The Experts below are selected from a list of 276 Experts worldwide ranked by ideXlab platform
Zygmunt L Kruk - One of the best experts on this subject based on the ideXlab platform.
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comparison of somatodendritic and Axon Terminal dopamine release in the ventral tegmental area and the nucleus accumbens
Neuroscience, 1996Co-Authors: Mahmoud M Iravani, Richard Muscat, Zygmunt L KrukAbstract:Fast cyclic voltammetry at a carbon fibre microelectrode was used to measure dopamine release following electrical or chemical stimulation in rat brain slices incorporating either the ventral tegmental area or the core region of the nucleus accumbens. Electrical or chemical stimulation gave clear voltammetric signals which corresponded to dopamine; less dopamine was released in the ventral tegmental area than in the nucleus accumbens. In contrast to the nucleus accumbens, electrically stimulated dopamine release in the ventral tegmental area was not sensitive to tetrodotoxin, was not modified by the presence of dopamine uptake inhibitors, or agonist or blockers acting at dopamine D2 autoreceptors.
Cesare Montecucco - One of the best experts on this subject based on the ideXlab platform.
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animal models for studying motor Axon Terminal paralysis and recovery
Journal of Neurochemistry, 2017Co-Authors: Michela Rigoni, Cesare MontecuccoAbstract:An extraordinary property of the peripheral nervous system is that nerve Terminals can regenerate after damage caused by different physical, chemical, or biological pathogens. Regeneration is the result of a complex and ill-known interplay among the nerve, the glia, the muscle, the basal lamina and, in some cases, the immune system. This phenomenon has been studied using different injury models mainly in rodents, particularly in mice, where a lesion can be produced in a chosen anatomical area. These approaches differ significantly among them for the nature of the lesion and the final outcomes. We have reviewed here the most common experimental models employed to induce motor Axon injury, the relative advantages and drawbacks, and the principal read-outs used to monitor the regenerative process. Recently introduced tools for inducing reversible damage to the motor Axon Terminal that overcome some of the drawbacks of the more classical approaches are also discussed. Animal models have provided precious information about the cellular components involved in the regenerative process and on its electrophysiological features. Methods and tools made available recently allow one to identify and study molecules that are involved in the crosstalk among the components of the endplate. The time-course of the intercellular signaling and of the intracellular pathways activated will draw a picture of the entire process of regeneration as seen from a privileged anatomical site of observation. This is an article for the special issue XVth International Symposium on Cholinergic Mechanisms.
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Mitochondrial alarmins released by degenerating motor Axon Terminals activate perisynaptic Schwann cells
Proceedings of the National Academy of Sciences of the United States of America, 2015Co-Authors: Elisa Duregotti, Samuele Negro, Michele Scorzeto, Irene Zornetta, Bryan C. Dickinson, Christopher J. Chang, Cesare Montecucco, Michela RigoniAbstract:An acute and highly reproducible motor Axon Terminal degeneration followed by complete regeneration is induced by some animal presynaptic neurotoxins, representing an appropriate and controlled system to dissect the molecular mechanisms underlying degeneration and regeneration of peripheral nerve Terminals. We have previously shown that nerve Terminals exposed to spider or snake presynaptic neurotoxins degenerate as a result of calcium overload and mitochondrial failure. Here we show that toxin-treated primary neurons release signaling molecules derived from mitochondria: hydrogen peroxide, mitochondrial DNA, and cytochrome c. These molecules activate isolated primary Schwann cells, Schwann cells cocultured with neurons and at neuromuscular junction in vivo through the MAPK pathway. We propose that this inter- and intracellular signaling is involved in triggering the regeneration of peripheral nerve Terminals affected by other forms of neurodegenerative diseases.
Wilkie A. Wilson - One of the best experts on this subject based on the ideXlab platform.
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Axon Terminal hyperexcitability associated with epileptogenesis in vitro. II. Pharmacological regulation by NMDA and GABAA receptors
Journal of neurophysiology, 1993Co-Authors: Steven F. Stasheff, David D. Mott, Wilkie A. WilsonAbstract:1. The preceding report presented evidence that the kindling-like induction of electrographic seizures (EGSs) in the hippocampal slice is accompanied by a lasting increase in the excitability of CA3 Axon Terminals, which is manifested by an increase in action-potential initiation at this site. In this report we explore the role of the N-methyl-D-aspartate (NMDA) receptor in the induction and maintenance of this antidromic firing, as well as the role of the gamma-aminobutyric acid type A (GABAA) receptor in regulating this activity once it has been induced. 2. Kindling-like stimulus trains (60 Hz, 2 s) were delivered to s. radiatum of CA3 at 10-min intervals. As EGSs developed in control artificial cerebrospinal fluid (ACSF), the frequency of Axon Terminal firing increased markedly (by 10.33 +/- 3.29 spikes/min, mean +/- SE P > 0.1). Thus the NMDA receptor is required for the induction but not maintenance of increased Axon Terminal firing, as we previously have shown to be the case for EGSs.(ABSTRACT TRUNCATED AT 250 WORDS)
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Axon Terminal hyperexcitability associated with epileptogenesis in vitro i origin of ectopic spikes
Journal of Neurophysiology, 1993Co-Authors: Steven F. Stasheff, M Hines, Wilkie A. WilsonAbstract:1. Intracellular and extracellular recording techniques were used to study the increase in ectopic (i.e., nonsomatic) action-potential generation occurring among CA3 pyramidal cells during the kind...
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Axon Terminal hyperexcitability seen in epileptogenesis in vitro
Ion channels, 1992Co-Authors: Steven F. Stasheff, Wilkie A. WilsonAbstract:In the study of epilepsy, a great deal of attention has been devoted to synaptic mechanisms of seizure induction and expression. Many efforts have focused on understanding changes in the balance between synpatic excitation and inhibition. For example, the application of a number of excitatory amino acids can evoke epileptiform activity (Lehman et al., 1987; McCaslin and Morgan, 1986;. Meldrum, 1986; Piredda and Gale, 1986; Turski et al., 1987a,b), and, conversely, antagonists of excitatory amino acid receptors can suppress seizures or seizurelike activity in some models (Czuczwar et al., 1985; Czuczwar and Meldrum, 1982; De Sarro et al., 1985; Heinemann et al., 1985; Lehman et al., 1987; McNamara et al., 1988; Meldrum, 1986; Sagratella et al., 1987; Traynelis and Dingledine, 1988; Turski et al., 1987a; Walther et al., 1986). Changes in responses to excitatory amino acids are associated with pathological neuroplasticity and accompany both in vivo kindling and similar in vitro stimulation models of epileptogenesis (Mody et al., 1988; Stelzer et al., ss1987). In addition to altering the receptor mediation of synaptic responses, excitation within a neural network may be increased by altering the frequency and probability of synaptic transmission. Thus, in the hippocampal slice, the application of convulsant drugs, disturbances in extracellular ion concentrations, and tetanic stimulation which leads to epileptiform activity can all result in a greater number of excitatory synaptic interactions between cells.
Mahmoud M Iravani - One of the best experts on this subject based on the ideXlab platform.
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comparison of somatodendritic and Axon Terminal dopamine release in the ventral tegmental area and the nucleus accumbens
Neuroscience, 1996Co-Authors: Mahmoud M Iravani, Richard Muscat, Zygmunt L KrukAbstract:Fast cyclic voltammetry at a carbon fibre microelectrode was used to measure dopamine release following electrical or chemical stimulation in rat brain slices incorporating either the ventral tegmental area or the core region of the nucleus accumbens. Electrical or chemical stimulation gave clear voltammetric signals which corresponded to dopamine; less dopamine was released in the ventral tegmental area than in the nucleus accumbens. In contrast to the nucleus accumbens, electrically stimulated dopamine release in the ventral tegmental area was not sensitive to tetrodotoxin, was not modified by the presence of dopamine uptake inhibitors, or agonist or blockers acting at dopamine D2 autoreceptors.
Michela Rigoni - One of the best experts on this subject based on the ideXlab platform.
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animal models for studying motor Axon Terminal paralysis and recovery
Journal of Neurochemistry, 2017Co-Authors: Michela Rigoni, Cesare MontecuccoAbstract:An extraordinary property of the peripheral nervous system is that nerve Terminals can regenerate after damage caused by different physical, chemical, or biological pathogens. Regeneration is the result of a complex and ill-known interplay among the nerve, the glia, the muscle, the basal lamina and, in some cases, the immune system. This phenomenon has been studied using different injury models mainly in rodents, particularly in mice, where a lesion can be produced in a chosen anatomical area. These approaches differ significantly among them for the nature of the lesion and the final outcomes. We have reviewed here the most common experimental models employed to induce motor Axon injury, the relative advantages and drawbacks, and the principal read-outs used to monitor the regenerative process. Recently introduced tools for inducing reversible damage to the motor Axon Terminal that overcome some of the drawbacks of the more classical approaches are also discussed. Animal models have provided precious information about the cellular components involved in the regenerative process and on its electrophysiological features. Methods and tools made available recently allow one to identify and study molecules that are involved in the crosstalk among the components of the endplate. The time-course of the intercellular signaling and of the intracellular pathways activated will draw a picture of the entire process of regeneration as seen from a privileged anatomical site of observation. This is an article for the special issue XVth International Symposium on Cholinergic Mechanisms.
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Mitochondrial alarmins released by degenerating motor Axon Terminals activate perisynaptic Schwann cells
Proceedings of the National Academy of Sciences of the United States of America, 2015Co-Authors: Elisa Duregotti, Samuele Negro, Michele Scorzeto, Irene Zornetta, Bryan C. Dickinson, Christopher J. Chang, Cesare Montecucco, Michela RigoniAbstract:An acute and highly reproducible motor Axon Terminal degeneration followed by complete regeneration is induced by some animal presynaptic neurotoxins, representing an appropriate and controlled system to dissect the molecular mechanisms underlying degeneration and regeneration of peripheral nerve Terminals. We have previously shown that nerve Terminals exposed to spider or snake presynaptic neurotoxins degenerate as a result of calcium overload and mitochondrial failure. Here we show that toxin-treated primary neurons release signaling molecules derived from mitochondria: hydrogen peroxide, mitochondrial DNA, and cytochrome c. These molecules activate isolated primary Schwann cells, Schwann cells cocultured with neurons and at neuromuscular junction in vivo through the MAPK pathway. We propose that this inter- and intracellular signaling is involved in triggering the regeneration of peripheral nerve Terminals affected by other forms of neurodegenerative diseases.