the plus end oriented toward the cell body and the other half with the minus end oriented toward the cell body. The tubules and filaments consist of a polymer of repeating subunits that are in a dynamic state of flux, continuously growing longer or shorter.
  33. Kinesin has the means to power their rapid movement via fast axonal anterograde transport to the plus (+) end of each neurotubule toward the nerve terminals. The motor is presumed to be transported back to the cell body in an inactive form. The organelle-bound kinesin molecules interact transiently with the microtubule during the anterograde transport via the neurotubule. The retrograde motor protein dynein is transported to the terminal in an inactive form, becomes activated, binds to degraded membranes and organelles, and then is conveyed by retrograde transport to the minus (–) end of the microtubules toward the cell body for disposal.
  34. The cell body is kept informed of the metabolic needs and condition of its most distal parts. Through axonal uptake of extracellular substances, such as nerve growth factor followed by retrograde transport, the cell body can sample the extracellular environment However, retrograde transport has its debit side, in that through this mechanism, neurotropic viruses such as rabies, herpes simplex, and poliomyelitis are conveyed to the central nervous system. Defects in microtubules might be involved in some human neurologic disorders.
  35. These dendritic spines increase the surface area of the membrane of the receptive segment of the neuron. Located on them are over 90% of all the excitatory synapses in the central nervous system (CNS). Because of their widespread occurrence on neurons of the cortical areas of the cerebrum, they are thought to be involved in learning and memory
  36. Dendrodendritic synapses (between two dendrites) have been noted (e.g., in the olfactory bulb and retina).
  37. There is a threedimensional dendritic field, formed by the branching of the dendrites
  38. Outline of an electron micrograph segment of a spiny dendrite illustrating a variety of shapes and sizes of spines described as simple to branched and with spine heads ranging from stubby to mushroom shaped. In vivo imaging has demonstrated that dendritic spine s form, collapse and reform, and rapidly change size and shape in response to a diverse array of stimuli. Spine morphology is activity dependent and dynamically responsive
  39. Early in the nineteenth century, the cell was recognized as the fundamental unit of all living organisms. It was not until well into the twentieth century, however, that neuroscientists agreed that nervous tissue, like all other organs, is made up of these fundamental units. The major reason was that the first generation of “modern” neurobiologists in the nineteenth century had difficulty resolving the unitary nature of nerve cells with the microscopes and cell staining techniques that were then available. This inadequacy was exacerbated by the extraordinarily complex shapes and extensive branches of individual nerve cells, which further obscured their resemblance to the geometrically simpler cells of other tissues (Figures 1.2–1.4). As a result, some biologists of that era concluded that each nerve cell was connected to its neighbors by protoplasmic links, forming a continuous nerve cell network, or reticulum. The “reticular theory” of nerve cell communication, which was championed by the Italian neuropathologist Camillo Golgi (for whom the Golgi apparatus in cells is named), eventually fell from favor and was replaced by what came to be known as the “neuron doctrine.” The major proponents of this new perspective were the Spanish neuroanatomist Santiago Ramón y Cajal and the British physiologist Charles Sherrington. The contrasting views represented by Golgi and Cajal occasioned a spirited debate in the early twentieth century that set the course of modern neuroscience. Based on light microscopic examination of nervous tissue stained with silver salts according to a method pioneered by Golgi, Cajal argued persuasively that nerve cells are discrete entities, and that they communicate with one another by means of specialized contacts that Sherrington called “ synapses.” The work that framed this debate was recognized by the award of the Nobel Prize for Physiology or Medicine in 1906 to both Golgi and Cajal ( the joint award suggests some ongoing concern about just who was correct, despite Cajal’s overwhelming evidence). The subsequent work of Sherrington and others demonstrating the transfer of electrical signals at synaptic junctions between nerve cells provided strong support of the “neuron doctrine,” but challenges to the autonomy of individual neurons remained. It was not until the advent of electron microscopy in the 1950s that any lingering doubts about the discreteness of neurons were resolved. The high-magnification, high-resolution pictures that could be obtained with the electron microscope clearly established that nerve cells are functionally independent units; such pictures also identified the specialized cellular junctions that Sherrington had named synapses
  40. The axon of one neuron might terminate in only a few synapses or up to many thousands of synapses. The dendrite–cell body complex might receive synaptic contacts from many different neurons (up to well over 15,000 synapses).
  41. The axon of one neuron might terminate in only a few synapses or up to many thousands of synapses. The dendrite–cell body complex might receive synaptic contacts from many different neurons (up to well over 15,000 synapses). A concentration of mitochondria and presynaptic vesicles is present in the cytoplasm of the bouton; none are present in the cytoplasm adjacent to the subsynaptic membrane.
  42. Most neurons contain at least two distinct types of vesicle: (1) small vesicles 50 nm in diameter and (2) large vesicles from 70 to 200 nm in diameter
  43. At electrical synapses, current flows through gap junctions, which are specialized membrane channels that connect two cells. Chemical synapses enable cell-to-cell communication via the secretion of neurotransmitters; these chemical agents released by the presynaptic neurons produce secondary current flow in postsynaptic neurons by activating specific receptor molecules. The total number of neurotransmitters is not known, but is well over 100. They are a distinct minority, electrical synapses
  44. Transmission can be bidirectional. Transmission is extraordinarily fast. Such synapses interconnect many of the neurons within the circuit that allows the crayfish to escape from its predators, thus minimizing the time between the presence of a threatening stimulus and a potentially life-saving motor response. A more general purpose of electrical synapses is to synchronize electrical activity among populations of neurons. For example, the brainstem neurons that generate rhythmic electrical activity underlying breathing are synchronized by electrical synapses, as are populations of interneurons in the cerebral cortex, thalamus, cerebellum, and other brain regions. Electrical transmission between certain hormone-secreting neurons within the mammalian hypothalamus ensures that all cells fire action potentials at about the same time, thus facilitating a burst of hormone secretion into the circulation. The fact that gap junction pores are large enough to allow molecules such as ATP and second messengers to diffuse intercellularly also permits electrical synapses to coordinate the intracellular signaling and metabolism of coupled cells. This property may be particularly important for glial cells, which form large intracellular signaling networks via their gap junctions.
  45. Gap junctions consist of hexameric complexes formed by the coming together of subunits called connexons, which are present in both the pre- and postsynaptic membranes.
  46. Rapid transmission of signals at an electrical synapse in the crayfish. An action potential in the presynaptic neuron causes the postsynaptic neuron to be depolarized within a fraction of a millisecond. The change in membrane potential caused by the arrival of the action potential leads to the opening of voltage-gated calcium channels in the presynaptic membrane. Because of the steep concentration gradient of Ca2+ across the presynaptic membrane (the external Ca2+ concentration is approximately 10–3 M, whereas the internal Ca2+ concentration is approximately 10–7 M), the opening of these channels causes a rapid influx of Ca2+ into the presynaptic terminal, with the result that the Ca2+ concentration of the cytoplasm in the terminal transiently rises to a much higher value. Elevation of the presynaptic Ca2+ concentration, in turn, allows synaptic vesicles to fuse with the plasma membrane of the presynaptic neuron. The Ca2+-dependent fusion of synaptic vesicles with the terminal membrane causes their contents, most importantly neurotransmitters, to be released into the synaptic cleft.
  47. The notion that electrical information can be transferred from one neuron to the next by means of chemical signaling was the subject of intense debate through the first half of the twentieth century. A key experiment that supported this idea was performed in 1926 by German physiologist Otto Loewi. Acting on an idea that allegedly came to him in the middle of the night, Loewi proved that electrical stimulation of the vagus nerve slows the heartbeat by releasing a chemical signal. He isolated and perfused the hearts of two frogs, monitoring the rates at which they were beating (Figure 5.4). His experiment collected the perfusate flowing through the stimulated heart and transferred this solution to the second heart. When the vagus nerve to the first heart was stimulated, the beat of this heart slowed. Remarkably, even though the vagus nerve of the second heart had not been stimulated, its beat also slowed when exposed to the perfusate from the first heart. This result showed that the vagus nerve regulates the heart rate by releasing a chemical that accumulates in the perfusate. Originally referred to as “vagus substance,” the agent was later shown to be acetylcholine (ACh).
  48. The neurotransmitters, includes substances which are responsible for intersynaptic signal transmission The neuromodulators, exerts a modulatory function on postsynaptic events. Neurons can synthesize and release individual neurotransmitters and are able to produce and release co-transmitter in the form of the neuromodulators.
  49. For decades, neurons were believed to constitute monofunctional units with respect to neurotransmitter production and secretion (Dale’s principle). However, a large body of evidence now indicates that individual neurons are able to synthesize different neuroactive substances and process them for secretion. This evidence does not, in principle, violate Dale’s idea that the neuron is a monofunctional entity, but it does lead to a modification of this paradigm, i.e. the functional phenotype of a differentiated neuron is monospecific in respcet of its neurotransmitter efficacy. The synthesis and release of more than one neuroactive substance from a single neuron substantially augments the range of variability of chemically coded signals. The full significance of this increase is far from being understood.
  50. For decades, neurons were believed to constitute monofunctional units with respect to neurotransmitter production and secretion (Dale’s principle). However, a large body of evidence now indicates that individual neurons are able to synthesize different neuroactive substances and process them for secretion. This evidence does not, in principle, violate Dale’s idea that the neuron is a monofunctional entity, but it does lead to a modification of this paradigm, i.e. the functional phenotype of a differentiated neuron is monospecific in respcet of its neurotransmitter efficacy. The synthesis and release of more than one neuroactive substance from a single neuron substantially augments the range of variability of chemically coded signals. The full significance of this increase is far from being understood.
  51. The “glial” cells of the PNS consist of Schwann cells that surround nerve fibers and perineuronal satellite cells surrounding the cell body. These cell types, now considered to be functionally indistinguishable, are collectively called neurolemma cells.
  52. Astroglia constitute a heterogeneous morphologic and functional population occupying the spaces surrounding each CNS neuron. There are protoplasmic astrocytes in the gray matter and fibrous astrocytes in white matter. Others include Bergmann cells in the cerebellum, Muller’s cells in the retina, pinealocytes in the pineal gland, and pituicytes located in the posterior lobe of the pituitary gland. These cells contain 8- to 10-nmwide microfilaments composed of polymerized strands of glial fibrillary acidic protein (GFAP), a specific biochemical marker for astrocytes that can be revealed through immunohistochemistry. Thus, astroglia can be distinguished from neurons for diagnostic purposes.
  53. Following intense neuronal activity, they take up glutamate and neurotoxins that accumulate in the extracellular spaces and synaptic clefts.
  54. Following the uptake of excess potassium ions from focal high-concentration sinks, the astrocytes can then transfer the excess ions via their gap junctions to regions within the astrocytic syncytium, where the potassium ion concentration is lower (known as spatial buffering). This prevents the spreading depression that results from the presence of high extracellular concentrations of potassium ions that can trigger excessive neuronal depolarization. In essence, astrocytes have roles in regulating and maintaining the homeostatic composition of the extracellular fluid (ionic microenvironment and pH) essential to the normal functioning of the neurons of the CNS.
  55. There are two types of oligodendroglia: perineuronal satellite cells, which are closely associated with cell bodies and dendrites in the gray matter, and (2) interfascicular cells, which are involved in myelination of axons in white matter
  56. There are two types of oligodendroglia: perineuronal satellite cells, which are closely associated with cell bodies and dendrites in the gray matter, and (2) interfascicular cells, which are involved in myelination of axons in white matter
  57. There are two types of oligodendroglia: perineuronal satellite cells, which are closely associated with cell bodies and dendrites in the gray matter, and (2) interfascicular cells, which are involved in myelination of axons in white matter
  58. Oligodendrocytes can participate in the remyelination that can occur following acute or chronic demyelination. This so-called spontaneous remyelination takes place in such diseases as multiple sclerosis and could explain the clinical improvement observed in different demyelinating diseases.