1 NEURONS AND THEIR PROPERTIES Anatomical Properties 1.1. Neuronal Structure 1.2. Types of Synapses 1.3. Neuronal Cell Types 1.4. Glial Cell Types 1.5. The Blood-Brain Barrier 1.6. Myelination of CNS and PNS Axons 1.7. Development of Myelination and Axon Ensheathment 1.8. High-Magnification View of a Central Myelin Sheath Neurotransmission 1.9. Chemical Neurotransmission 1.10. Synaptic Morphology Electrical Properties 1.11. Neuronal Resting Potential 1.12. Graded Potentials in Neurons 1.13. Action Potentials 1.14. Propagation of the Action Potential 1.15. Conduction Velocity 1.16. Classification of Peripheral Nerve Fibers by Size and Conduction Velocity 1.17. Electromyography and Conduction Velocity Studies 1.18. Presynaptic and Postsynaptic Inhibition 1.19. Spatial and Temporal Summation 1.20. Normal Electrical Firing Patterns of Cortical Neurons and the Origin and Spread of Seizures 1.21. Electroencephalography ANATOMICAL PROPERTIES 1.1 NEURONAL STRUCTURE Neuronal structure reflects the functional characteristics of the individual neuron. Incoming information is projected to a neuron mainly through axonal terminations on the cell body and dendrites. These synapses are isolated and are protected by astrocytic processes. The dendrites usually make up the greatest surface area of the neuron. Some protrusions from dendritic branches (dendritic spines) are sites of specific axodendritic synapses. Each specific neuronal type has a characteristic dendritic branching pattern called the dendritic tree, or dendritic arborizations. The neuronal cell body varies from a few micrometers (μm) in diameter to more than 100 μm. The neuronal cytoplasm contains extensive rough endoplasmic reticulum (rough ER), reflecting the massive amount of protein synthesis necessary to maintain the neuron and its processes. The Golgi apparatus is involved in packaging potential signal molecules for transport and release. Large numbers of mitochondria are necessary to meet the huge energy demands of neurons, particularly those related to the maintenance of ion pumps and membrane potentials. Each neuron has a single (or occasionally no) axon. The cell body tapers to the axon at the axon hillock, followed by the initial segment of the axon, which contains the Na+ channels, the first site where action potentials are initiated. The axon extends for a variable distance from the cell body (up to 1 m or more). An axon larger than 1 to 2 μm in diameter is insulated by a sheath of myelin provided by oligodendroglia in the central nervous system (CNS) or Schwann cells in the peripheral nervous system (PNS). An axon may branch into more than 500,000 axon terminals, and may terminate in a highly localized and circumscribed zone (e.g., primary somatosensory axon projections used for fine discriminative touch) or may branch to many disparate regions of the brain (e.g., noradrenergic axonal projections of the locus coeruleus). A neuron whose axon terminates at a distance from its cell body and dendritic tree is called a macroneuron or a Golgi type I neuron; a neuron whose axon terminates locally, close to its cell body and dendritic tree, is called a microneuron, a Golgi type II neuron, a local circuit neuron, or an interneuron. There is no typical neuron because each type of neuron has its own specialization. However, pyramidal cells and lower motor neurons are commonly used to portray a so-called typical neuron. CLINICAL POINT Neurons require extraordinary metabolic resources to sustain their functional integrity, particularly that related to the maintenance of membrane potentials for the initiation and propagation of action potentials. Neurons require aerobic metabolism for the generation of adenosine triphosphate (ATP) and have virtually no ATP reserve, so they require continuous delivery of glucose and oxygen, generally in the range of 15% to 20% of the body’s resources, which is a disproportionate consumption of resources. During starvation, when glucose availability is limited, the brain can shift gradually to using beta-hydroxybutyrate and acetoacetate as energy sources for neuronal metabolism; however, this is not an instant process and is not available to buffer acute hypoglycemic episodes. An ischemic episode of even 5 minutes, resulting from a heart attack or an ischemic stroke, can lead to permanent damage in some neuronal populations such as pyramidal cells in the CA1 region of the hippocampus. In cases of longer ischemia, widespread neuronal death can occur. Because neurons are postmitotic cells, except for a small subset of interneurons, dead neurons are not replaced. One additional consequence of the postmitotic state of most neurons is that they are not sources of tumor formation. Brain tumors derive mainly from glial cells, ependymal cells, and meningeal cells. 1.2 TYPES OF SYNAPSES A synapse is a site where an arriving action potential, through excitation-secretion coupling involving Ca2+ influx, triggers the release of one or more neurotransmitters into the synaptic cleft (typically 20 μm across). The neurotransmitter acts on receptors on the target neuronal membrane, altering the membrane potential from its resting state. These postsynaptic potentials are called graded potentials. Most synapses carrying information toward a target neuron terminate as axodendritic or axosomatic synapses. Specialized synapses, such as reciprocal synapses or complex arrays of synaptic interactions, provide specific regulatory control over the excitability of their target neurons. Dendrodendritic synapses aid in the coordinated firing of groups of related neurons such as the phrenic nucleus neurons that cause contraction of the diaphragm. CLINICAL POINT The configurations of the synapses of key neuronal populations in particular regions of the brain and of target cells in the periphery determine the relative influence of that input. At the neuromuscular junction, a sufficient amount of acetylcholine is usually released by an action potential in the motor axon to guarantee that the muscle end plate potential reaches threshold and initiates an action potential. In contrast, the neuronal inputs into reticular formation neurons and many other types of neurons require either temporal or spatial summation to allow the target neuron to reach threshold; this orchestration involves coordinated multisynaptic regulation. In some key neurons such as lower motor neurons (LMNs), input from brain stem upper motor neurons (UMNs) is directed mainly through spinal cord interneurons and requires extensive summation to activate the LMNs; in contrast, direct monosynaptic corticospinal UMNs input into some LMNs, such as those regulating fine finger movements, terminate close to the axon hillock/initial segment; and can directly initiate an action potential in the LMNs. Some complex arrays of synapses among several neuronal elements, such as those seen in structures such as the cerebellum and retina, permit modulation of key neurons by both serial and parallel arrays of connections, providing lateral modulation of neighboring neuronal excitability. 1.3 NEURONAL CELL TYPES Local interneurons and projection neurons demonstrate characteristic size, dendritic arborizations, and axonal projections. In the CNS (denoted by dashed lines), glial cells (astrocytes, microglia, oligodendroglia) provide support, protection, and maintenance of neurons. Schwann cells and satellite cells provide these functions in the PNS. The primary sensory neurons (blue) provide sensory transduction of incoming energy or stimuli into electrical signals that are carried into the CNS. The neuronal outflow from the CNS is motor (red) to skeletal muscle fibers via neuromuscular junctions, or is autonomic preganglionic (red) to autonomic ganglia, whose neurons innervate cardiac muscle, smooth muscle, secretory glands, metabolic cells, or cells of the immune system. Neurons other than primary sensory neurons, LMNs, and preganglionic autonomic neurons are located in the CNS in the brain (enclosed by upper dashed lines) or spinal cord (enclosed by lower dashed lines). CLINICAL POINT Neuronal form and configuration provide evidence of the role of that particular type of neuron. Dorsal root ganglion cells have virtually no synapses on the cell body; the sensory receptor is contiguous with the initial segment of the axon to permit direct activation of the initial segment upon reaching a threshold stimulus. This arrangement provides virtually no opportunity for centrifugal control of the initial sensory input; rather, control and analysis of the sensory input occurs in the CNS. Purkinje neurons in the cerebellum have huge planar dendritic trees, with activation occurring via hundreds of parallel fibers and the background excitability influenced by climbing fiber control. This type of array allows network modulation of Purkinje cell output to UMNs, a control mechanism that permits fine-grained, ongoing adjustments to smooth and coordinated motor activities. Small interneurons in many regions have local and specialized functions that have local circuit connections, whereas large isodendritic neurons of the reticular formation receive widespread, polymodal, nonlocal input, which is important for general arousal of the cerebral cortex and consciousness. Damage to these key neurons may result in coma. LMNs and preganglionic autonomic neurons receive tremendous convergence upon their dendrites and cell bodies to orchestrate the final pattern of activation of these final common pathway neurons through which the peripheral effector tissues are signaled and through which all behavior is achieved. 1.4 GLIAL CELL TYPES Astrocytes provide structural isolation of neurons and their synapses and provide ionic (K+) sequestration, trophic support, and support for growth and signaling functions to neurons. Oligodendroglia provide myelination of axons in the CNS. Microglia are scavenger cells that participate in phagocytosis, inflammatory responses, cytokine and growth factor secretion, and some immune reactivity in the CNS. Perivascular cells participate in similar activities at sites near the blood vessels. Schwann cells provide myelination, ensheathment, trophic support, and actions that contribute to the growth and repair of peripheral neurons. Activated T lymphocytes normally can enter and traverse the CNS for immune surveillance for a period of approximately 24 hours. 1.5 THE BLOOD-BRAIN BARRIER The blood-brain barrier (BBB) is the cellular interface between the blood and the CNS. It serves to protect the brain from unwanted intrusion by many large molecules and potentially toxic substances and to maintain the interstitial fluid environment to ensure optimal functioning of the neurons and their associated glial cells. The major cellular basis for the BBB consists of the capillary endothelial cells which have an elaborate network of tight junctions; these tight junctions restrict access by many large molecules, including many drugs, to the CNS. Endothelial cells in the CNS also exhibit a low level of pinocytotic activity across the cell, providing selected specific carrier systems for the transport of essential substrates of energy production and amino acid metabolism into the CNS. Astrocytic endfoot processes abut the endothelial cells and their basement membranes; these processes help to transfer important metabolites from the blood to neurons and can influence the expression of some specific gene products in the endothelial cells. These astrocytic processes also can remove excess K+ and some neurotransmitters from the interstitial fluid. CLINICAL POINT Only gold members can continue reading. Log In or Register to continue Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window) Related Related posts: SPINAL CORD VENTRICLES AND THE CEREBROSPINAL FLUID SPINAL CORD VASCULATURE DEVELOPMENTAL NEUROSCIENCE SENSORY SYSTEMS Stay updated, free articles. Join our Telegram channel Join Tags: Netters Atlas of Neuroscience with STUDENT CONSULT Online Access Jun 4, 2016 | Posted by admin in NEUROLOGY | Comments Off on NEURONS AND THEIR PROPERTIES Full access? Get Clinical Tree
1 NEURONS AND THEIR PROPERTIES Anatomical Properties 1.1. Neuronal Structure 1.2. Types of Synapses 1.3. Neuronal Cell Types 1.4. Glial Cell Types 1.5. The Blood-Brain Barrier 1.6. Myelination of CNS and PNS Axons 1.7. Development of Myelination and Axon Ensheathment 1.8. High-Magnification View of a Central Myelin Sheath Neurotransmission 1.9. Chemical Neurotransmission 1.10. Synaptic Morphology Electrical Properties 1.11. Neuronal Resting Potential 1.12. Graded Potentials in Neurons 1.13. Action Potentials 1.14. Propagation of the Action Potential 1.15. Conduction Velocity 1.16. Classification of Peripheral Nerve Fibers by Size and Conduction Velocity 1.17. Electromyography and Conduction Velocity Studies 1.18. Presynaptic and Postsynaptic Inhibition 1.19. Spatial and Temporal Summation 1.20. Normal Electrical Firing Patterns of Cortical Neurons and the Origin and Spread of Seizures 1.21. Electroencephalography ANATOMICAL PROPERTIES 1.1 NEURONAL STRUCTURE Neuronal structure reflects the functional characteristics of the individual neuron. Incoming information is projected to a neuron mainly through axonal terminations on the cell body and dendrites. These synapses are isolated and are protected by astrocytic processes. The dendrites usually make up the greatest surface area of the neuron. Some protrusions from dendritic branches (dendritic spines) are sites of specific axodendritic synapses. Each specific neuronal type has a characteristic dendritic branching pattern called the dendritic tree, or dendritic arborizations. The neuronal cell body varies from a few micrometers (μm) in diameter to more than 100 μm. The neuronal cytoplasm contains extensive rough endoplasmic reticulum (rough ER), reflecting the massive amount of protein synthesis necessary to maintain the neuron and its processes. The Golgi apparatus is involved in packaging potential signal molecules for transport and release. Large numbers of mitochondria are necessary to meet the huge energy demands of neurons, particularly those related to the maintenance of ion pumps and membrane potentials. Each neuron has a single (or occasionally no) axon. The cell body tapers to the axon at the axon hillock, followed by the initial segment of the axon, which contains the Na+ channels, the first site where action potentials are initiated. The axon extends for a variable distance from the cell body (up to 1 m or more). An axon larger than 1 to 2 μm in diameter is insulated by a sheath of myelin provided by oligodendroglia in the central nervous system (CNS) or Schwann cells in the peripheral nervous system (PNS). An axon may branch into more than 500,000 axon terminals, and may terminate in a highly localized and circumscribed zone (e.g., primary somatosensory axon projections used for fine discriminative touch) or may branch to many disparate regions of the brain (e.g., noradrenergic axonal projections of the locus coeruleus). A neuron whose axon terminates at a distance from its cell body and dendritic tree is called a macroneuron or a Golgi type I neuron; a neuron whose axon terminates locally, close to its cell body and dendritic tree, is called a microneuron, a Golgi type II neuron, a local circuit neuron, or an interneuron. There is no typical neuron because each type of neuron has its own specialization. However, pyramidal cells and lower motor neurons are commonly used to portray a so-called typical neuron. CLINICAL POINT Neurons require extraordinary metabolic resources to sustain their functional integrity, particularly that related to the maintenance of membrane potentials for the initiation and propagation of action potentials. Neurons require aerobic metabolism for the generation of adenosine triphosphate (ATP) and have virtually no ATP reserve, so they require continuous delivery of glucose and oxygen, generally in the range of 15% to 20% of the body’s resources, which is a disproportionate consumption of resources. During starvation, when glucose availability is limited, the brain can shift gradually to using beta-hydroxybutyrate and acetoacetate as energy sources for neuronal metabolism; however, this is not an instant process and is not available to buffer acute hypoglycemic episodes. An ischemic episode of even 5 minutes, resulting from a heart attack or an ischemic stroke, can lead to permanent damage in some neuronal populations such as pyramidal cells in the CA1 region of the hippocampus. In cases of longer ischemia, widespread neuronal death can occur. Because neurons are postmitotic cells, except for a small subset of interneurons, dead neurons are not replaced. One additional consequence of the postmitotic state of most neurons is that they are not sources of tumor formation. Brain tumors derive mainly from glial cells, ependymal cells, and meningeal cells. 1.2 TYPES OF SYNAPSES A synapse is a site where an arriving action potential, through excitation-secretion coupling involving Ca2+ influx, triggers the release of one or more neurotransmitters into the synaptic cleft (typically 20 μm across). The neurotransmitter acts on receptors on the target neuronal membrane, altering the membrane potential from its resting state. These postsynaptic potentials are called graded potentials. Most synapses carrying information toward a target neuron terminate as axodendritic or axosomatic synapses. Specialized synapses, such as reciprocal synapses or complex arrays of synaptic interactions, provide specific regulatory control over the excitability of their target neurons. Dendrodendritic synapses aid in the coordinated firing of groups of related neurons such as the phrenic nucleus neurons that cause contraction of the diaphragm. CLINICAL POINT The configurations of the synapses of key neuronal populations in particular regions of the brain and of target cells in the periphery determine the relative influence of that input. At the neuromuscular junction, a sufficient amount of acetylcholine is usually released by an action potential in the motor axon to guarantee that the muscle end plate potential reaches threshold and initiates an action potential. In contrast, the neuronal inputs into reticular formation neurons and many other types of neurons require either temporal or spatial summation to allow the target neuron to reach threshold; this orchestration involves coordinated multisynaptic regulation. In some key neurons such as lower motor neurons (LMNs), input from brain stem upper motor neurons (UMNs) is directed mainly through spinal cord interneurons and requires extensive summation to activate the LMNs; in contrast, direct monosynaptic corticospinal UMNs input into some LMNs, such as those regulating fine finger movements, terminate close to the axon hillock/initial segment; and can directly initiate an action potential in the LMNs. Some complex arrays of synapses among several neuronal elements, such as those seen in structures such as the cerebellum and retina, permit modulation of key neurons by both serial and parallel arrays of connections, providing lateral modulation of neighboring neuronal excitability. 1.3 NEURONAL CELL TYPES Local interneurons and projection neurons demonstrate characteristic size, dendritic arborizations, and axonal projections. In the CNS (denoted by dashed lines), glial cells (astrocytes, microglia, oligodendroglia) provide support, protection, and maintenance of neurons. Schwann cells and satellite cells provide these functions in the PNS. The primary sensory neurons (blue) provide sensory transduction of incoming energy or stimuli into electrical signals that are carried into the CNS. The neuronal outflow from the CNS is motor (red) to skeletal muscle fibers via neuromuscular junctions, or is autonomic preganglionic (red) to autonomic ganglia, whose neurons innervate cardiac muscle, smooth muscle, secretory glands, metabolic cells, or cells of the immune system. Neurons other than primary sensory neurons, LMNs, and preganglionic autonomic neurons are located in the CNS in the brain (enclosed by upper dashed lines) or spinal cord (enclosed by lower dashed lines). CLINICAL POINT Neuronal form and configuration provide evidence of the role of that particular type of neuron. Dorsal root ganglion cells have virtually no synapses on the cell body; the sensory receptor is contiguous with the initial segment of the axon to permit direct activation of the initial segment upon reaching a threshold stimulus. This arrangement provides virtually no opportunity for centrifugal control of the initial sensory input; rather, control and analysis of the sensory input occurs in the CNS. Purkinje neurons in the cerebellum have huge planar dendritic trees, with activation occurring via hundreds of parallel fibers and the background excitability influenced by climbing fiber control. This type of array allows network modulation of Purkinje cell output to UMNs, a control mechanism that permits fine-grained, ongoing adjustments to smooth and coordinated motor activities. Small interneurons in many regions have local and specialized functions that have local circuit connections, whereas large isodendritic neurons of the reticular formation receive widespread, polymodal, nonlocal input, which is important for general arousal of the cerebral cortex and consciousness. Damage to these key neurons may result in coma. LMNs and preganglionic autonomic neurons receive tremendous convergence upon their dendrites and cell bodies to orchestrate the final pattern of activation of these final common pathway neurons through which the peripheral effector tissues are signaled and through which all behavior is achieved. 1.4 GLIAL CELL TYPES Astrocytes provide structural isolation of neurons and their synapses and provide ionic (K+) sequestration, trophic support, and support for growth and signaling functions to neurons. Oligodendroglia provide myelination of axons in the CNS. Microglia are scavenger cells that participate in phagocytosis, inflammatory responses, cytokine and growth factor secretion, and some immune reactivity in the CNS. Perivascular cells participate in similar activities at sites near the blood vessels. Schwann cells provide myelination, ensheathment, trophic support, and actions that contribute to the growth and repair of peripheral neurons. Activated T lymphocytes normally can enter and traverse the CNS for immune surveillance for a period of approximately 24 hours. 1.5 THE BLOOD-BRAIN BARRIER The blood-brain barrier (BBB) is the cellular interface between the blood and the CNS. It serves to protect the brain from unwanted intrusion by many large molecules and potentially toxic substances and to maintain the interstitial fluid environment to ensure optimal functioning of the neurons and their associated glial cells. The major cellular basis for the BBB consists of the capillary endothelial cells which have an elaborate network of tight junctions; these tight junctions restrict access by many large molecules, including many drugs, to the CNS. Endothelial cells in the CNS also exhibit a low level of pinocytotic activity across the cell, providing selected specific carrier systems for the transport of essential substrates of energy production and amino acid metabolism into the CNS. Astrocytic endfoot processes abut the endothelial cells and their basement membranes; these processes help to transfer important metabolites from the blood to neurons and can influence the expression of some specific gene products in the endothelial cells. These astrocytic processes also can remove excess K+ and some neurotransmitters from the interstitial fluid. CLINICAL POINT Only gold members can continue reading. Log In or Register to continue Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window) Related Related posts: SPINAL CORD VENTRICLES AND THE CEREBROSPINAL FLUID SPINAL CORD VASCULATURE DEVELOPMENTAL NEUROSCIENCE SENSORY SYSTEMS Stay updated, free articles. Join our Telegram channel Join Tags: Netters Atlas of Neuroscience with STUDENT CONSULT Online Access Jun 4, 2016 | Posted by admin in NEUROLOGY | Comments Off on NEURONS AND THEIR PROPERTIES Full access? Get Clinical Tree
