
Neuroscience in Medicine.
Title:
Neuroscience in Medicine.
Author:
Conn, P.Michael.
ISBN:
9781603274555
Personal Author:
Edition:
3rd ed.
Physical Description:
1 online resource (813 pages)
Contents:
145198_1_En_FM_Chapter_OnlinePDF.pdf -- Neuroscience in Medicine -- Preface -- Contents -- Contributors -- List of Color Plates -- 145198_1_En_2_Chapter_OnlinePDF.pdf -- Anatomy of the Spinal Cord and Brain -- 1 Introduction -- 2 Spinal Cord External Anatomy -- 2.1 Spinal Cord Internal Anatomy -- 2.1.1 Spinal Gray Matter Anatomy -- 2.1.2 The Spinal Autonomic Nervous System -- 2.1.3 Spinal Cord Sexual Dimorphism -- 2.2 Blood Supply of the Spinal Cord -- 2.3 Venous Drainage of the Spinal Cord -- 2.4 Meninges of the Spinal Cord -- 3 Brain -- 3.1 Medulla Oblongata -- 3.2 Pons -- 3.3 Midbrain -- 3.4 Cerebellum -- 3.5 Forebrain -- 3.6 Arterial Supply of the Brain -- 3.7 Venous Drainage of the Brain -- 3.8 Ventricular System -- 3.9 Meninges of the Brain -- Selected Readings -- 145198_1_En_3_Chapter_OnlinePDF.pdf -- Ion Channels, Transporters, and Electrical Signaling -- 1. Overview -- 2. Resting Membrane Potentials -- 2.1. Lipid Bilayer Separates Cells from Their Environment -- 2.2. Ion Pumps and Ion Channels Transport Ions in Opposite Directions -- 2.3. Signaling Proteins Other than Channels and Transporters -- 2.4. Ion Concentrations Differ Across the Cell Membrane -- 2.5. Every Neuron Has a Membrane Potential -- 2.6. The Membrane Potential as Cellular Force -- 2.7. Membrane Potential and Ion Movements -- 2.8. Single-Ion Electrochemical Equilibrium -- 2.9. Real Cells Are Not at Equilibrium -- 2.10. Multi-ion Electrochemical Equilibrium -- 3. Electrical Excitability of the Cell Membrane -- 3.1. Excitable Cells Fire Action Potentials -- 3.2. Neurons Also Generate a Variety of Slow Potentials -- 3.3. Action Potential and Ion Movements -- 3.4. How Does the Action Potential Propagate? -- 3.5. Myelin Enhances the Speed of Action Potential -- 3.6. Neurons Do Not Require Energy to Conduct Action Potential.
3.7. Action Potentials Can Have Different Shapes and Functions -- 4. VoltagehypnGated Channels -- 4.1. Gigaseal and Patch-Clamp Methods -- 4.2. Voltage-Gated Na+ Channels Depolarize Cells -- 4.3. Voltage-Gated Calcium Channels Have Dual Functions -- 4.4. Potassium Channels Tend to Reduce Excitation -- 4.5. Cyclic Nucleotide-Modulated Channels Are Nonselective Cation Channels -- 4.6. TRP Ion Channels in the Nervous System -- 4.7. Chloride Channels Also Tend to Reduce Excitation -- 5. Extracellular LigandhypnGated Channels -- 5.1. Nicotinic Acetylcholine and 5-Hydroxytryptamine Receptors Are Cation-Permeable Channels -- 5.2. GABA and Glycine Receptors Are Anion-Permeable Channels -- 5.3. Some Glutamate Channels Are Voltage- and Ligand-Gated -- 5.4. ATP-Gated Channels Are Expressed in Excitable and Nonexcitable Cells -- 6. ENaC/Degenerin Family of Channels -- 7. Intracellular and Intercellular Channels -- 7.1. Voltage-Gated Ca2+ Influx Activates Ryanodine Receptors -- 7.2. IP3 Receptors Are Intracellular Ligand-Gated Channels -- 7.3. Calcium Release Is Coupled to Capacitative Ca2+ Entry -- 7.4. Electrical, Ca2+, and Chemical Coupling by Gap-Junction Channels -- 8. Active Transporters -- 8.1. Na-K-ATPase Has Multiple Functions -- 8.2. Na-Ca Exchanger and Ca-ATPase Control Intracellular Calcium -- 8.3. Several Transporters Maintain Chloride Gradient -- 8.4. Acid-Base Transporters -- 8.5. Other Na+ Gradient-Driven Transporters -- 9. A CrosshypnCommunication Between Electrical and ReceptorhypnMediated Signaling Pathways -- Selected Readings -- 1. Impaired or Blocked Impulse Conduction -- 2. Diseases That Affect Myelin -- 3. MS Has a Distinct Age, Gender, Race, and Geographic Profile -- 4. MS is Characterized by the Presence of Numerous Discrete Areas of Demyelination Throughout the Brain and Spinal Cord.
5. The Symptoms of MS Remit and Reappear in Characteristic Fashion -- 6. The Diagnosis of MS Can be Aided by Imaging Studies and Laboratory Tests -- 7. Immunosuppression Is The Most Common Form of Therapy Used in Ms -- Selected Readings -- 145198_1_En_4_Chapter_OnlinePDF.pdf -- Synaptic Transmission -- Overview -- 1. Properties of Chemical and Electrical Synapses -- 2. A Model Synapse: The Neuromuscular Junction -- 3. Presynaptic Exocytosis is Ca2+ Dependent -- 4. Neurotransmitters and Their Receptors in the Mammalian Brain -- 5. The Interplay of Excitation and Inhibition -- 6. Synapses are Heterogeneous and can be Specialized -- 7. Short-Term and Long-Term Synaptic Plasticity -- Selected Readings -- 145198_1_En_5_Chapter_OnlinePDF.pdf -- Presynaptic and Postsynaptic Receptors -- 1. Receptor Classification Schemes: Anatomic, Pharmacologic, and Structural/Mechanistic -- 2. Receptor Structure and Function -- 2.1. Receptors Can Be Mathematically Characterized Using Biochemical Kinetic Parameters Developed to Understand Enzymes -- 2.2. Receptors Can Be Multisubunit Ion Channels in the Membrane or Single Polypeptides That Modulate an Effector System -- 2.3. Ligand-Gated Ion Channel Receptors -- 2.4. G Protein-Coupled Receptors -- 2.4.1. G Proteins -- 2.4.2. Effector Mechanisms -- 2.4.3. Constitutive Activity and Inverse Agonism -- 2.4.4. Receptor Dynamics: Membrane Trafficking -- 2.5. Nitric Oxide -- 2.6. Receptors as Part of the Effector Pathway -- 3. Neurotransmitters and their Receptors -- 3.1. Cholinergic Receptors Are Found in Both Main Genetic Families of Transmitter Receptors -- 3.1.1. Nicotinic Cholinergic Receptors -- 3.1.2. Muscarinic Cholinergic Receptors -- 3.2. Catecholamine Receptors -- 3.2.1. alpha-Adrenergic Receptors -- 3.2.2. beta-Adrenergic Receptors -- 3.3. Dopamine Receptors -- 3.4. Serotonin Receptors -- 3.5. Histamine Receptors.
3.6. Receptors for Amino Acid Neurotransmitters -- 3.6.1. GABA Receptors -- 3.6.2. Glycine Receptor -- 3.6.3. Glutamate Receptors -- 3.7. Peptide Receptors -- 4. Conclusion -- Suggested Readings -- 145198_1_En_6_Chapter_OnlinePDF.pdf -- Neuroembryology and Neurogenesis -- 1. Introduction -- 2. Embryonic Development or the Nervous System -- 2.1. Early Development of the Neural Tube -- 2.1.1. Proliferation and Differentiation of the Neuroepithelial Cells -- 2.2. Formation of Neural Crest and Migration of Cells -- 2.3. Spinal Cord and Brain Stem -- 2.4. The Primary Brain Vesicles -- 2.5. Myelencephalon and Metencephalon -- 2.6. Mesencephalon -- 2.7. Diencephalon -- 2.8. Telencephalon -- 3. Neurogenesis in the Embryonic Nervous System -- 3.1. The Origin and Formation of Cortical Neurons -- 3.2. Extracellular Molecules for Developing Neurons -- 4. Neuronal Apoptosis in the Developing Nervous System -- 4.1. The Function of Neuronal Apoptosis -- 4.2. Underlying Mechanisms of Regulating Developing Neuronal Apoptosis -- Selected Readings -- Clinical Correlation -- Disorders of Neuronal Migration -- Cortical Neurons in Neuronal Migration Disorders -- Epilepsy as a Symptom of Abnormal Cortical Neuronal Migration -- Kallmann's Syndrome as a Prototype of the Heritable Disorders of Neuronal Migration -- Selected Readings -- 145198_1_En_7_Chapter_OnlinePDF.pdf -- The Vasculature of the Human Brain -- 1. Introduction -- 1.1. Human Vasculature Can Be Visualized In Vivo by Four Different Modalities -- 2. Intracranial Arterial System (TABLE 1) -- 2.1. Anterior (Carotid) Circulation -- 2.1.1. The Internal Carotid Artery (Table 2) -- 2.1.2. The Anterior Cerebral Artery (Table 3) -- 2.1.3. The Middle Cerebral Artery (Table 4) -- 2.1.4. The Posterior Cerebral Artery (Table 5) -- 2.2. Posterior (Vertebrobasilar) Circulation -- 2.2.1. The Vertebral Arteries (Table 6).
2.2.2. The Basilar Artery (Table 7) -- 2.2.3. Leptomeningeal or Pial Vessels -- 2.2.4. Intraparenchymal or Penetrating Arteries -- 2.3. The Structure of Intradural Arteries Is Different from That of Extracranial Arteries -- 2.4. Three Types of Nerve Fibers Have Endings on the Walls of Large Intracranial Arteries -- 2.4.1. Pain-Sensitive Fibers -- 2.4.2. Sympathetic Fibers -- 2.4.3. Parasympathetic Fibers -- 3. Collateral Circulation (TABLE 8) -- 4. Capillaries -- 4.1. The Blood-Brain Barrier Refers to a Complex Array of Physical, Metabolic, and Transport Properties of the Capillary Endothelium -- 4.2. Capillaries at the Circumventricular Organs Are Permeable to Circulating Macromolecules -- 4.3. Immune and Inflammatory Mediators Play an Important Role in a Variety of Pathophysiologic Pathways Such as in Cerebral Ischemia -- 4.3.1. Adhesion Receptors -- 4.3.2. Cytokines -- 4.4. Complement Activation -- 5. Intracranial Venous System (TABLE 9) -- 5.1. The Deep Venous System (Table 10) -- 5.1.1. The Deep Cerebral Venous System Primarily Drains Veins Originating in Midline Structures -- 5.2. Superficial Cerebral Veins (Table 11) -- 5.2.1. Superficial Cerebral Veins Drain into Either the Superior Sagittal Sinus, Transverse Sinuses, or Sigmoid Sinuses -- 5.3. Posterior Fossa (Infratentorial) Veins (Table 12) -- 5.4. Dural Venous Sinuses (Table 13) -- Selected Readings -- Clinical Correlation -- Stroke -- Pathologic Mechanisms of Stroke -- Loss of Energy-Dependent Homeostatic Mechanisms Leads the Neurologic Symptoms That Result from a Stroke -- Normal Homeostatic Mechanisms in the Cerebral Vascular System May Be Lost Because of Cerebral Ischemia -- The Normal Blood Supply to the Brain can be Disrupted by Several Mechanisms -- Transient Ischemic Symptoms Often Precede Cerebral Infarction.
The Neurologic Deficit in Ischemic Stroke Depends on which Blood Vessel is Involved.
Abstract:
This up-to-date edition alternates scientific and clinical chapters that explain the basic science underlying neurological processes and then relates that science to the understanding of neurological disorders and their treatment.
Local Note:
Electronic reproduction. Ann Arbor, Michigan : ProQuest Ebook Central, 2017. Available via World Wide Web. Access may be limited to ProQuest Ebook Central affiliated libraries.
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