Academic literature on the topic 'Neurotransmitter release process'
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Journal articles on the topic "Neurotransmitter release process"
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Keighron, Jacqueline D., Yuanmo Wang, and Ann-Sofie Cans. "Electrochemistry of Single-Vesicle Events." Annual Review of Analytical Chemistry 13, no. 1 (June 12, 2020): 159–81. http://dx.doi.org/10.1146/annurev-anchem-061417-010032.
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Neuronal transmission relies on electrical signals and the transfer of chemical signals from one neuron to another. Chemical messages are transmitted from presynaptic neurons to neighboring neurons through the triggered fusion of neurotransmitter-filled vesicles with the cell plasma membrane. This process, known as exocytosis, involves the rapid release of neurotransmitter solutions that are detected with high affinity by the postsynaptic neuron. The type and number of neurotransmitters released and the frequency of vesicular events govern brain functions such as cognition, decision making, learning, and memory. Therefore, to understand neurotransmitters and neuronal function, analytical tools capable of quantitative and chemically selective detection of neurotransmitters with high spatiotemporal resolution are needed. Electrochemistry offers powerful techniques that are sufficiently rapid to allow for the detection of exocytosis activity and provides quantitative measurements of vesicle neurotransmitter content and neurotransmitter release from individual vesicle events. In this review, we provide an overview of the most commonly used electrochemical methods for monitoring single-vesicle events, including recent developments and what is needed for future research.
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Omote, Hiroshi, and Yoshinori Moriyama. "Vesicular Neurotransmitter Transporters: An Approach for Studying Transporters With Purified Proteins." Physiology 28, no. 1 (January 2013): 39–50. http://dx.doi.org/10.1152/physiol.00033.2012.
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Vesicular storage and subsequent release of neurotransmitters are the key processes of chemical signal transmission. In this process, vesicular neurotransmitter transporters are responsible for loading the signaling molecules. The use of a “clean biochemical” approach with purified, recombinant transporters has helped in the identification of novel vesicular neurotransmitter transporters and in the analysis of the control of signal transmission.
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Chang, Che-Wei, Chung-Wei Chiang, and Meyer B. Jackson. "Fusion pores and their control of neurotransmitter and hormone release." Journal of General Physiology 149, no. 3 (February 6, 2017): 301–22. http://dx.doi.org/10.1085/jgp.201611724.
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Ca2+-triggered exocytosis functions broadly in the secretion of chemical signals, enabling neurons to release neurotransmitters and endocrine cells to release hormones. The biological demands on this process can vary enormously. Although synapses often release neurotransmitter in a small fraction of a millisecond, hormone release can be orders of magnitude slower. Vesicles usually contain multiple signaling molecules that can be released selectively and conditionally. Cells are able to control the speed, concentration profile, and content selectivity of release by tuning and tailoring exocytosis to meet different biological demands. Much of this regulation depends on the fusion pore—the aqueous pathway by which molecules leave a vesicle and move out into the surrounding extracellular space. Studies of fusion pores have illuminated how cells regulate secretion. Furthermore, the formation and growth of fusion pores serve as a readout for the progress of exocytosis, thus revealing key kinetic stages that provide clues about the underlying mechanisms. Herein, we review the structure, composition, and dynamics of fusion pores and discuss the implications for molecular mechanisms as well as for the cellular regulation of neurotransmitter and hormone release.
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Grabner, Chad P., and Aaron P. Fox. "Stimulus-Dependent Alterations in Quantal Neurotransmitter Release." Journal of Neurophysiology 96, no. 6 (December 2006): 3082–87. http://dx.doi.org/10.1152/jn.00017.2006.
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Neurotransmitter release is a steep function of the intracellular calcium ion concentration ([Ca2+]i) at the release sites. Both the Ca2+ amplitude and the time course appear to be important for specifying neurotransmitter release. Ca2+ influx regulates the number of vesicles exocytosed as well as the amount of neurotransmitter each individual vesicle releases. In our study we stimulated mouse chromaffin cells in two different ways to alter Ca2+ presentation at the release sites. One method, digitonin permeabilization followed by exposure to Ca2+, allows for a large uniform global elevation of [Ca2+]i, whereas the second method, application of nicotine, depolarizes chromaffin cells and activates voltage-dependent Ca2+ channels, thereby producing more phasic and localized changes in [Ca2+]i. Using amperometry to monitor catecholamine release, we show that both kinds of stimuli elicit the exocytosis of similar quantities of neurotransmitter per large dense core vesicles (LDCVs) released. Even so, the release process was quite different for each stimulus; nicotine-elicited events were small and slow, whereas digitonin events were, in comparison, large and fast. In addition, the transient opening of the fusion pore, called the “foot,” was essentially absent in digitonin-stimulated cells, but was quite common in nicotine-stimulated cells. Thus even though both strong stimuli used in this study elicited the release of many vesicles it appears that the differences in the Ca2+ levels at the release sites were key determinants for the fusion and release of individual vesicles.
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Benfenati, Fabio, Franco Onofri, and Silvia Giovedí. "Protein–protein interactions and protein modules in the control of neurotransmitter release." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 354, no. 1381 (February 28, 1999): 243–57. http://dx.doi.org/10.1098/rstb.1999.0376.
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Information transfer among neurons is operated by neurotransmitters stored in synaptic vesicles and released to the extracellular space by an efficient process of regulated exocytosis. Synaptic vesicles are organized into two distinct functional pools, a large reserve pool in which vesicles are restrained by the actin–based cytoskeleton, and a quantitatively smaller releasable pool in which vesicles approach the presynaptic membrane and eventually fuse with it on stimulation. Both synaptic vesicle trafficking and neurotransmitter release depend on a precise sequence of events that include release from the reserve pool, targeting to the active zone, docking, priming, fusion and endocytotic retrieval of synaptic vesicles. These steps are mediated by a series of specific interactions among cytoskeletal, synaptic vesicle, presynaptic membrane and cytosolic proteins that, by acting in concert, promote the spatial and temporal regulation of the exocytotic machinery. The majority of these interactions are mediated by specific protein modules and domains that are found in many proteins and are involved in numerous intracellular processes. In this paper, the possible physiological role of these multiple protein–protein interactions is analysed, with ensuing updating and clarification of the present molecular model of the process of neurotransmitter release.
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Kupchik, Yonatan M., Ofra Barchad-Avitzur, Jürgen Wess, Yair Ben-Chaim, Itzchak Parnas, and Hanna Parnas. "A novel fast mechanism for GPCR-mediated signal transduction—control of neurotransmitter release." Journal of Cell Biology 192, no. 1 (January 3, 2011): 137–51. http://dx.doi.org/10.1083/jcb.201007053.
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Reliable neuronal communication depends on accurate temporal correlation between the action potential and neurotransmitter release. Although a requirement for Ca2+ in neurotransmitter release is amply documented, recent studies have shown that voltage-sensitive G protein–coupled receptors (GPCRs) are also involved in this process. However, how slow-acting GPCRs control fast neurotransmitter release is an unsolved question. Here we examine whether the recently discovered fast depolarization-induced charge movement in the M2-muscarinic receptor (M2R) is responsible for M2R-mediated control of acetylcholine release. We show that inhibition of the M2R charge movement in Xenopus oocytes correlated well with inhibition of acetylcholine release at the mouse neuromuscular junction. Our results suggest that, in addition to Ca2+ influx, charge movement in GPCRs is also necessary for release control.
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Liu, Tianshu, Pankaj Singh, James T. Jenkins, Anand Jagota, Maria Bykhovskaia, and Chung-Yuen Hui. "A continuum model of docking of synaptic vesicle to plasma membrane." Journal of The Royal Society Interface 12, no. 102 (January 2015): 20141119. http://dx.doi.org/10.1098/rsif.2014.1119.
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Neurotransmitter release from neuronal terminals is governed by synaptic vesicle fusion. Vesicles filled with transmitters are docked at the neuronal membrane by means of the SNARE machinery. After a series of events leading up to the fusion pore formation, neurotransmitters are released into the synaptic cleft. In this paper, we study the mechanics of the docking process. A continuum model is used to determine the deformation of a spherical vesicle and a plasma membrane, under the influence of SNARE-machinery forces and electrostatic repulsion. Our analysis provides information on the variation of in-plane stress in the membranes, which is known to affect fusion. Also, a simple model is proposed to study hemifusion.
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Mochida, S., S. Orita, G. Sakaguchi, T. Sasaki, and Y. Takai. "Role of the Doc2 -Munc13-1 interaction in the neurotransmitter release process." Proceedings of the National Academy of Sciences 95, no. 19 (September 15, 1998): 11418–22. http://dx.doi.org/10.1073/pnas.95.19.11418.
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Arroyo, Gloria, Jorge Fuentealba, Natalia Sevane-Fernández, Marcos Aldea, Antonio G. García, and Almudena Albillos. "Amperometric Study of the Kinetics of Exocytosis in Mouse Adrenal Slice Chromaffin Cells: Physiological and Methodological Insights." Journal of Neurophysiology 96, no. 3 (September 2006): 1196–202. http://dx.doi.org/10.1152/jn.00088.2006.
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This study was designed to examine the kinetics of neurotransmitter release using the carbon fiber amperometric technique on cells in slices of mouse adrenal glands superfused with bicarbonate phosphate buffer–based solutions. The exocytotic amperometric response evoked by electrical stimulation was significantly faster than that produced after exogenous application of ACh or K+. Splanchnic nerve–evoked neurotransmitter release was blocked by hexamethonium, indicating the involvement of ACh nicotinic receptors. We discuss the implications of our data for understanding the mechanisms underlying the vesicle fusion process.
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Boll, Inga, Pia Jensen, Veit Schwämmle, and Martin R. Larsen. "Depolarization-dependent Induction of Site-specific Changes in Sialylation on N-linked Glycoproteins in Rat Nerve Terminals." Molecular & Cellular Proteomics 19, no. 9 (June 9, 2020): 1418–35. http://dx.doi.org/10.1074/mcp.ra119.001896.
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Synaptic transmission leading to release of neurotransmitters in the nervous system is a fast and highly dynamic process. Previously, protein interaction and phosphorylation have been thought to be the main regulators of synaptic transmission. Here we show that sialylation of N-linked glycosylation is a novel potential modulator of neurotransmitter release mechanisms by investigating depolarization-dependent changes of formerly sialylated N-linked glycopeptides. We suggest that negatively charged sialic acids can be modulated, similarly to phosphorylation, by the action of sialyltransferases and sialidases thereby changing local structure and function of membrane glycoproteins. We characterized site-specific alteration in sialylation on N-linked glycoproteins in isolated rat nerve terminals after brief depolarization using quantitative sialiomics. We identified 1965 formerly sialylated N-linked glycosites in synaptic proteins and found that the abundances of 430 glycosites changed after 5 s depolarization. We observed changes on essential synaptic proteins such as synaptic vesicle proteins, ion channels and transporters, neurotransmitter receptors and cell adhesion molecules. This study is to our knowledge the first to describe ultra-fast site-specific modulation of the sialiome after brief stimulation of a biological system.
Dissertations / Theses on the topic "Neurotransmitter release process"
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Wardell, Claire Frances. "Mechanisms of transmitter release in vascular and non-vascular smooth muscle." Thesis, University of Oxford, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.303665.
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Gentile, Luigi. "Voltage-gated calcium channel kinetics implicated in the process of fast neurotransmitter release." 2005. http://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=362561&T=F.
Full textBooks on the topic "Neurotransmitter release process"
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Gentile, Luigi. Voltage-gated calcium channel kinetics implicated in the process of fast neurotransmitter release. 2005.
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Gentile, Luigi. Voltage-gated calcium channel kinetics implicated in the process of fast neurotransmitter release. 2005.
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Mason, Peggy. Neurotransmitter Release. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0011.
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The biochemical and physiological processes of neurotransmitter release from an active zone, a specialized region of synaptic membrane, are examined. Synaptic vesicles containing neurotransmitters are docked at the active zone and then primed for release by SNARE complexes that bring them into extreme proximity to the plasma membrane. Entry of calcium ions through voltage-gated calcium channels triggers synaptic vesicle fusion with the synaptic terminal membrane and the consequent diffusion of neurotransmitter into the synaptic cleft. Release results when the fusion pore bridging the synaptic vesicle and plasma membrane widens and neurotransmitter from the inside of the synaptic vesicle diffuses into the synaptic cleft. Membrane from the active zone membrane is endocytosed, and synaptic vesicle proteins are then reassembled into recycled synaptic vesicles, allowing for more rounds of neurotransmitter release.
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Arnold, Monica M., Lauren M. Burgeno, and Paul E. M. Phillips. Fast-Scan Cyclic Voltammetry in Behaving Animals. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199939800.003.0005.
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Gaining insight into the mechanisms by which neural transmission governs behavior remains a central goal of behavioral neuroscience. Multiple applications exist for monitoring neurotransmission during behavior, including fast-scan cyclic voltammetry (FSCV). This technique is an electrochemical detection method that can be used to monitor subsecond changes in concentrations of electroactive molecules such as neurotransmitters. In this technique, a triangular waveform voltage is applied to a carbon fiber electrode implanted into a selected brain region. During each waveform application, specific molecules in the vicinity of the electrode will undergo electrolysis and produce a current, which can be detected by the electrode. In order to monitor subsecond changes in neurotransmitter release, waveform application is repeated every 100 ms, yielding a 10 Hz sampling rate. This chapter describes the fundamental principles behind FSCV and the basic instrumentation required, using as an example system the detection of in vivo phasic dopamine changes in freely-moving animals over the course of long-term experiments. We explain step-by-step, how to construct and surgically implant a carbon fiber electrode that can readily detect phasic neurotransmitter fluctuations and that remains sensitive over multiple recordings across months. Also included are the basic steps for recording FSCV during behavioral experiments and how to process voltammetric data in which signaling is time-locked to behavioral events of interest. Together, information in this chapter provides a foundation of FSCV theory and practice that can be applied to the assembly of an FSCV system and execution of in vivo experiments.
Book chapters on the topic "Neurotransmitter release process"
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Levitan, Irwin B., and Leonard K. Kaczmarek. "Synaptic Release of Neurotransmitters." In The Neuron, 187–212. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199773893.003.0009.
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Several specialized synapses, including those in squid stellate ganglion, frog neuromuscular junction, and calyx of Held, have been instrumental in advancing our understanding of the release of neurotransmitters from presynaptic terminals. Studies of rapid synaptic transmission have shown that neurotransmitters are released in packets, or quanta, which may correspond to the exocytosis of individual synaptic vesicles. Following an action potential, release is linked in space and time to the entry of calcium though voltage-dependent channels. The amount of transmitter released by a single action potential varies through depression, facilitation, or potentiation during and after repetitive stimulation of a synapse. Mechanisms that induce neurotransmitter release and proteins, such as synapsins, that modulate their release are still not completely understood. Biochemical and genetic experiments that characterize, modify, or eliminate components of synaptic vesicles and release sites, coupled with physiological experiments at specific synapses, provide further insights into the release process.
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Benarroch, Eduardo E., Jeremy K. Cutsforth-Gregory, and Kelly D. Flemming. "Neurochemistry." In Mayo Clinic Medical Neurosciences, edited by Eduardo E. Benarroch, Jeremy K. Cutsforth-Gregory, and Kelly D. Flemming, 167–206. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190209407.003.0006.
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Communication between neurons occurs primarily at the level of synapses. The most common form of communication in the nervous system is through chemical synapses, which consist of presynaptic and postsynaptic components separated by a synaptic cleft. The presynaptic terminals contain synaptic vesicles, which are involved in the storage and release of neurotransmitters by the process of exocytosis. Complex mechanisms control the synthesis, vesicular storage, and release of neurotransmitters and regulate the availability of neurotransmitter at the level of the synaptic cleft. The effects of the neurochemical transmitter on its target are mediated by neurotransmitter receptors. Specific neurotransmitter systems are responsible for fast neuronal excitation or inhibition, while other neurotransmitter systems regulate the excitability of neurons in the nervous system. Abnormalities in neurochemical transmission are responsible for many disorders, including acute neuronal death, seizures, neurodegenerative disorders, and psychiatric diseases. Most importantly, neurochemical systems provide the target for pharmacologic treatment of these disorders. The aims of this chapter are to review the basis of neurochemical transmission and the distribution, biochemistry, and function of specific neurotransmitter systems.
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Levitan, Irwin B., and Leonard K. Kaczmarek. "How Neurons Communicate: Gap Junctions and Neurosecretion." In The Neuron, 153–86. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199773893.003.0008.
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Two ways that neurons communicate with one another are by direct electrical coupling and by the secretion of neurotransmitters. Electrical coupling arises from the existence of proteins, known as connexins, that form pores linking the cytoplasm of adjacent cells. Ions and small molecules can carry signals from one cell to another through these pores. Neurosecretion is a more complex process whereby different categories of molecules are sorted into cytoplasmic vesicles. Chemical processes within these vesicles ensure that they contain biologically active transmitters or hormones. SNARE complex proteins cooperate with other proteins to allow synaptic vesicles containing neurotransmitter to release their components into the external medium following calcium entry into nerve terminals. Such exocytosis of synaptic vesicles can be monitored with imaging techniques using fluorescent dyes or proteins, or by capacitance measurements. A second set of molecules retrieves the membrane of synaptic vesicles back from the plasma membrane through endocytosis.
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Emmett, Stevan R., Nicola Hill, and Federico Dajas-Bailador. "Psychiatry." In Clinical Pharmacology for Prescribing. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780199694938.003.0018.
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Anxiety disorders fall mainly into the category of neurotic, stress, or somatoform disorders, as defined by the international classification of disease system (ICD- 11, WHO, 2018). They refer to several disorders that include generalized anxiety disorder (GAD), phobic anxiety disorders, panic disorder (± agoraphobia), obsessive compulsive disorder (OCD) and post- traumatic stress disorder (PTSD). Collectively, anxiety disorders affect almost 30% of people in the western world during their lifetime, with PTSD and GAD amongst the most prevalent. In general, anxiety disorders are associated with neurotransmitter dysregulation and amygdala hyperactivity. Insomnia is the unsatisfactory quantity and/ or quality of sleep, which persists for sufficient time to affect quality of life. It is often associated with other mental health (e.g. depression, anxiety, alcohol dependence) and physical (e.g. pain, neoplasms) pathologies, or iatrogenic effects (e.g. diuretic, β- blockers, statins, levodopa). It may require treatment if symptoms are troublesome. Chronic insomnia can last for years, and affects almost 10% of the population. Around 30% have symptoms that are occasionally worse, with higher prevalence in older age. Many factors interplay to generate a state of anxiety, but from a biological perspective one of the key central brain pathways involved in this process is the limbic system, which regulates an array of functions, including emotion, fear, behaviour, and memory. One vital brain area that processes fear reactions from the thalamus and cortex is the amygdala, with connections to the hypothalamus, which can activate sympathetic reactions and the hypothalamic– pituitary axis (HPA). Activation/ inhibition within this pathway leads to altered neurotransmitter activity. Corticotrophin- releasing factor (CRF) is known to be released from the hypothalamus in response to stress, under the regulation of the amygdala. CRF acts to drive the HPA, promoting the release of ACTH from the pituitary and then cortisol from the adrenal gland. In effect, sustained CRF exposure may lead to limbic system up- regulation and the heightening of anxiety states. Moreover, dysregulation in this system and changes in central cortisol sensing systems (e.g. decreased receptor expression) may cause chronic anxiety. The locus coeruleus (LC), is another brain region partly responsible for regulating the sympathetic effects of stress, again under the control of CRF.
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Benarroch, Eduardo E. "Neurotransmission, Neuromodulation, and Plasticity." In Neuroscience for Clinicians, edited by Eduardo E. Benarroch, 276–95. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190948894.003.0016.
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Neurochemical signals released at synapses or by perisynaptic glial cell processes include excitatory and inhibitory amino acids, acetylcholine, monoamines, neuropeptides, purines, lipid mediators, nitric oxide, growth factors, cytokines, and extracellular matrix proteins. These signals produce three fundamental effects on their target: classical neurotransmission, neuromodulation, and plasticity. Classical neurotransmission is the rapid, precise transmission of excitatory or inhibitory signals. Neuromodulation affects the probability of neurotransmitter release or responsiveness of the postsynaptic cells to the neurotransmitter. Synaptic plasticity refers to the use-dependent changes in efficacy of transmission of excitatory signals, eventually associated with change in dendritic structure and connectivity. Plasticity also involves interactions among synapses, glial cell, and the extracellular matrix. Abnormalities of synaptic transmission and plasticity are common disease mechanisms in neurologic disorders and are therapeutic targets.
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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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Levitan, Irwin B., and Leonard K. Kaczmarek. "Neurotransmitters and Neurohormones." In The Neuron, 213–38. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199773893.003.0010.
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A multitude of chemicals called neurotransmitters mediate intercellular communication in the nervous system. These include acetylcholine, the catecholamines, serotonin, glutamate, GABA, glycine, and a wide variety of neuropeptides. Although they exhibit great diversity in many of their properties, all are stored in vesicles in nerve terminals and are released to the extracellular space via a process requiring calcium ions. Their actions are terminated by reuptake into the presynaptic terminal or nearby glial cells by specific transporter proteins or by their destruction in the extracellular space. The role of neurotransmitters is to alter the properties—chemical, electrical, or both—of some target cell. With the arrival on the scene of the neuropeptides, it has become evident that signaling in the nervous system occurs through the use of rich and varied forms of chemical currency, and that some neurons use more than one type of currency simultaneously.
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Ahlskog, J. Eric. "Symptoms, Related Brain Regions, and Diagnosis." In Dementia with Lewy Body and Parkinson's Disease Patients. Oxford University Press, 2013. http://dx.doi.org/10.1093/oso/9780199977567.003.0008.
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As a prelude to the treatment chapters that follow, we need to define and describe the types of problems and symptoms encountered in DLB and PDD. The clinical picture can be quite varied: problems encountered by one person may be quite different from those encountered by another person, and symptoms that are problematic in one individual may be minimal in another. In these disorders, the Lewy neurodegenerative process potentially affects certain nervous system regions but spares others. Affected areas include thinking and memory circuits, as well as movement (motor) function and the autonomic nervous system, which regulates primary functions such as bladder, bowel, and blood pressure control. Many other brain regions, by contrast, are spared or minimally involved, such as vision and sensation. The brain and spinal cord constitute the central nervous system. The interface between the brain and spinal cord is by way of the brain stem, as shown in Figure 4.1. Thought, memory, and reasoning are primarily organized in the thick layers of cortex overlying lower brain levels. Volitional movements, such as writing, throwing, or kicking, also emanate from the cortex and integrate with circuits just below, including those in the basal ganglia, shown in Figure 4.2. The basal ganglia includes the striatum, globus pallidus, subthalamic nucleus, and substantia nigra, as illustrated in Figure 4.2. Movement information is integrated and modulated in these basal ganglia nuclei and then transmitted down the brain stem to the spinal cord. At spinal cord levels the correct sequence of muscle activation that has been programmed is accomplished. Activated nerves from appropriate regions of the spinal cord relay the signals to the proper muscles. Sensory information from the periphery (limbs) travels in the opposite direction. How are these signals transmitted? Brain cells called neurons have long, wire-like extensions that interface with other neurons, effectively making up circuits that are slightly similar to computer circuits; this is illustrated in Figure 4.3. At the end of these wire-like extensions are tiny enlargements (terminals) that contain specific biological chemicals called neurotransmitters. Neurotransmitters are released when the electrical signal travels down that neuron to the end of that wire-like process.
Conference papers on the topic "Neurotransmitter release process"
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Ball, John M., Ali H. Hummos, and Satish S. Nair. "A Firing-Rate Lateral Amygdala Network Model With Calcium-Dependent Synaptic Learning." In ASME 2011 Dynamic Systems and Control Conference and Bath/ASME Symposium on Fluid Power and Motion Control. ASMEDC, 2011. http://dx.doi.org/10.1115/dscc2011-6117.
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Neurons in the nervous system communicate by spiking, which activates synaptic connections via the release of neurotransmitter molecules. Modification of the strength of these synaptic connections, known as plasticity, is a mechanism by which networks of neurons can exhibit learning. Previously, a biophysical model of a rodent lateral amygdala was developed that could learn and store auditory fear and extinction memories following classical Pavlovian fear conditioning [1]. We propose a novel reduced order model that preserves the learning capabilities of the detailed model with considerably fewer computations while providing additional insights into the synaptic learning process. To capture the dynamics of individual cells, we propose enhancements to the Wilson-Cowan firing rate model that permit “full” spike frequency adaptation and a non-zero threshold. To incorporate synaptic learning dynamics, we propose a regression technique to capture the nonlinear relationship between firing rate and synaptic [Ca2+]. The resulting method provides a general technique to develop neuronal networks that employ [Ca2+]-dependent synaptic learning.