Academic literature on the topic 'Afferent pathways – Diseases'
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Journal articles on the topic "Afferent pathways – Diseases"
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Mazzone, Stuart B., and Bradley J. Undem. "Vagal Afferent Innervation of the Airways in Health and Disease." Physiological Reviews 96, no. 3 (July 2016): 975–1024. http://dx.doi.org/10.1152/physrev.00039.2015.
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Vagal sensory neurons constitute the major afferent supply to the airways and lungs. Subsets of afferents are defined by their embryological origin, molecular profile, neurochemistry, functionality, and anatomical organization, and collectively these nerves are essential for the regulation of respiratory physiology and pulmonary defense through local responses and centrally mediated neural pathways. Mechanical and chemical activation of airway afferents depends on a myriad of ionic and receptor-mediated signaling, much of which has yet to be fully explored. Alterations in the sensitivity and neurochemical phenotype of vagal afferent nerves and/or the neural pathways that they innervate occur in a wide variety of pulmonary diseases, and as such, understanding the mechanisms of vagal sensory function and dysfunction may reveal novel therapeutic targets. In this comprehensive review we discuss historical and state-of-the-art concepts in airway sensory neurobiology and explore mechanisms underlying how vagal sensory pathways become dysfunctional in pathological conditions.
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Canning, Brendan J. "Reflex regulation of airway smooth muscle tone." Journal of Applied Physiology 101, no. 3 (September 2006): 971–85. http://dx.doi.org/10.1152/japplphysiol.00313.2006.
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Autonomic nerves in most mammalian species mediate both contractions and relaxations of airway smooth muscle. Cholinergic-parasympathetic nerves mediate contractions, whereas adrenergic-sympathetic and/or noncholinergic parasympathetic nerves mediate relaxations. Sympathetic-adrenergic innervation of human airway smooth muscle is sparse or nonexistent based on histological analyses and plays little or no role in regulating airway caliber. Rather, in humans and in many other species, postganglionic noncholinergic parasympathetic nerves provide the only relaxant innervation of airway smooth muscle. These noncholinergic nerves are anatomically and physiologically distinct from the postganglionic cholinergic parasympathetic nerves and differentially regulated by reflexes. Although bronchopulmonary vagal afferent nerves provide the primary afferent input regulating airway autonomic nerve activity, extrapulmonary afferent nerves, both vagal and nonvagal, can also reflexively regulate autonomic tone in airway smooth muscle. Reflexes result in either an enhanced activity in one or more of the autonomic efferent pathways, or a withdrawal of baseline cholinergic tone. These parallel excitatory and inhibitory afferent and efferent pathways add complexity to autonomic control of airway caliber. Dysfunction or dysregulation of these afferent and efferent nerves likely contributes to the pathogenesis of obstructive airways diseases and may account for the pulmonary symptoms associated with extrapulmonary disorders, including gastroesophageal reflux disease, cardiovascular disease, and rhinosinusitis.
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Korneva, E. A. "Pathways of neuro-immune communication: past and present time, clinical application." Medical Immunology (Russia) 22, no. 3 (May 21, 2020): 405–18. http://dx.doi.org/10.15789/1563-0625-pon-1974.
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Fundamental studies in neuroimmunophysiology are the keystone for development of new therapeutic approaches to the treatment of infectious, allergic, oncologic and autoimmune diseases. The achievements in this field allowed approving new treatment methods based on irritation of afferent and efferent fibers of autonomic nerves. That became possible due to numerous studies of pathways between the immune and nervous systems performed over last two decades. The milestones in the history of neuroimmune communication research are represented here. The immune system organs – bone marrow, thymus and spleen are coupled to central nervous system (CNS) via sympathetic nerves. Information about LPS and bacteria emergence in peritoneum, intestine and parenchymal organs reaches the brain via parasympathetic pathways. After vagotomy, the brain neurons do not respond to this kind of antigens. The pattern of brain responses to different applied antigens (the EEG changes and the quantity of c-Fos-positive neurons) is specific for definite antigen, like as algorithms of electroneurogram after exposure to different cytokines. Activation of parasympathetic nerves causes the inhibition of inflammation. The entry of any antigens into the body initiates production of cytokines (IL-1, TNFα, IL-6, IFNγ etc.), via specific receptors which are present on peripheral neurons and terminals of vagus nerve, i.e. the vagal afferent terminals and neurons respond to cytokine action, and these signals are transmitted to CNS neurons. The afferent vagal fibers end on the dorsal vagal complex neurons in the caudal part of medulla oblongata. The information about bacterial antigens, LPS and inflammation is transmitted to the brain via afferent autonomic neural pathways. The speed of this process is high and significantly depends on the rates of cytokine production that are transmitters of signals upon the antigen exposure. It is important to emphasize that this events occur within minutes, and the response to the received information proceeds by reflex mechanisms, i.e., within fraction of a second, as exemplified by inflammation (“inflammation reflex”). This is a fundamentally new and revolutionary discovery in the functional studies of immune system regulation. Clinical efficiency of n. vagus stimulation by pulsed ultrasound was shown, being used for the treatment of inflammatory, allergic and autoimmune diseases, e.g., multiple sclerosis, rheumatoid arthritis, renal inflammatory diseases. Electrical stimulation of the vagus nerve reduces the death of animals in septic shock by 80%. The mentioned data have made a revolution in understanding the functional arrangement of immune system in the body. A hypothesis is represented, which suggests how the information on the antigen exposure is transmitted to the brain.
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Burke, Melissa L., Michael de Veer, Jill Pleasance, Melanie Neeland, Martin Elhay, Paul Harrison, and Els Meeusen. "Innate immune pathways in afferent lymph following vaccination with poly(I:C)-containing liposomes." Innate Immunity 20, no. 5 (September 17, 2013): 501–10. http://dx.doi.org/10.1177/1753425913501213.
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Vibert, D., R. Häusler, and A. B. Safran. "Subjective visual vertical in peripheral unilateral vestibular diseases*." Journal of Vestibular Research 9, no. 2 (April 1, 1999): 145–52. http://dx.doi.org/10.3233/ves-1999-9209.
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In humans, the perception of vertical is provided by input from various sensorineural organs and pathways: vision, eye-movements, and proprioceptive and vestibular cues, particularly from the otolithic organs and graviceptive pathways. Well known in several types of brainstem lesions, subjective visual vertical (SVV) abnormalities may also be observed after peripheral vestibular lesions, such as surgical deafferentation, with a deviation directed toward the operated ear. Subjective visual vertical abnormalities are presumably related to a lesion of the otolithic organs and/or to changes in the afferent graviceptive pathways. The goal of this prospective study was to measure the SVV and to define the influence of the otolithic organs in patients suffering from various types of peripheral vestibular diseases: unilateral sudden cochleo-vestibular loss, so-called “viral labyrinthitis” (VL), sudden idiopathic unilateral peripheral vestibular loss, so-called “vestibular neuritis” (Ne). Data were compared with findings after unilateral surgical deafferentations such as vestibular neurectomy (VN) and labyrinthectomy (Lab). Subjective visual vertical was measured with a binocular test (vertical frame) and a monocular test (Maddox rod). In all patients, after VN and Lab, the SVV showed a 10 – 30 ∘ tilt with the vertical frame (N: 0 ± 2 ∘ ), 5 – 15 ∘ with the Maddox rod (N: 0 ± 4 ∘ ). With the vertical frame, SVV was tilted > 2 ∘ in VL (47%) VL (41%) Our results demonstrate that SVV is frequently tilted in acute peripheral vestibulopathies such as VL and Ne. These findings suggest that otolithic function is implicated in the deficit depending on the extent and/or the localisation of the peripheral vestibular lesion.
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Noh, Mi, Hee-Seong Jang, Jinu Kim, and Babu Padanilam. "Renal Sympathetic Nerve-Derived Signaling in Acute and Chronic Kidney Diseases." International Journal of Molecular Sciences 21, no. 5 (February 28, 2020): 1647. http://dx.doi.org/10.3390/ijms21051647.
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The kidney is innervated by afferent sensory and efferent sympathetic nerve fibers. Norepinephrine (NE) is the primary neurotransmitter for post-ganglionic sympathetic adrenergic nerves, and its signaling, regulated through adrenergic receptors (AR), modulates renal function and pathophysiology under disease conditions. Renal sympathetic overactivity and increased NE level are commonly seen in chronic kidney disease (CKD) and are critical factors in the progression of renal disease. Blockade of sympathetic nerve-derived signaling by renal denervation or AR blockade in clinical and experimental studies demonstrates that renal nerves and its downstream signaling contribute to progression of acute kidney injury (AKI) to CKD and fibrogenesis. This review summarizes our current knowledge of the role of renal sympathetic nerve and adrenergic receptors in AKI, AKI to CKD transition and CKDand provides new insights into the therapeutic potential of intervening in its signaling pathways.
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Baj, Andreina, Michela Bistoletti, Annalisa Bosi, Elisabetta Moro, Cristina Giaroni, and Francesca Crema. "Marine Toxins and Nociception: Potential Therapeutic Use in the Treatment of Visceral Pain Associated with Gastrointestinal Disorders." Toxins 11, no. 8 (July 31, 2019): 449. http://dx.doi.org/10.3390/toxins11080449.
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Visceral pain, of which the pathogenic basis is currently largely unknown, is a hallmark symptom of both functional disorders, such as irritable bowel syndrome, and inflammatory bowel disease. Intrinsic sensory neurons in the enteric nervous system and afferent sensory neurons of the dorsal root ganglia, connecting with the central nervous system, represent the primary neuronal pathways transducing gut visceral pain. Current pharmacological therapies have several limitations, owing to their partial efficacy and the generation of severe adverse effects. Numerous cellular targets of visceral nociception have been recognized, including, among others, channels (i.e., voltage-gated sodium channels, VGSCs, voltage-gated calcium channels, VGCCs, Transient Receptor Potential, TRP, and Acid-sensing ion channels, ASICs) and neurotransmitter pathways (i.e., GABAergic pathways), which represent attractive targets for the discovery of novel drugs. Natural biologically active compounds, such as marine toxins, able to bind with high affinity and selectivity to different visceral pain molecular mediators, may represent a useful tool (1) to improve our knowledge of the physiological and pathological relevance of each nociceptive target, and (2) to discover therapeutically valuable molecules. In this review we report the most recent literature describing the effects of marine toxin on gastrointestinal visceral pain pathways and the possible clinical implications in the treatment of chronic pain associated with gut diseases.
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Guilloteau, P., V. Le Meuth-Metzinger, J. Morisset, and R. Zabielski. "Gastrin, cholecystokinin and gastrointestinal tract functions in mammals." Nutrition Research Reviews 19, no. 2 (December 2006): 254–83. http://dx.doi.org/10.1017/s0954422407334082.
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The aim of the present review is to synthesise and summarise our recent knowledge on the involvement of cholecystokinin (CCK) and gastrin peptides and their receptors in the control of digestive functions and more generally their role in the field of nutrition in mammals. First, we examined the release of these peptides from the gut, focusing on their molecular forms, the factors regulating their release and the signalling pathways mediating their effects. Second, general physiological effects of CCK and gastrin peptides are described with regard to their specific receptors and the role of CCK on vagal mucosal afferent nerve activities. Local effects of CCK and gastrin in the gut are also reported, including gut development, gastrointestinal motility and control of pancreatic functions through vagal afferent pathways, including NO. Third, some examples of the intervention of the CCK and gastrin peptides are exposed in diseases, taking into account intervention of the classical receptor subtypes (CCK1and CCK2receptors) and their heterodimerisation as well as CCK-C receptor subtype. Finally, applications and future challenges are suggested in the nutritional field (performances) and in therapy with regards to the molecular forms or in relation with the type of receptor as well as new techniques to be utilised in detection or in therapy of disease. In conclusion, the present review underlines recent developments in this field: CCK and gastrin peptides and their receptors are the key factor of nutritional aspects; a better understanding of the mechanisms involved may increase the efficiency of the nutritional functions and the treatment of abnormalities under pathological conditions.
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Vits, Sabine, Elvir Cesko, Paul Enck, Uwe Hillen, Dirk Schadendorf, and Manfred Schedlowski. "Behavioural conditioning as the mediator of placebo responses in the immune system." Philosophical Transactions of the Royal Society B: Biological Sciences 366, no. 1572 (June 27, 2011): 1799–807. http://dx.doi.org/10.1098/rstb.2010.0392.
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Current placebo research postulates that conditioning processes are one of the major mechanisms of the placebo response. Behaviourally conditioned changes in peripheral immune functions have been demonstrated in experimental animals, healthy subjects and patients. The physiological mechanisms responsible for this ‘learned immune response’ are not yet fully understood, but some relevant afferent and efferent pathways in the communication between the brain and the peripheral immune system have been identified. In addition, possible benefits and applicability in clinical settings have been demonstrated where behaviourally conditioned immunosuppression attenuated the exacerbation of autoimmune diseases, prolonged allograft survival and affected allergic responses. Here, we summarize data describing the mechanisms and the potential clinical benefit of behaviourally conditioned immune functions, with particular focus on learned placebo effects on allergic reactions.
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Gaier, E. D., R. M. Rodriguiz, J. Zhou, M. Ralle, W. C. Wetsel, B. A. Eipper, and R. E. Mains. "In vivo and in vitro analyses of amygdalar function reveal a role for copper." Journal of Neurophysiology 111, no. 10 (May 15, 2014): 1927–39. http://dx.doi.org/10.1152/jn.00631.2013.
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Mice with a single copy of the peptide amidating monooxygenase ( Pam) gene (PAM+/−) are impaired in contextual and cued fear conditioning. These abnormalities coincide with deficient long-term potentiation (LTP) at excitatory thalamic afferent synapses onto pyramidal neurons in the lateral amygdala. Slice recordings from PAM+/− mice identified an increase in GABAergic tone (Gaier ED, Rodriguiz RM, Ma XM, Sivaramakrishnan S, Bousquet-Moore D, Wetsel WC, Eipper BA, Mains RE. J Neurosci 30: 13656–13669, 2010). Biochemical data indicate a tissue-specific deficit in Cu content in the amygdala; amygdalar expression of Atox-1 and Atp7a, essential for transport of Cu into the secretory pathway, is reduced in PAM+/− mice. When PAM+/− mice were fed a diet supplemented with Cu, the impairments in fear conditioning were reversed, and LTP was normalized in amygdala slice recordings. A role for endogenous Cu in amygdalar LTP was established by the inhibitory effect of a brief incubation of wild-type slices with bathocuproine disulfonate, a highly selective, cell-impermeant Cu chelator. Interestingly, bath-applied CuSO4 had no effect on excitatory currents but reversibly potentiated the disynaptic inhibitory current. Bath-applied CuSO4 was sufficient to potentiate wild-type amygdala afferent synapses. The ability of dietary Cu to affect signaling in pathways that govern fear-based behaviors supports an essential physiological role for Cu in amygdalar function at both the synaptic and behavioral levels. This work is relevant to neurological and psychiatric disorders in which disturbed Cu homeostasis could contribute to altered synaptic transmission, including Wilson's, Menkes, Alzheimer's, and prion-related diseases.
Dissertations / Theses on the topic "Afferent pathways – Diseases"
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McMahon, Catherine. "The mechanisms underlying normal spike activity of the primary afferent synapse in the cochlea and its dysfunction : an investigation of the possible mechanisms of peripheral tinnitus and auditory neuropathy." University of Western Australia. School of Biomedical and Chemical Sciences, 2004. http://theses.library.uwa.edu.au/adt-WU2003.0034.
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[Truncated abstract] One of the problems in researching tinnitus is that it has often been assumed that the physiological mechanisms underlying the tinnitus percept cannot be objectively measured. Nonetheless, it is generally accepted that the percept results from altered spontaneous neural activity at some site along the auditory pathway, although it is still debated whether it is produced by: synchronisation of activity of adjacent neurones; a change in the temporal pattern of activity of individual neurones; or an increase in the spontaneous firing rate per se. Similarly, it is possible that the recently coined “auditory neuropathy” is produced by under-firing of the primary afferent synapse, although several other mechanisms can also produce the symptoms described by this disorder (normal cochlear mechanical function but absent, or abnormal, synchronous neural firing arising from the cochlea and auditory brainstem, known as the auditory brainstem response, or ABR). Despite an absent ABR, some subjects can detect pure tones at near-normal levels, although their ability to integrate complex sounds, such as speech, is severely degraded in comparison with the pure-tone audiogram. The aim of the following study was to investigate the normal mechanisms underlying neural firing at the primary afferent synapse, and its regulation, to determine the possible mechanisms underlying over-firing (tinnitus) or under-firing (auditory neuropathy) of primary afferent neurones.
Books on the topic "Afferent pathways – Diseases"
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Falk Symposium (103 1997 Freiburg, Germany). Liver and nervous system: Proceedings of the Falk Symposium 103 (Part III of the Liver Week in Freiburg 1997) held in Freiburg, Germany, October 4-5, 1997. Dordrecht: Kluwer Academic Publishers, 1998.
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1951-, Häussinger D., and Jungermann Kurt, eds. Liver and nervous system: Proceedings of the Falk Symposium 103 (Part III of the Liver Week in Freiburg 1997) held in Freiburg, Germany, October 4-5, 1997. Dordrecht: Kluwer Academic, 1998.
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George, N. J. R. 1946- and Gosling J. A. 1939-, eds. Sensory disorders of the bladder and urethra. Berlin: Springer-Verlag, 1986.
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Goode, Jamie A., and Gregory R. Bock. Growth Factors As Drugs for Neurological and Sensory Disorders. Wiley & Sons, Incorporated, John, 2008.
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Kennard, Christopher. Ocular motor disorders. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0274.
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This chapter discusses motor disorders of the eye. The first part of the chapter describes the proper examination of eye movements to facilitate identification of ocular motor disorder pathology. The effects of nerve palsies on ocular motor function are then described.Eye movement disorders can also have their cause in the central nervous system; both the brainstem, and cerebellum have been implicated as causal factors in some eye movement disorders. Disorders of the pupil, which affect the pupillary light reflex, can be caused by lesions to central, afferent and efferent pupillary pathways as well as sympathetic pathways lesions.Finally, this chapter describes diseases of the eye orbits, including dysthyroid eye disease, idiopathic orbital inflammation, orbital tumours, vascular disorders and orbital infections.
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Gregory, Bock, and Goode Jamie, eds. Growth factors as drugs for neurological and sensory disorders. Chichester: Wiley, 1996.
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Growth Factors as Drugs for Neurological and Sensory Disorders - Symposium No. 196. John Wiley & Sons, 1996.
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Price, Chane, Zahid Huq, Eellan Sivanesan, and Constantine Sarantopoulos. Pain Pathways and Pain Physiology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190457006.003.0001.
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Pain is a multidimensional sensory experience that is mediated by complex peripheral and central neuroanatomical pathways and mechanisms. Typically, noxious stimuli activate specific peripheral nerve terminals onto Aδ and C nerve fibers that convey pain and generate signals that are relayed and processed in the spinal cord and then conveyed via the spinothalamic tracts to the contralateral thalamus and from there to the brain. Acute pain is self-limited and resolves with the healing process, but conditions of extensive injury or inflammation sensitize the pain pathways and generate aberrant, augmented responses. Peripheral and central sensitization of neurons (as a result of spatially and temporally excessive inflammation or intense afferent signal traffic) may result in hyperexcitability and chronicity of pain, with spontaneous pain and abnormal evoked responses to stimuli (allodynia, hyperalgesia). Finally, neuropathic pain follows injury or disease to nerves as a result of hyperexcitability augmented by various sensitizing mechanisms.
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Mason, Peggy. Somatosensation. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0017.
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Under normal circumstances, the somatosensory system contributes more to shaping movements than to perception. Yet damage to the somatosensory system can result in spontaneous pain and other abnormal somatic perceptions. An exploration of the mechanisms and pathways involved in touch perception is slanted toward understanding the contribution of the dorsal column–medial lemniscus pathway to the generation of paresthesia and dysesthesia. Peripheral somatosensory afferents that contribute to the perception of sharp or aching pain, temperature, and itch are described. The properties of transient receptor potential (TRP) channels on nociceptors and thermoreceptors are described. Physiological and pharmacological mechanisms that lead to neurogenic inflammation are considered. How peripheral and central changes triggered by acute injury or disease can lead to long-lasting changes that support chronic pain is described. Persistent pain that occurs independently of any stimulus is termed neuropathic. Mechanisms of referred pain from deep structures including viscera are introduced.
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Valls-Solé, Josep. Reflex studies. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0010.
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Reflex studies are an important part of clinical neurophysiology assessment in health and disease. They are essential to get information on conduction in proximal segments of peripheral nerves, spinal and supraspinal integration of sensory inputs on the motor pathway, and excitability of motor structures. They do not require special equipment, except for a sweep-triggering hammer that is essential, for instance, to elicit monosynaptic reflexes, such as the jaw jerk. For consensual reflexes, it is also recommended to use two recording channels, which facilitate recognition of potential disturbances in the afferent or efferent path of the reflex. What follows is a review of some of the most relevant reflexes that can be studied for neurophysiology assessment in clinical practice.
Book chapters on the topic "Afferent pathways – Diseases"
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Benarroch, Eduardo E. "Spinal Motor Control." In Neuroscience for Clinicians, edited by Eduardo E. Benarroch, 578–94. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190948894.003.0031.
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Motor neurons in the spinal cord brainstem motor nuclei (motoneurons) are the final effectors of central motor control and provide the output to skeletal muscles, forming motor units. The activity of spinal motoneurons is controlled by descending cortical and brainstem inputs largely via premotor circuits involving excitatory or inhibitory interneurons. These circuits elicit specific patterns of motoneuron activation controlling muscle synergies under the influence of descending corticospinal and brainstem motor pathways. Central pattern generators are interneuron circuits that can autonomously generate activation of motoneurons in the absence of descending commands or afferent feedback and include those involved in locomotion, respiration, and swallowing. Disorders affecting motor neurons or their control by afferent, cortical, or cerebellar influences constitute a large proportion of neurological diseases.
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A. Vega, José, and Juan Cobo. "Structural and Biological Basis for Proprioception." In Proprioception [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96787.
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The proprioception is the sense of positioning and movement. It is mediate by proprioceptors, a small subset of mechanosensory neurons localized in the dorsal root ganglia that convey information about the stretch and tension of muscles, tendons, and joints. These neurons supply of afferent innervation to specialized sensory organs in muscles (muscle spindles) and tendons (Golgi tendon organs). Thereafter, the information originated in the proprioceptors travels throughout two main nerve pathways reaching the central nervous system at the level of the spinal cord and the cerebellum (unconscious) and the cerebral cortex (conscious) for processing. On the other hand, since the stimuli for proprioceptors are mechanical (stretch, tension) proprioception can be regarded as a modality of mechanosensitivity and the putative mechanotransducers proprioceptors begins to be known now. The mechanogated ion channels acid-sensing ion channel 2 (ASIC2), transient receptor potential vanilloid 4 (TRPV4) and PIEZO2 are among candidates. Impairment or poor proprioception is proper of aging and some neurological diseases. Future research should focus on treating these defects. This chapter intends provide a comprehensive update an overview of the anatomical, structural and molecular basis of proprioception as well as of the main causes of proprioception impairment, including aging, and possible treatments.
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Canning, Brendan, and Stuart Mazzone. "Afferent Pathways Regulating the Cough Reflex." In Lung Biology in Health and Disease, 25–48. CRC Press, 2005. http://dx.doi.org/10.1201/b14188-3.
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Romo-Nava, Francisco, and Susan L. McElroy. "Neurobiology of Bipolar Disorder." In Bipolar Disorder, 141–54. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780190908096.003.0010.
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As frequently occurs in science, progress made on the neurobiology of bipolar disorder has followed a nonlinear course that often revisits deserted concepts. The neurobiological blueprint of bipolar disorder continues to unfold from a neurotransmitter-based hypothesis to include peptides and intracellular signaling pathways, and into a broader neuronal network perspective that involves cortical and subcortical regions in the brain. Moreover, new evidence makes it increasingly clear that the mechanisms of disease in bipolar disorder extend beyond the brain, providing plausible “missing links” between psychopathology and the elevated medical comorbidities. This is illustrated by the expanding role of the circadian system in bipolar disorder and the emerging evidence on the contribution of spinal afferents to the construct of mood, portraying that brain–body communication pathways are relevant to the pathophysiology of bipolar disorder. This chapter provides an overview of the current and emerging neurobiological frameworks for bipolar disorder.
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"Nerve and muscle." In Oxford Assess and Progress: Medical Sciences, edited by Jade Chow, John Patterson, Kathy Boursicot, and David Sales. Oxford University Press, 2012. http://dx.doi.org/10.1093/oso/9780199605071.003.0016.
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Higher animals have four basic tissue types: epithelial tissue, connective tissue, nervous tissue, and muscle. Of these, nerve and muscle are grouped together as ‘excitable cells’ because the cell membrane has the ability to vary membrane ion conductance and membrane voltage so as to transmit meaningful signals within and between cells. Within excitable cells information is transmitted using either an amplitude-modulated (AM) code using slow, electrotonic potentials, or a frequency-modulated (FM) code when signalling is by action potentials. Much of the signalling between excitable cells occurs at chemical synapses where a chemical neurotransmitter is released from presynaptic cells and then interacts with postsynaptic membrane receptors. Clinical symptoms can arise when the release of chemical neurotransmitters is disturbed, or when availability of postsynaptic receptors is altered. Thus, a reduction in dopamine release from basal ganglia substantia nigra cells is found in Parkinson’s disease, while myasthenia gravis results from loss of nicotinic acetylcholine receptors at the neuromuscular junction of skeletal muscle. Sometimes transmission from cell to cell is not by chemical neurotransmitter but by electrical synapses, where gap-junctions provide direct electrical connectivity. Transmission between cardiac muscle cells occurs in this way. Some cardiac arrhythmias, such as Wolff –Parkinson–White syndrome, are a consequence of an abnormal path of electrical conduction between cardiac muscle fibres. Sensory cells on and within the body pass information via afferent pathways from the peripheral nervous system into the central nervous system (CNS). CNS processes and sensory information are integrated to produce outputs from the CNS. These outputs pass by various efferent routes to the effector organs: skeletal muscle, cardiac muscle, smooth muscle, and glands. It is through these effectors that the CNS is able to exert control over the body and to interact with the environment. Alterations of function anywhere in the afferent, integrative, or efferent aspects of the system, as well as defects in the effectors themselves, are likely to lead to significant clinical symptoms and signs. The efferent outflow from the CNS has two major components. One, the somatic nervous system, innervates only skeletal muscle. The other is the autonomic nervous system (ANS), which innervates cardiac muscle, smooth muscle, and the glands of the viscera and skin.
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Schaible, Hans-Georg, and Rainer H. Straub. "Pain neurophysiology." In Oxford Textbook of Rheumatology, 431–36. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0059_update_002.
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Physiological pain is evoked by intense (noxious) stimuli acting on healthy tissue functioning as a warning signal to avoid damage of the tissue. In contrast, pathophysiological pain is present in the course of disease, and it is often elicited by low-intensity stimulation or occurs even as resting pain. Causes of pathophysiological pain are either inflammation or injury causing pathophysiological nociceptive pain or damage to nerve cells evoking neuropathic pain. The major peripheral neuronal mechanism of pathophysiological nociceptive pain is the sensitization of peripheral nociceptors for mechanical, thermal and chemical stimuli; the major peripheral mechanism of neuropathic pain is the generation of ectopic discharges in injured nerve fibres. These phenomena are created by changes of ion channels in the neurons, e.g. by the influence of inflammatory mediators or growth factors. Both peripheral sensitization and ectopic discharges can evoke the development of hyperexcitability of central nociceptive pathways, called central sensitization, which amplifies the nociceptive processing. Central sensitization is caused by changes of the synaptic processing, in which glial cell activation also plays an important role. Endogenous inhibitory neuronal systems may reduce pain but some types of pain are characterized by the loss of inhibitory neural function. In addition to their role in pain generation, nociceptive afferents and the spinal cord can further enhance the inflammatory process by the release of neuropeptides into the innervated tissue and by activation of sympathetic efferent fibres. However, in inflamed tissue the innervation is remodelled by repellent factors, in particular with a loss of sympathetic nerve fibres.