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Journal of Neurophysiology Dec 2019Semicircular canal afferent neurons transmit information about head rotation to the brain. Mathematical models of how they do this have coevolved with concepts of how... (Review)
Review
Semicircular canal afferent neurons transmit information about head rotation to the brain. Mathematical models of how they do this have coevolved with concepts of how brains perceive the world. A 19th-century "camera" metaphor, in which sensory neurons project an image of the world captured by sense organs into the brain, gave way to a 20th-century view of sensory nerves as communication channels providing inputs to dynamical control systems. Now, in the 21st century, brains are being modeled as Bayesian observers who infer what is happening in the world given noisy, incomplete, and distorted sense data. The semicircular canals of the vestibular apparatus provide an experimentally accessible, low-dimensional system for developing and testing dynamical Bayesian generative models of sense data. In this review, we summarize advances in mathematical modeling of information transmission by semicircular canal afferent sensory neurons since the first such model was proposed nearly a century ago. Models of information transmission by vestibular afferent neurons may provide a foundation for developing realistic models of how brains perceive the world by inferring the causes of sense data.
Topics: Animals; Models, Biological; Neurons, Afferent; Semicircular Canals; Vestibule, Labyrinth
PubMed: 31693427
DOI: 10.1152/jn.00087.2019 -
Current Opinion in Pharmacology Jun 2002The activation of airway afferent neurons initiates a variety of reflexes including cough and bronchoconstriction. Like somatic afferent neurons involved in... (Review)
Review
The activation of airway afferent neurons initiates a variety of reflexes including cough and bronchoconstriction. Like somatic afferent neurons involved in inflammation-induced hyperalgesia, the excitability of airway afferent neurons is not fixed but, rather, can be increased by the action of a variety of mediators produced during inflammation. A variety of techniques have been applied to study the pharmacological modulation of the excitability of afferent neurons. Although airway afferent neurons have not been studied to the same extent as fibers involved in hyperalgesia, similar pathways may control their excitability. The ability to study the pharmacological modulation of airway afferent neuron excitability is crucial to our understanding of airway afferent neurophysiology and may also provide insight into novel therapeutic targets for various inflammatory lung diseases.
Topics: Animals; Humans; Neurons, Afferent; Respiratory System; Respiratory Tract Diseases
PubMed: 12020460
DOI: 10.1016/s1471-4892(02)00147-9 -
Nature Sep 2001The sensation of pain alerts us to real or impending injury and triggers appropriate protective responses. Unfortunately, pain often outlives its usefulness as a warning... (Review)
Review
The sensation of pain alerts us to real or impending injury and triggers appropriate protective responses. Unfortunately, pain often outlives its usefulness as a warning system and instead becomes chronic and debilitating. This transition to a chronic phase involves changes within the spinal cord and brain, but there is also remarkable modulation where pain messages are initiated - at the level of the primary sensory neuron. Efforts to determine how these neurons detect pain-producing stimuli of a thermal, mechanical or chemical nature have revealed new signalling mechanisms and brought us closer to understanding the molecular events that facilitate transitions from acute to persistent pain.
Topics: Animals; Forecasting; Humans; Neurons, Afferent; Pain; Signal Transduction
PubMed: 11557989
DOI: 10.1038/35093019 -
Advances in Nutrition (Bethesda, Md.) Jul 2014It is well established that food intake behavior and energy balance are regulated by crosstalk between peripheral organ systems and the central nervous system (CNS), for... (Review)
Review
It is well established that food intake behavior and energy balance are regulated by crosstalk between peripheral organ systems and the central nervous system (CNS), for instance, through the actions of peripherally derived leptin on hindbrain and hypothalamic loci. Diet- or obesity-associated disturbances in metabolic and hormonal signals to the CNS can perturb metabolic homeostasis bodywide. Although interrelations between metabolic status and diet with CNS biology are well characterized, afferent networks (those sending information to the CNS from the periphery) have received far less attention. It is increasingly appreciated that afferent neurons in adipose tissue, the intestines, liver, and other tissues are important controllers of energy balance and feeding behavior. Disruption in their signaling may have consequences for cardiovascular, pancreatic, adipose, and immune function. This review discusses the diverse ways that afferent neurons participate in metabolic homeostasis and highlights how changes in their function associate with dysmetabolic states, such as obesity and insulin resistance.
Topics: Animals; Diet; Energy Intake; Energy Metabolism; Feeding Behavior; Homeostasis; Humans; Insulin Resistance; Metabolic Diseases; Neurons, Afferent; Obesity
PubMed: 25022988
DOI: 10.3945/an.113.005439 -
The Journal of Nutrition Apr 2015Emerging evidence has suggested a possible physiologic role for peripheral glucagon-like peptide 1 (GLP-1) in regulating glucose metabolism and food intake. The likely... (Review)
Review
Emerging evidence has suggested a possible physiologic role for peripheral glucagon-like peptide 1 (GLP-1) in regulating glucose metabolism and food intake. The likely site of action of GLP-1 is on vagal afferent neurons (VANs). The vagal afferent pathway is the major neural pathway by which information about ingested nutrients reaches the central nervous system and influences feeding behavior. Peripheral GLP-1 acts on VANs to inhibit food intake. The mechanism of the GLP-1 receptor (GLP-1R) is unlike other gut-derived receptors; GLP-1Rs change their cellular localization according to feeding status rather than their protein concentrations. It is possible that several gut peptides are involved in mediating GLP-1R translocation. The mechanism of peripheral GLP-1R translocation still needs to be elucidated. We review data supporting the role of peripheral GLP-1 acting on VANs in influencing glucose homeostasis and feeding behavior. We highlight evidence demonstrating that GLP-1 interacts with ghrelin and leptin to induce satiation. Our aim was to understand the mechanism of peripheral GLP-1 in the development of noninvasive antiobesity treatments.
Topics: Animals; Blood Glucose; Eating; Gastrointestinal Tract; Ghrelin; Glucagon-Like Peptide 1; Glucagon-Like Peptide-1 Receptor; Humans; Leptin; Neurons, Afferent; Receptors, Glucagon; Satiation; Signal Transduction
PubMed: 25833771
DOI: 10.3945/jn.114.206029 -
American Journal of Physiology.... Sep 2019The distal colon is innervated by the splanchnic and pelvic nerves, which relay into the thoracolumbar and lumbosacral spinal cord, respectively. Although the peripheral...
The distal colon is innervated by the splanchnic and pelvic nerves, which relay into the thoracolumbar and lumbosacral spinal cord, respectively. Although the peripheral properties of the colonic afferent nerves within these pathways are well studied, their input into the spinal cord remain ill defined. The use of dual retrograde tracing from the colon wall and lumen, in conjunction with in vivo colorectal distension and spinal neuronal activation labeling with phosphorylated MAPK ERK 1/2 (pERK), allowed us to identify thoracolumbar and lumbosacral spinal cord circuits processing colonic afferent input. In the thoracolumbar dorsal horn, central projections of colonic afferents were primarily labeled from the wall of the colon and localized in laminae I and V. In contrast, lumbosacral projections were identified from both lumen and wall tracing, present within various dorsal horn laminae, collateral tracts, and the dorsal gray commissure. Nonnoxious in vivo colorectal distension evoked significant neuronal activation (pERK-immunoreactivity) within the lumbosacral dorsal horn but not in thoracolumbar regions. However, noxious in vivo colorectal distension evoked significant neuronal activation in both the thoracolumbar and lumbosacral dorsal horn, with the distribution of activated neurons correlating to the pattern of traced projections. Dorsal horn neurons activated by colorectal distension were identified as possible populations of projection neurons or excitatory and inhibitory interneurons based on their neurochemistry. Our findings demonstrate how colonic afferents in splanchnic and pelvic pathways differentially relay mechanosensory information into the spinal cord and contribute to the recruitment of spinal cord pathways processing non-noxious and noxious stimuli. In mice, retrograde tracing from the colon wall and lumen was used to identify unique populations of afferent neurons and central projections within the spinal cord dorsal horn. We show that there are pronounced differences between the spinal cord regions in the distribution pattern of colonic afferent central projections and the pattern of dorsal horn neuron activation evoked by colorectal distension. These findings demonstrate how colonic afferent input influences spinal processing of colonic mechanosensation.
Topics: Afferent Pathways; Animals; Colon; Male; Mice, Inbred C57BL; Neurons, Afferent; Posterior Horn Cells; Spinal Cord
PubMed: 31188624
DOI: 10.1152/ajpgi.00013.2019 -
The Lancet. Neurology Jun 2005Sensory neuron diseases (SND) are a distinct subgroup of peripheral-nervous-system diseases, first acknowledged in 1948. Acquired SND have a subacute or chronic course... (Review)
Review
Sensory neuron diseases (SND) are a distinct subgroup of peripheral-nervous-system diseases, first acknowledged in 1948. Acquired SND have a subacute or chronic course and are associated with systemic immune-mediated diseases, vitamin intoxication or deficiency, neurotoxic drugs, and life-threatening diseases such as cancer. SND are commonly idiopathic but can be genetic diseases; the latter tend to involve subtypes of sensory neurons and are associated with certain clinical pictures. The loss of sensory neurons in dorsal root ganglia causes the degeneration of short and long peripheral axons and central sensory projections in the posterior columns. This pathological process leads to a pattern of sensory nerve degeneration that is not length dependent and explains distinct clinical and neurophysiological abnormalities. Here we propose a comprehensive approach to the diagnosis of acquired and hereditary SND and discuss clinical, genetic, neurophysiological, neuroradiological, and neuropathological assessments.
Topics: Ganglia, Spinal; Humans; Neural Pathways; Neurons, Afferent; Peripheral Nervous System Diseases
PubMed: 15907739
DOI: 10.1016/S1474-4422(05)70096-X -
Progress in Brain Research 1996Sympathetic post-ganglionic neurons may be involved in the generation of pain, hyperalgesia and inflammation under pathophysiological conditions. Two categories of... (Review)
Review
Sympathetic post-ganglionic neurons may be involved in the generation of pain, hyperalgesia and inflammation under pathophysiological conditions. Two categories of influence of the sympathetic neuron on afferent neurons can be distinguished and this distinction seems to be related to whether the coupling between afferent and sympathetic neuron develops after nerve lesion or after tissue trauma with inflammation (Fig. 15): A. Peripheral nerve lesion generates plastic changes of the afferent and sympathetic postganglionic neurons, depending on the type of nerve lesion (e.g. complete, partial). Both afferent and post-ganglionic neurons exhibit degenerative and regenerative changes and unlesioned neurons may show collateral sprouting in the periphery as well as in the dorsal root ganglion. This reorganization of the peripheral neurons may lead to chemical coupling between sympathetic and afferent neurons. The coupling is responsible for sensitization and/or activation of primary afferent neurons by the sympathetic neurons. The mediator probably is norepinephrine, but other substances cannot be excluded. The afferent neuron expresses or upregulates functional adrenoceptors. The type of adrenoceptor involved is probably alpha 2. The coupling may occur at different sites of the primary afferent neuron, e.g. at the lesion site, remote from the lesion site in the dorsal root ganglion or between nonlesioned sympathetic and afferent neurons which show collateral sprouting. The biochemical signals which trigger these changes probably are neurotrophic substances, their receptors which are synthesized by the peripheral neurons, Schwann cells and other cells in response to the peripheral lesions. B. Sympathetic nerve terminals in peripheral tissues may serve as mediator elements in hyperalgesia and inflammation following tissue trauma without nerve lesion. Experiments show that these functions are largely independent of activity in the sympathetic neurons and independent of vesicular release of transmitter substances (such as norepinephrine). Sensitization of nociceptive afferents for mechanical stimuli and venular plasma extravasation in the synovium which are induced by the inflammatory mediator bradykinin are, at least in part, dependent on the sympathetic terminal. The signal to venules and afferent receptors is synthesized and released from the sympathetic terminal or in association with it. It is a prostaglandin (probably PGE2). Sympathetically mediated (neurogenic) inflammation and neurogenic inflammation mediated by afferents may interact reciprocally and enhance the inflammatory process as well as the sensitization of nociceptive afferents. Norepinephrine may also lead to sensitization of nociceptive afferents under inflammatory conditions. This sensitization is presumably mediated by alpha 2-adrenoceptors in the sympathetic varicosities and by a prostaglandin (probably PGI2) which is synthesized and released by or in association with the sympathetic varicosities.
Topics: Extremities; Hyperalgesia; Neurons, Afferent; Pain; Sympathetic Nervous System
PubMed: 9009734
DOI: 10.1016/s0079-6123(08)61087-0 -
Current Opinion in Neurobiology Aug 2003Mechanosensory hair cells of the cochlea must serve as both transducers and presynaptic terminals, precisely releasing neurotransmitter to encode acoustic signals for... (Review)
Review
Mechanosensory hair cells of the cochlea must serve as both transducers and presynaptic terminals, precisely releasing neurotransmitter to encode acoustic signals for the postsynaptic afferent neuron. Remarkably, each inner hair cell serves as the sole input for 10-30 individual afferent neurons, which requires extraordinary precision and reliability from the synaptic ribbons that marshal vesicular release onto each afferent. Recent studies of hair cell membrane capacitance and postsynaptic currents suggest that the synaptic ribbon may operate by simultaneous multi-vesicular release. This mechanism could serve to ensure the accurate timing of transmission, and further challenges our understanding of this synaptic nano-machine.
Topics: Afferent Pathways; Animals; Cochlea; Excitatory Amino Acid Transporter 1; Excitatory Amino Acid Transporter 2; Hair Cells, Auditory; Humans; Synapses
PubMed: 12965293
DOI: 10.1016/s0959-4388(03)00098-9 -
Advances in Experimental Medicine and... 2001
Review
Topics: Afferent Pathways; Animals; Aortic Bodies; Brain Stem; Cats; Neurons, Afferent; Respiratory Mechanics
PubMed: 11729938
DOI: 10.1007/978-1-4615-1375-9_13