Introducción a la Neurología

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Introducción a la Neurología - Asociación Guatemalteca de Neurología Virtual

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  • Terminología Organización Somatotópica o Topográfica Porciones específicas de ciertos tractos, núcleos, o áreas de la corteza cerebral asociadas con regiones restringidas y específicas del cuerpo
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  • 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.
  • Gracias a los glicolípidos y glicoproteínas
  • 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
  • Tráfico contínuo de estos elementos
  • 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.
  • 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.
  • 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.
  • 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.
  • 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.”
  • 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.
  • 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).
  • 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.
  • Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  • Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  • Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  • Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  • Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  • Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  • Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  • Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  • Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  • Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  • Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  • Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  • Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  • Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  • Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  • Mitochondria are present in the ovum but not in sperm. Thus, mtDNA inheritance is said to be matrilineal and independent of nuclear inheritance.
  • Detoxify, with the enzyme catalase, by hydrolyzing hydrogen peroxide
  • 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
  • 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.
  • 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.
  • 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.
  • 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.
  • 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
  • Dendrodendritic synapses (between two dendrites) have been noted (e.g., in the olfactory bulb and retina).
  • There is a threedimensional dendritic field, formed by the branching of the dendrites
  • 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
  • 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
  • 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).
  • 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.
  • 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
  • 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
  • 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.
  • 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.
  • 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.
  • 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).
  • 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.
  • 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.
  • 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.
  • 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.
  • 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.
  • Following intense neuronal activity, they take up glutamate and neurotoxins that accumulate in the extracellular spaces and synaptic clefts.
  • 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.
  • 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
  • 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
  • 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
  • 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.
  • Introducción a la Neurología

    1. 1. Introducción a la Neurología Dr. Edgar Avalos Herrera Neurólogo Internista
    2. 2. El Cerebro Humano <ul><li>Es lo que separa a los humanos del resto de las especies, permitiéndonos lograr maravillas como caminar sobre la luna y crear obras maestras de literatura, arte y música. (SfN) </li></ul>
    3. 3. El Cerebro Humano <ul><li>Ha sido comparado con una super-computadora, pero el cerebro es mucho más complicado, un hecho que los científicos confirma diariamente con cada nuevo descubrimiento.(SfN) </li></ul>
    4. 4. El Cerebro Humano <ul><li>La extensión de las capacidades del cerebro es desconocida, pero es la estructura viviente más compleja en todo el universo. (SfN) </li></ul>
    5. 5. El Cerebro Humano <ul><li>Cómo es que 100 billones de células nerviosas son producidas, crecen, se organizan y forman sistemas activos y funcionales. </li></ul><ul><li>De forma breve, el cerebro es lo que nos hace humanos. (SfN) </li></ul>
    6. 6. Divisiones <ul><li>Anatómica </li></ul><ul><ul><li>SN Central </li></ul></ul><ul><ul><li>SN Periférico </li></ul></ul><ul><li>Funcional </li></ul><ul><ul><li>SN Somático </li></ul></ul><ul><ul><li>SN Autonómico </li></ul></ul>
    7. 7. Divisiones <ul><li>SN Periférico </li></ul><ul><ul><li>Nervios Craneales (Cerebro) </li></ul></ul><ul><ul><li>Nervios Espinales (Médula Espinal) </li></ul></ul>
    8. 8. Divisiones <ul><li>Señales SN Periférico </li></ul><ul><ul><li>Órganos de los Sentidos y Receptores Sensitivos hacia el SNC (AFERENTE) </li></ul></ul><ul><ul><li>Del SNC hacia músculos y glándulas del cuerpo (EFERENTE) </li></ul></ul>
    9. 9. Divisiones <ul><li>Señales SN Somático (SNP - SNC) </li></ul><ul><ul><li>Procesamiento y transmisión de informacion consciente e inconsciente. Visión, dolor, tacto, aferencias musculares inconscientes desde músculos de la cabeza, tronco y extremidades hacia el SNC </li></ul></ul>
    10. 10. Divisiones <ul><li>Señales SN Somático (SNP - SNC) </li></ul><ul><ul><li>Eferencias para el control motor voluntario del músculo estriado </li></ul></ul>
    11. 11. Divisiones <ul><li>Señales SN Autonómico (SNC - SNP) </li></ul><ul><ul><li>Procesamiento y transmisión de información sensitiva desde órganos viscerales (sistema digestivo, sistema cardiovascular, otros) </li></ul></ul>
    12. 12. Divisiones <ul><li>Señales SN Autonómico (SNC - SNP) </li></ul><ul><ul><li>Control motor del músculo liso, músculo cardíaco y glándulas </li></ul></ul>
    13. 13. Información <ul><li>La información sensitiva de receptores periféricos es transmitida a través del sistema nervioso por medio de vías sensitivas </li></ul><ul><ul><li>Vías de dolor </li></ul></ul><ul><ul><li>Vías de temperatura </li></ul></ul><ul><ul><li>Vías visuales </li></ul></ul><ul><ul><li>Otras </li></ul></ul>
    14. 14. Información <ul><li>La información que llega al sistema nervioso central puede ser utilizada </li></ul><ul><ul><li>De forma consciente </li></ul></ul><ul><ul><li>De forma inconsciente </li></ul></ul>
    15. 15. Información <ul><li>La información nerviosa para la actividad motora es transmitida a través del sistema nervioso central hacia los músculos y glándulas por medio de vías motoras </li></ul>
    16. 16. Información <ul><li>Cada vía sensitiva (aferente, ascendente) y motora (eferente, descendete) tiene centros de procesamiento (núcleos, ganglios, cortezas) a distintos niveles en la médula espinal y en el cerebro </li></ul>
    17. 17. Información <ul><li>Los centros de procesamiento de la información constituyen las computadoras de estas vías de alta velocidad </li></ul>
    18. 18. Información <ul><li>Desde los receptores periféricos hacia los centros más altos del cerebro las señales eléctricas siguen una misma secuencia básica: </li></ul>
    19. 19. Información <ul><li>Receptores Sensitivos Fibras Nerviosas Centros de Procesamiento en Médula Espinal y Cerebro Fibras Nerviosas que ascienden de forma ipsilateral o se decusan Centros Superiores de Procesamiento Fibras ipsilaterales que ascienden y terminan en Los Centros más altos en la Corteza Cerebral </li></ul>
    20. 20. Orientación <ul><li>El eje largo trazado a través de la médula espinal y el cerebro se denomina neuroeje, en forma de letra “T” </li></ul>
    21. 21. Orientación
    22. 22. Orientación
    23. 23. Terminología
    24. 24. Organización <ul><li>Sistema Nervioso Central </li></ul><ul><ul><li>Sustancia Gris </li></ul></ul><ul><ul><ul><li>Cuerpos Neuronales, Dendritas, Terminaciones Axónales, Sinapsis, Células Gliales, muy vascularizada </li></ul></ul></ul><ul><ul><li>Sustancia Blanca </li></ul></ul><ul><ul><ul><li>Axones, Células Gliales, sin neuronas excepto en los núcleos basales, menos vascularizada. Su color más blanco se debe a la mielina. </li></ul></ul></ul>
    25. 25. Terminología <ul><li>Comisuras </li></ul><ul><ul><li>Haces de fibras nerviosas que cruzan la línea media y que interconectan estructuras pares de ambos hemisferios cerebrales </li></ul></ul>
    26. 26. Terminología <ul><li>Modalidad </li></ul><ul><ul><li>Cualidad de un estímulo, tipo de sensación transmitida (tacto, dolor, sonido, visión) </li></ul></ul>
    27. 27. Terminología <ul><li>Organización Somatotópica o Topográfica </li></ul><ul><ul><li>Porciones específicas de ciertos tractos, núcleos, o áreas de la corteza cerebral asociadas con regiones restringidas y específicas del cuerpo </li></ul></ul>
    28. 28. Terminología <ul><li>Organización Somatotópica o Topográfica </li></ul><ul><ul><li>Algunas estructuras de la vía visual están topográficamente relacionadas con regiones específicas de la retina: Organización Retinotópica </li></ul></ul>
    29. 29. Terminología <ul><li>Organización Somatotópica o Topográfica </li></ul><ul><ul><li>Algunas estructuras de la vía auditiva están organizadas funcionalmente con respecto a diferentes frecuencias o tonos: Organización Tonotópica </li></ul></ul>
    30. 31. La Neurona <ul><li>Célula especializada diseñada para transmitir información a otras neuronas, múlculos y glándulas. Es la unidad funcional del cerebro. </li></ul><ul><li>El cerebro se debe a las propiedades funcionales y estructurales de las neuronas interconectadas. </li></ul><ul><li>Recibe, transmite y almacena información </li></ul>
    31. 32. La Neurona <ul><li>Cuerpo celular </li></ul><ul><li>Dendritas </li></ul><ul><li>Axón </li></ul><ul><li>Terminaciones Sinápticas </li></ul>
    32. 33. La Neurona
    33. 34. La Neurona
    34. 35. La Neurona
    35. 42. Núcleo <ul><li>Separado del citoplasma por una doble capa, la cubierta nuclear </li></ul><ul><li>La membrana nuclear esta perforada por los poros nucleares </li></ul><ul><li>La parte externa de la membrana se continúa con el retículo endoplásmico liso </li></ul>
    36. 43. Núcleo <ul><li>La parte interna de la membrana se une a la cromatina nuclear y con estructuras que controlan el diámetro de los poros nucleares </li></ul>
    37. 44. Núcleo <ul><li>Se sintetizan 3 clases de proteínas </li></ul><ul><ul><li>Sintetizadas en el citosol por ribosomas y polisomas, que permanecen en el citosol </li></ul></ul><ul><ul><ul><li>Distribuidas por transporte axoplásmico lento, incluidas enzimas esenciales para catalizar procesos metabólicos del citoesqueleto </li></ul></ul></ul>
    38. 45. Núcleo <ul><li>Se sintetizan 3 clases de proteínas </li></ul><ul><ul><li>Sintetizadas en el citosol por ribosomas y polisomas, que son incorporadas al núcleo, mitocondrias, peroxisomas </li></ul></ul><ul><ul><ul><li>Enzimas incluidas en la síntesis de ADN, ARN, factores de transcripción que regulan expresión genética </li></ul></ul></ul>
    39. 46. Núcleo <ul><li>Se sintetizan 3 clases de proteínas </li></ul><ul><ul><li>Sintetizadas en asociación con el retículo endoplásmico y el aparato de Golgi </li></ul></ul><ul><ul><ul><li>Distribuidas por transporte axonal rápido hacia organelas, hacia vesículas secretoras (neurotransmisores) y hacia la membrana plasmática para mantenimiento estructural </li></ul></ul></ul>
    40. 47. Nucléolo <ul><li>Maquinaria productora de ribosomas </li></ul><ul><li>Constituido principalmente por ARN y menos ADN </li></ul><ul><li>Sitio de ensamblaje inicial y producción de ARNr </li></ul><ul><li>Bastante desarrollado en neuronas activamente productoras de péptidos y proteínas </li></ul>
    41. 48. Nucléolo <ul><li>El cerebro utiliza más genes que cualquier otro órgano del cuerpo </li></ul><ul><li>15,000 genes son únicos al tejido neural </li></ul><ul><li>Neuronas femeninas </li></ul><ul><ul><li>Cuerpos de Barr </li></ul></ul>
    42. 49. Núcleo
    43. 50. Membrana Plasmática <ul><li>Bicapa de fosfolípidos asociada a proteínas, carbohidratos, glicolípidos y colesterol </li></ul><ul><li>Porción hidrofílica (polar) </li></ul><ul><li>Porción hidrofóbica (no-polar) </li></ul>
    44. 51. Membrana Plasmática <ul><li>Proteínas intrínsecas o integrales </li></ul><ul><li>Proteínas periféricas </li></ul>
    45. 52. Membrana Plasmática <ul><li>Reconocimiento Molecular </li></ul><ul><li>Reconocimiento Celular </li></ul><ul><li>Adhesión Celular </li></ul>
    46. 53. Membrana Plasmática <ul><li>Difusión de moléculas hidrosolubles </li></ul><ul><li>Permeabilidad selectiva a ciertas moléculas </li></ul><ul><li>Transducción </li></ul>
    47. 54. Membrana Plasmática <ul><li>Sodio, Potasio, Calcio, Cloro </li></ul><ul><li>Oxígeno </li></ul><ul><li>Nutrientes </li></ul><ul><li>Desechos moleculares </li></ul>
    48. 55. Membrana Plasmática <ul><li>Transporte Pasivo </li></ul><ul><li>Difusión Facilitada </li></ul><ul><li>Transporte Activo </li></ul><ul><li>Endocitosis </li></ul><ul><li>Exocitosis </li></ul>
    49. 56. Membrana Plasmática <ul><li>Bomba Na-K ATPasa </li></ul><ul><ul><li>Integral ? </li></ul></ul><ul><ul><li>Periférica ? </li></ul></ul><ul><ul><li>Intrínseca ? </li></ul></ul>
    50. 57. Membrana Plasmática <ul><li>Bomba Na-K ATPasa </li></ul><ul><ul><li>Integral ? </li></ul></ul><ul><ul><li>Periférica ? </li></ul></ul><ul><ul><li>Intrínseca ? </li></ul></ul>
    51. 58. Membrana Plasmática <ul><li>Proteínas Funcionales </li></ul><ul><ul><li>Ionóforos </li></ul></ul><ul><ul><li>Bombas </li></ul></ul><ul><ul><li>Receptores </li></ul></ul><ul><ul><li>Transductores </li></ul></ul><ul><ul><li>Proteínas Estructurales </li></ul></ul><ul><ul><li>Transportadores de Neurotransmisores </li></ul></ul>
    52. 59. Membrana Plasmática <ul><li>Ionóforos </li></ul><ul><ul><li>Canales activados por acetilcolina </li></ul></ul><ul><ul><ul><li>1 ms </li></ul></ul></ul><ul><ul><ul><li>20,000 Na </li></ul></ul></ul><ul><ul><ul><li>K </li></ul></ul></ul>
    53. 60. Membrana Plasmática <ul><li>Bombas Iónicas </li></ul><ul><ul><li>A favor de gradiente ? </li></ul></ul><ul><ul><li>Contra gradiente ? </li></ul></ul>
    54. 61. Membrana Plasmática <ul><li>Receptores protéicos </li></ul><ul><ul><li>Hormonas </li></ul></ul><ul><ul><li>Neurotransmisores </li></ul></ul>
    55. 62. Membrana Plasmática <ul><li>Transductores </li></ul><ul><ul><li>Ligando </li></ul></ul><ul><ul><li>Receptor </li></ul></ul><ul><ul><li>Enzimas </li></ul></ul><ul><ul><li>Segundos Mensajeros (AMPc) </li></ul></ul>
    56. 63. Membrana Plasmática <ul><li>Proteínas Estructurales </li></ul><ul><ul><li>Moléculas de adhesión celular (MAC) </li></ul></ul><ul><ul><li>MAC-N: Moléculas de adhesión celular neuronal </li></ul></ul><ul><ul><ul><li>Reconocimiento interneuronal </li></ul></ul></ul><ul><ul><ul><li>Redes neuronales funcionales </li></ul></ul></ul><ul><ul><ul><li>Migración neuronal </li></ul></ul></ul><ul><ul><ul><li>Afinidad de terminaciones nerviosas </li></ul></ul></ul><ul><ul><ul><li>Interacciones neurona-neurona neurona-glia </li></ul></ul></ul>
    57. 64. Membrana Plasmática <ul><li>MAC-N: Moléculas de adhesión celular neuronal </li></ul><ul><ul><ul><li>Adherencia neuronal </li></ul></ul></ul><ul><ul><ul><li>Interactúan con integrinas y cadherinas </li></ul></ul></ul>
    58. 65. Membrana Plasmática <ul><li>Integrinas </li></ul><ul><ul><li>Crecimiento celular. </li></ul></ul><ul><ul><li>División celular. </li></ul></ul><ul><ul><li>Supervivencia celular. </li></ul></ul><ul><ul><li>Diferenciación celular. </li></ul></ul><ul><ul><li>Apoptosis. </li></ul></ul>
    59. 66. Membrana Plasmática <ul><li>Cadherinas </li></ul><ul><ul><li>Cadherinas clásicas o tradicionales: </li></ul></ul><ul><ul><ul><li>Cadherina-E </li></ul></ul></ul><ul><ul><ul><li>Cadherina-N </li></ul></ul></ul><ul><ul><ul><li>Cadherina-P </li></ul></ul></ul><ul><ul><ul><li>Cadherina-V </li></ul></ul></ul>
    60. 67. Membrana Plasmática <ul><li>Cadherinas </li></ul><ul><ul><li>Cadherinas no clásicas o no tradicionales: </li></ul></ul><ul><ul><ul><li>Demogleína y desmocolina </li></ul></ul></ul><ul><ul><ul><li>Cadherina-T </li></ul></ul></ul><ul><ul><ul><li>Protocadherina </li></ul></ul></ul>
    61. 68. Membrana Plasmática <ul><li>Transportadores de Neurotransmisores </li></ul><ul><ul><li>Recaptación y reciclaje de Serotonina, Glutamato, Dopamina </li></ul></ul>
    62. 69. Membrana Plasmática
    63. 70. Cuerpos de Nissl <ul><li>Sustancia Cromofílica </li></ul><ul><ul><li>Agregados basofílicos localizados en el soma y dendritas </li></ul></ul><ul><ul><li>No se encuentra en el cono axónico (axon hillock) ni en el axón </li></ul></ul>
    64. 71. Cuerpos de Nissl
    65. 72. Cuerpos de Nissl <ul><li>Cisternas aplanadas de Retículo Endoplásmico Rugoso </li></ul><ul><li>Ribosomas Libres </li></ul><ul><li>Polisomas </li></ul>
    66. 73. Ribosomas <ul><li>Proteínas (Ribonucleoproteínas) </li></ul><ul><li>ARNr </li></ul><ul><li>ARNm </li></ul>
    67. 74. ARN - ADN
    68. 75. Tipos de ARN <ul><li>ARNr </li></ul><ul><li>ARNm </li></ul><ul><li>ARNt </li></ul><ul><li>ARNi </li></ul><ul><li>ARNmt </li></ul><ul><li>ARN antisentido </li></ul><ul><li>ARNnc largo </li></ul><ul><li>Riboswitch </li></ul>
    69. 76. Codones <ul><li>UAG, UAA, UGA </li></ul><ul><li>AUG </li></ul>
    70. 77. RER <ul><li>Proteínas Neurosecretoras </li></ul><ul><li>Proteínas Integrales de la Membrana Plasmática </li></ul><ul><li>Proteínas Lisosomales </li></ul><ul><li>Ribosomas libres y polisomas </li></ul><ul><ul><li>Proteínas citosólicas </li></ul></ul><ul><ul><li>Proteínas no integrales de la membrana plasmática </li></ul></ul>
    71. 78. REL <ul><li>Triglicéridos </li></ul><ul><li>Colesterol </li></ul><ul><li>Esteroides </li></ul>
    72. 79. Mitocondrias <ul><li>Plantas de Energía de las neuronas </li></ul><ul><li>Energía (ATP), Agua, CO2 </li></ul>
    73. 80. Mitocondrias <ul><li>Fosforilación Oxidativa - Complejos I a V ? </li></ul>
    74. 81. Mitocondrias <ul><li>Deleciones y Duplicaciones esporádicas de ADNmt </li></ul><ul><ul><li>Síndrome de Kearns-Sayre </li></ul></ul><ul><ul><li>Síndrome de Pearson </li></ul></ul><ul><ul><li>Oftalmoplejía Externa Crónica Progresiva Esporádica </li></ul></ul><ul><ul><li>Diabetes y Sordera </li></ul></ul><ul><ul><li>Oftalmoplejía Externa Crónica Progresiva de herencia materna </li></ul></ul>
    75. 82. Mitocondrias <ul><li>Mutaciones Puntuales de ADNmt </li></ul><ul><ul><li>Polipéptidos </li></ul></ul><ul><ul><ul><li>Encefalomiopatía mitocondrial con acidosis láctica y episodios parecidos a eventos cerebrovasculares ( Mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes - MELAS ) </li></ul></ul></ul>
    76. 83. Mitocondrias <ul><li>Mutaciones Puntuales de ADNmt </li></ul><ul><ul><li>Polipéptidos </li></ul></ul><ul><ul><ul><li>Intolerancia al ejercicio </li></ul></ul></ul><ul><ul><ul><li>Miopatía aislada </li></ul></ul></ul><ul><ul><ul><li>Neuropatía óptica hereditaria de Leber </li></ul></ul></ul><ul><ul><ul><li>Síndrome de Neuropatía Ataxia y Retinitis Pigmentosa </li></ul></ul></ul><ul><ul><ul><li>Síndrome de Leigh </li></ul></ul></ul>
    77. 84. Mitocondrias <ul><li>Mutaciones Puntuales de ADNmt </li></ul><ul><ul><li>ARNt mitocondrial </li></ul></ul><ul><ul><ul><li>MELAS </li></ul></ul></ul><ul><ul><ul><li>Epilepsia Mioclónica con Fibras Rojas Rasgadas ( Myoclonic epilepsy with ragged-red fibers MERRF ) </li></ul></ul></ul><ul><ul><ul><li>Cardiomiopatía-Miopatía </li></ul></ul></ul><ul><ul><ul><li>Oftalmoplejía Externa Crónica Progresiva </li></ul></ul></ul><ul><ul><ul><li>Miopatía aislada </li></ul></ul></ul>
    78. 85. Mitocondrias <ul><li>Mutaciones Puntuales de ADNmt </li></ul><ul><ul><li>ARNt mitocondrial </li></ul></ul><ul><ul><ul><li>Diabetes y Sordera </li></ul></ul></ul><ul><ul><ul><li>Sordera Neurosensorial </li></ul></ul></ul><ul><ul><ul><li>Cardiomiopatía Hipertrófica </li></ul></ul></ul><ul><ul><ul><li>Tubulopatía </li></ul></ul></ul>
    79. 86. Mitocondrias <ul><li>Mutaciones Puntuales de ADNmt </li></ul><ul><ul><li>ARNr mitocondrial </li></ul></ul><ul><ul><ul><li>Sordera no sindrómica inducida por aminoglucósidos </li></ul></ul></ul><ul><ul><ul><li>Cardiomiopatía Hipertrófica </li></ul></ul></ul>
    80. 87. Mitocondrias <ul><li>Enfermedad de Alzheimer </li></ul><ul><ul><li>Gen: APP </li></ul></ul><ul><ul><li>Proteína: Precursor Proteína Amiloide beta A4 </li></ul></ul><ul><ul><li>OMIM: 104760 </li></ul></ul><ul><ul><li>Cromosoma: 21q21 </li></ul></ul><ul><ul><li>Herencia: Autosómica dominante </li></ul></ul>
    81. 88. Mitocondrias <ul><li>Enfermedad de Huntington </li></ul><ul><ul><li>Gen: IT-15 </li></ul></ul><ul><ul><li>Proteína: Proteína Huntingtina </li></ul></ul><ul><ul><li>OMIM: 143100 </li></ul></ul><ul><ul><li>Cromosoma: 4p16.3 </li></ul></ul><ul><ul><li>Herencia: Autosómica dominante </li></ul></ul>
    82. 89. Mitocondrias <ul><li>Enfermedad de Parkinson </li></ul><ul><ul><li>Gen: HTRA2 </li></ul></ul><ul><ul><li>Proteína: PRSS25 </li></ul></ul><ul><ul><li>OMIM: 606441 </li></ul></ul><ul><ul><li>Cromosoma: 2p12 </li></ul></ul><ul><ul><li>Herencia: Esporádica </li></ul></ul>
    83. 90. Mitocondrias <ul><li>Enfermedad de Parkinson </li></ul><ul><ul><li>Gen: LRRK2 </li></ul></ul><ul><ul><li>Proteína: Quinasa de repeticiones ricas en leucina 2 </li></ul></ul><ul><ul><li>OMIM: 609007 </li></ul></ul><ul><ul><li>Cromosoma: 12q12 </li></ul></ul><ul><ul><li>Herencia: Autosómica dominante </li></ul></ul>
    84. 91. Mitocondrias <ul><li>Enfermedad de Parkinson </li></ul><ul><ul><li>Gen: PARK2 </li></ul></ul><ul><ul><li>Proteína: Parkina </li></ul></ul><ul><ul><li>OMIM: 602544 </li></ul></ul><ul><ul><li>Cromosoma: 6q25.2-q27 </li></ul></ul><ul><ul><li>Herencia: Autosómica recesiva </li></ul></ul>
    85. 92. Mitocondrias <ul><li>Enfermedad de Parkinson </li></ul><ul><ul><li>Gen: PARK7 </li></ul></ul><ul><ul><li>Proteína: DJ-1 </li></ul></ul><ul><ul><li>OMIM: 606324 </li></ul></ul><ul><ul><li>Cromosoma: 1p36 </li></ul></ul><ul><ul><li>Herencia: Autosómica recesiva </li></ul></ul>
    86. 93. Mitocondrias <ul><li>Enfermedad de Parkinson </li></ul><ul><ul><li>Gen: PINK1 </li></ul></ul><ul><ul><li>Proteína: Quinasa putativa inducida por PTEN (Fosfatasa y Homólogo de Tensina) </li></ul></ul><ul><ul><li>OMIM: 608309 </li></ul></ul><ul><ul><li>Cromosoma: 1p36 </li></ul></ul><ul><ul><li>Herencia: Autosómica recesiva </li></ul></ul>
    87. 94. Mitocondrias <ul><li>Enfermedad de Parkinson </li></ul><ul><ul><li>Gen: SNCA </li></ul></ul><ul><ul><li>Proteína: α - sinucleína </li></ul></ul><ul><ul><li>OMIM: 163890 </li></ul></ul><ul><ul><li>Cromosoma: 4q21 </li></ul></ul><ul><ul><li>Herencia: Autosómica dominante </li></ul></ul>
    88. 95. Mitocondrias <ul><li>Criterios de Clasificación </li></ul><ul><ul><li>Walker modificados (2002) </li></ul></ul><ul><ul><li>Nijmegen (2002) </li></ul></ul><ul><ul><li>Nonaka (2002) </li></ul></ul><ul><ul><li>Wolfson (1999) </li></ul></ul>
    89. 96. Peroxisomas <ul><li>Detoxificación </li></ul><ul><li>Neuroprotección del H2O2 </li></ul>
    90. 97. Peroxisomas <ul><li>Síndrome de Zellweger </li></ul><ul><li>Adrenoleucodistrofia Neonatal </li></ul><ul><li>Enfermedad de Refsum </li></ul><ul><li>Condrodisplasia punctata rizomélica </li></ul>
    91. 98. Lisosomas <ul><li>Sistema digestivo intracelular </li></ul><ul><li>Enzimas hidrolíticas </li></ul><ul><li>Gránulos amarillos de lipofuscina </li></ul>
    92. 99. Lisosomas <ul><li>Mucopolisacaridosis </li></ul><ul><ul><li>Síndrome de Hurler-Scheie </li></ul></ul><ul><ul><li>Síndrome de Hunter </li></ul></ul><ul><ul><li>Síndrome de Sanfilippo (A-D) </li></ul></ul><ul><ul><li>Síndrome de Morquio (A-B) </li></ul></ul><ul><ul><li>Síndrome de Maroteaux-Lamy </li></ul></ul><ul><ul><li>Síndrome de Sly </li></ul></ul><ul><ul><li>Síndrome de Natowicz </li></ul></ul><ul><ul><li>Síndrome de Austin </li></ul></ul>
    93. 100. Lisosomas <ul><li>Esfingolipidosis </li></ul><ul><ul><li>Enfermedad de Fabry </li></ul></ul><ul><ul><li>Lipogranulomatosis de Farber </li></ul></ul><ul><ul><li>Enfermedad de Gaucher </li></ul></ul><ul><ul><li>Leucodistrofia de Células Globoides (Krabbe) </li></ul></ul><ul><ul><li>Leucodistrofia Metacromática </li></ul></ul><ul><ul><li>Niemann–Pick (A-B) </li></ul></ul><ul><ul><li>Gangliosidosis GM1 </li></ul></ul>
    94. 101. Lisosomas <ul><li>Esfingolipidosis </li></ul><ul><ul><li>Gangliosidosis GM1 </li></ul></ul><ul><ul><li>Gangliosidosis GM2 (Tay–Sachs) </li></ul></ul><ul><ul><li>Gangliosidosis GM3 (Sandhoff) </li></ul></ul>
    95. 102. Lisosomas <ul><li>Oligosacaridosis y glucoproteinosis </li></ul><ul><ul><li>Aspartilglucosaminuria </li></ul></ul><ul><ul><li>Fucosidosis </li></ul></ul><ul><ul><li>α- Mannosidosis </li></ul></ul><ul><ul><li>β- Mannosidosis </li></ul></ul><ul><ul><li>Sialidosis </li></ul></ul><ul><ul><li>Enfermedad de Schindler </li></ul></ul>
    96. 103. Lisosomas <ul><li>Glucogenosis </li></ul><ul><ul><li>Enfermedad de Pompe </li></ul></ul>
    97. 104. Aparato de Golgi <ul><li>Cisternas </li></ul><ul><li>Vesículas </li></ul><ul><li>Túbulos membranosos </li></ul>
    98. 105. Aparato de Golgi <ul><li>Proteínas integrales de membrana plasmática </li></ul><ul><li>Proteínas empacadas en vesículas secretoras liberadas en respuesta a señales </li></ul><ul><li>Enzimas lisosomales </li></ul>
    99. 106. Citoesqueleto <ul><li>Neurotúbulos </li></ul><ul><li>Neurofilamentos </li></ul><ul><li>Microfilamentos de actina </li></ul>
    100. 107. Neurotúbulos <ul><li>Cilindros no ramificados </li></ul><ul><li>Polímeros de tubulina </li></ul><ul><li>Transportan organelas por toda la neurona </li></ul>
    101. 108. Neurofilamentos <ul><li>Sólo en neuronas </li></ul><ul><li>Cilindros no ramificados </li></ul><ul><li>Actina y otras proteínas </li></ul><ul><li>Glia </li></ul><ul><ul><li>Glial fibrillary acidic protein (GFAP) </li></ul></ul>
    102. 109. Citoesqueleto <ul><li>Estructura dinámica </li></ul><ul><li>Fuerza mecánica de movimiento </li></ul><ul><li>Neurotúbulos </li></ul><ul><ul><li>Rieles de tranporte del soma a las terminales axonales </li></ul></ul><ul><li>Alta plasticidad durante desarrollo, crecimiento, regeneración nerviosa </li></ul>
    103. 110. Transporte Axoplásmico <ul><li>Transporte Axonal Anterógrado u Ortógrado </li></ul><ul><ul><li>Del soma hacia las dendritas o el axón </li></ul></ul><ul><li>Transporte Axonal Retrógrado </li></ul><ul><ul><li>De las dendritas y el axón hacia el cuerpo neuronal </li></ul></ul>
    104. 111. Transporte Axoplásmico <ul><li>Rápido </li></ul><ul><ul><li>200 – 400 mm al día </li></ul></ul><ul><ul><li>Anterógrado y retrógrado </li></ul></ul><ul><li>Lento </li></ul><ul><ul><li>1 – 5 mm al día </li></ul></ul><ul><ul><li>Anterógrado </li></ul></ul>
    105. 112. Transporte Axoplásmico <ul><li>Anterógrado Rápido </li></ul><ul><ul><li>Mitocondrias </li></ul></ul><ul><ul><li>Precursores de REL </li></ul></ul><ul><ul><li>Precursores de Vesículas Sinápticas </li></ul></ul><ul><ul><li>Precursores de Membrana Plasmática </li></ul></ul>
    106. 113. Transporte Axoplásmico <ul><li>Retrógrado Rápido </li></ul><ul><ul><li>Mitocondrias </li></ul></ul><ul><ul><li>Cuerpos multivesiculados (degradación) </li></ul></ul><ul><ul><li>Vesículas que contienen ligandos (factores de crecimiento neural) captados por endocitosis </li></ul></ul>
    107. 114. Transporte Axoplásmico <ul><li>Transporte dependiente de Neurotúbulos </li></ul><ul><ul><li>Proteínas generadoras de fuerza motora </li></ul></ul><ul><ul><ul><li>Kinesina </li></ul></ul></ul><ul><ul><ul><li>Dineína </li></ul></ul></ul><ul><ul><ul><li>ATP </li></ul></ul></ul>
    108. 115. Transporte Axoplásmico
    109. 116. Transporte Axoplásmico <ul><li>Un mismo neurotúbulo tiene distintas líneas de movimiento </li></ul><ul><li>Una vesícula puede adelantarse a otra que viaja en otra línea de movimiento </li></ul><ul><li>Dos vesículas pueden viajar en direcciones opuestas en distintas líneas de movimiento </li></ul><ul><li>Las vesículas pueden cambiarse de neurotúbulo </li></ul>
    110. 117. Transporte Axoplásmico <ul><li>Anterógrado Lento </li></ul><ul><ul><li>Enzimas solubles </li></ul></ul><ul><ul><li>Componentes del Citoesqueleto </li></ul></ul><ul><ul><li>Componentes de Membrana Plasmática </li></ul></ul><ul><ul><li>Dinamina ? </li></ul></ul>
    111. 118. Dendritas <ul><li>Mismas organelas que el soma (Cuerpos de Nissl, mitocondrias) </li></ul><ul><li>Recepción de Información </li></ul><ul><li>Espina Dendríticas </li></ul>
    112. 119. Axón <ul><li>Cono axónico </li></ul><ul><li>Segmento Inicial </li></ul><ul><li>< 1 mm a > 1 metro </li></ul><ul><li>No hay cuerpos de Nissl </li></ul><ul><li>Terminal bouton </li></ul><ul><li>Bouton terminaux </li></ul><ul><li>End-foot) </li></ul><ul><li>Boutons en passage </li></ul>
    113. 120. Tipos de Terminaciones
    114. 121. Neurópilo <ul><li>Axones </li></ul><ul><li>Dendritas </li></ul><ul><li>Sinapsis </li></ul><ul><li>Neuroglia </li></ul><ul><li>Sustancia gris </li></ul>
    115. 130. Sinapsis <ul><li>Sherrington </li></ul><ul><li>“ Doctrina de la Neurona” </li></ul><ul><li>Santiago Ramón y Cajal </li></ul><ul><li>“ Teoría Reticular” </li></ul><ul><li>Golgi </li></ul>
    116. 131. Sinapsis <ul><li>Conexión interneuronal </li></ul><ul><li>Hendidura sináptica (200 A) </li></ul><ul><li>De pocas a miles de sinapsis (axón) </li></ul><ul><li>Hasta 15,000 sinapsis (dendritas, neurona) </li></ul>
    117. 132. Sinapsis <ul><li>Membrana Presináptica </li></ul><ul><li>Membrana Postsináptica </li></ul><ul><li>Membrana Subsináptica </li></ul>
    118. 133. Sinapsis
    119. 134. Sinapsis <ul><li>Mecanismo de Transmisión </li></ul><ul><ul><li>Químicas </li></ul></ul><ul><ul><ul><li>Canal iónico y Receptor </li></ul></ul></ul><ul><ul><ul><li>Canal iónico receptor </li></ul></ul></ul><ul><ul><li>Eléctricas </li></ul></ul>
    120. 140. Sinapsis Químicas <ul><li>Neurotransmisores </li></ul><ul><li>Neuromoduladores </li></ul>
    121. 141. Sinapsis Químicas <ul><li>Una Neurona = Un Neurotransmisor </li></ul><ul><li>Neurotransmisor + Co-transmisor </li></ul>
    122. 142. Neurotransmisor <ul><li>Presente en la terminal presináptica </li></ul><ul><li>Liberado en respuesta a la despolarización presináptica, liberación calcio-dependiente </li></ul><ul><li>Receptores específicos en la membrana postsináptica </li></ul>
    123. 143. Neurotransmisor
    124. 144. Neuroglia <ul><li>Células de soporte que rodean las neuronas, dendritas y axones </li></ul><ul><li>Células no exitables </li></ul><ul><li>10-50 : 1 </li></ul><ul><li>Alta actividad metabólica </li></ul><ul><li>Tienen actividad mitótica </li></ul>
    125. 145. Neuroglia
    126. 146. Astrocitos <ul><li>Funcional y morfológicamente heterogéneos </li></ul><ul><li>Rodean a todas la neuronas </li></ul><ul><li>Protoplásmicos (Sustancia Gris) </li></ul><ul><li>Fibrosos (Sustancia Blanca) </li></ul>
    127. 147. Astrocitos <ul><li>Células de Bergmann </li></ul><ul><li>Células de Müller </li></ul><ul><li>Pinealocitos </li></ul><ul><li>Pituicitos </li></ul><ul><li>Tanicitos </li></ul><ul><li>Otros </li></ul><ul><li>Glial fibrillary acidic protein (GFAP) </li></ul>
    128. 148. Astrocitos <ul><li>Sincitio funcional </li></ul><ul><li>Procesos en forma de pies terminales </li></ul><ul><li>Aislan las sinapsis </li></ul><ul><li>Recubren la membrana basal de los capilares </li></ul><ul><li>Forman la barrera pial-glial </li></ul><ul><li>En contacto con células ependimarias en ventrículos </li></ul>
    129. 149. Astrocitos <ul><li>Almacenan y transfieren metabolitos como glucosa que llevan de los capilares a las neuronas </li></ul><ul><li>Eliminan es exceso de K del espacio extracelular </li></ul><ul><li>Eliminan el exceso de glutamato </li></ul><ul><li>Eliminan neurotoxinas </li></ul>
    130. 150. Astrocitos <ul><li>Spatial Buffering </li></ul><ul><li>Spreading Depression </li></ul><ul><li>Neurotrofinas </li></ul>
    131. 151. Astrocitos
    132. 152. Oligodendrocitos <ul><li>Producción de mielina en SNC </li></ul><ul><li>Mantenimiento estructural de mielina </li></ul>
    133. 153. Oligodendrocitos <ul><li>Células satélite perineuronales </li></ul><ul><li>Células interfasciculares </li></ul>
    134. 154. Oligodendrocitos
    135. 155. Oligodendrocitos <ul><li>Mielinización de internodos en hasta 70 axones </li></ul><ul><li>Mayoría de vías centrales no se mielinizan hasta los 2 años </li></ul><ul><li>Remielinización espontánea </li></ul>
    136. 156. Microglia <ul><li>Células microgliales en reposo </li></ul><ul><li>Microglia activada o reactiva no fagocítica </li></ul><ul><li>Microglia fagocítica </li></ul>
    137. 157. Microglia <ul><li>Activada por </li></ul><ul><ul><li>Cuerpos extraños </li></ul></ul><ul><ul><li>Lesión cerebral </li></ul></ul><ul><ul><li>Productos de degradación </li></ul></ul><ul><ul><li>Inflamación </li></ul></ul>
    138. 158. Microglia <ul><li>Sintetizan </li></ul><ul><ul><li>Factores de crecimiento </li></ul></ul><ul><ul><li>Moléculas de adhesión </li></ul></ul><ul><ul><li>Citoquinas </li></ul></ul>
    139. 159. Microglia <ul><li>Interacción inmune SNC-SNP </li></ul><ul><li>Vigilancia inmunológica de cerebro y médula espinal </li></ul>
    140. 160. Epéndimo <ul><li>Canal central de la médula espinal </li></ul><ul><li>Paredes ventriculares </li></ul><ul><li>Junto a los astrocitos forman la barrera LCR-Cerebro </li></ul><ul><li>Tanicitos </li></ul><ul><ul><li>Transporte entre ventrículos y vasos sanguíneos </li></ul></ul>

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