The Experts below are selected from a list of 4473 Experts worldwide ranked by ideXlab platform
Jeff W. Lichtman - One of the best experts on this subject based on the ideXlab platform.
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Multispectral labeling technique to map many neighboring axonal projections in the same tissue
Nature Methods, 2015Co-Authors: Shlomo Tsuriel, Sagi Gudes, Ryan W Draft, Alexander M Binshtok, Jeff W. LichtmanAbstract:We describe a method to map the location of axonal arbors of many individual neurons simultaneously via the spectral properties of retrogradely transported dye-labeled vesicles. We inject overlapping regions of an axon target area with three or more different colored retrograde tracers. On the basis of the combinations and intensities of the colors in the individual vesicles transported to neuronal somata, we calculate the projection sites of each neuron's axon. This neuronal positioning system (NPS) enables mapping of many axons in a simple automated way. In our experiments, NPS combined with spectral (Brainbow) labeling of the input to Autonomic Ganglion cells showed that the locations of Ganglion cell projections to a mouse salivary gland related to the identities of their preGanglionic axonal innervation. NPS could also delineate projections of many axons simultaneously in the mouse central nervous system. The topography of axonal projections can be deciphered by retrograde labeling with multiple overlapping dye injections, as the dye composition in retrogradely transported vesicles is indicative of axonal projection sites.
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Synaptic dynamism measured over minutes to months: age-dependent decline in an Autonomic Ganglion
Nature Neuroscience, 2003Co-Authors: Wen-biao Gan, Elaine Kwon, Guoping Feng, Joshua R Sanes, Jeff W. LichtmanAbstract:Naturally occurring rearrangements of synaptic terminals are common in the nervous systems of young mammals, but little is known about their incidence in adults. Using transgenic mice that express yellow fluorescent protein (YFP) in axons, we repeatedly imaged nerve terminals in the parasympathetic submandibular Ganglion. We found that the pattern of synaptic branches underwent significant rearrangements over several weeks in young adult mice. In older mice, rearrangements were less common, and synaptic patterns on individual neurons were recognizable for many months to years. Axonal branches frequently retracted or extended on a time scale of minutes in young adult mice, but seldom in mature animals. These results provide direct evidence for a decrease in plasticity of interneuronal connections as animals make the transition from young adulthood to middle age. The long-term stability of synaptic patterns could provide a structural basis for the persistence of memory in the adult nervous system.
Sheree M. Johnson - One of the best experts on this subject based on the ideXlab platform.
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Autonomic Ganglion cells: likely source of acetylcholine in the rat carotid body.
Advances in experimental medicine and biology, 2003Co-Authors: Estelle B. Gauda, Reed Cooper, Sheree M. JohnsonAbstract:Peripheral arterial chemoreceptors are essential to respiratory and cardiac homeostasis. Although the components of these chemoreceptors lie within a tiny structure, the carotid body, the physiological affects resulting from activation of the peripheral arterial chemoreceptors have profound effects on arousal responses and cardiorespiratory responses to hypoxia and asphyxia (Gonzalez et αl., 1994). In response to hypoxia, hypercapnia and acidosis the glomus cell within the arterial chemoreceptor depolarizes; intracellular calcium levels rises, and neurotransmitters are released. These neurotransmitters bind to autoreceptors on the glomus cell and postsynaptic receptors on the carotid sinus nerve. Binding of neurotransmitters to autoreceptors on glomus cells regulates further neurotransmitter release, while binding to postsynaptic receptors on chemoafferent nerve fibers results in electrical output through the carotid sinus nerve (for reviews, see Gonzalezet al., 1994; Prabhakar 1994).
Sandra A. Farrell - One of the best experts on this subject based on the ideXlab platform.
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Mutations in **FAM134B**, encoding a newly identified Golgi protein, cause severe sensory and Autonomic neuropathy
Nature genetics, 2009Co-Authors: Ingo Kurth, Torsten Pamminger, J. Christopher Hennings, Désirée Soehendra, Antje K. Huebner, Annelies Rotthier, Jonathan Baets, Jan Senderek, Haluk Topaloglu, Sandra A. FarrellAbstract:Hereditary sensory and Autonomic neuropathy type II (HSAN II) leads to severe mutilations because of impaired nociception and Autonomic dysfunction. Here we show that loss-of-function mutations in FAM134B, encoding a newly identified cis-Golgi protein, cause HSAN II. Fam134b knockdown results in structural alterations of the cis-Golgi compartment and induces apoptosis in some primary dorsal root Ganglion neurons. This implicates FAM134B as critical in long-term survival of nociceptive and Autonomic Ganglion neurons.
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mutations in fam134b encoding a newly identified golgi protein cause severe sensory and Autonomic neuropathy
Nature Genetics, 2009Co-Authors: Ingo Kurth, Torsten Pamminger, Désirée Soehendra, Antje K. Huebner, Annelies Rotthier, Jonathan Baets, Jan Senderek, Haluk Topaloglu, Christopher J Hennings, Sandra A. FarrellAbstract:Ingo Kurth and Christian Hubner report the identification of loss-of-function mutations in FAM134B, which encodes a novel cis-Golgi protein, in hereditary sensory and Autonomic neuropathy type II. Hereditary sensory and Autonomic neuropathy type II (HSAN II) leads to severe mutilations because of impaired nociception and Autonomic dysfunction. Here we show that loss-of-function mutations in FAM134B, encoding a newly identified cis-Golgi protein, cause HSAN II. Fam134b knockdown results in structural alterations of the cis-Golgi compartment and induces apoptosis in some primary dorsal root Ganglion neurons. This implicates FAM134B as critical in long-term survival of nociceptive and Autonomic Ganglion neurons.
Radan Čapek - One of the best experts on this subject based on the ideXlab platform.
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The pharmacology of the nicotinic antagonist, chlorisondamine, investigated in rat brain and Autonomic Ganglion
British Journal of Pharmacology, 1994Co-Authors: Paul B. S. Clarke, H. El‐bizri, Maryka Quik, B.a. Esplin, Patricia Boksa, Isabelle Chaudieu, Radan ČapekAbstract:1. A single administration of the Ganglion blocker, chlorisondamine (10 mg kg-1, s.c.) is known to produce a quasi-irreversible blockade of the central actions of nicotine in the rat. The mechanism of this persistent action is not known. It is also unclear whether chlorisondamine can block neuronal responses to excitatory amino acids and whether chronic blockade of nicotinic responses also occurs in the periphery. 2. Acute administration of chlorisondamine (10 mg kg-1, s.c.) to rats resulted in a blockade of central nicotinic effects (ataxia and prostration) when tested 1 to 14 days later, but caused no detectable cell death in tissue sections sampled throughout the rostrocaudal extent of the brain which were stained in order to reveal neuronal degeneration. 3. Long-term blockade of central nicotinic effects by chlorisondamine was not associated with significant alterations in the density (Bmax) of high-affinity [3H]-nicotine binding to forebrain cryostat-cut sections. 4. In cultured dissociated mesencephalic cells of the foetal rat, chlorisondamine and mecamylamine inhibited [3H]-dopamine release evoked by N-methyl-D-aspartate (NMDA, 10(-4) M), but only at high concentrations (IC50 approx. 600 and 70 microM, respectively). A high concentration of chlorisondamine (10(-3) M) had no effect on responses to quisqualate (10(-5) M) and only slightly reduced responses to kainate (10(-4) M). Mecamylamine (10(-3) M) was ineffective against both agonists. 5. In adult rat hippocampal slices, chlorisondamine depressed NMDA receptor-mediated synaptically-evoked field potentials, but again only at high concentrations (10(-4)-10(-3) M). Synaptic responses that were mediated by non-NMDA excitatory amino acid receptors were less affected.(ABSTRACT TRUNCATED AT 250 WORDS)
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The pharmacology of the nicotinic antagonist, chlorisondamine, investigated in rat brain and Autonomic Ganglion
British Journal of Pharmacology, 1994Co-Authors: Paul B. S. Clarke, H. El‐bizri, Maryka Quik, B.a. Esplin, Patricia Boksa, Isabelle Chaudieu, Radan ČapekAbstract:1. A single administration of the Ganglion blocker, chlorisondamine (10 mg kg-1, s.c.) is known to produce a quasi-irreversible blockade of the central actions of nicotine in the rat. The mechanism of this persistent action is not known. It is also unclear whether chlorisondamine can block neuronal responses to excitatory amino acids and whether chronic blockade of nicotinic responses also occurs in the periphery. 2. Acute administration of chlorisondamine (10 mg kg-1, s.c.) to rats resulted in a blockade of central nicotinic effects (ataxia and prostration) when tested 1 to 14 days later, but caused no detectable cell death in tissue sections sampled throughout the rostrocaudal extent of the brain which were stained in order to reveal neuronal degeneration. 3. Long-term blockade of central nicotinic effects by chlorisondamine was not associated with significant alterations in the density (Bmax) of high-affinity [3H]-nicotine binding to forebrain cryostat-cut sections. 4. In cultured dissociated mesencephalic cells of the foetal rat, chlorisondamine and mecamylamine inhibited [3H]-dopamine release evoked by N-methyl-D-aspartate (NMDA, 10(-4) M), but only at high concentrations (IC50 approx. 600 and 70 microM, respectively). A high concentration of chlorisondamine (10(-3) M) had no effect on responses to quisqualate (10(-5) M) and only slightly reduced responses to kainate (10(-4) M). Mecamylamine (10(-3) M) was ineffective against both agonists. 5. In adult rat hippocampal slices, chlorisondamine depressed NMDA receptor-mediated synaptically-evoked field potentials, but again only at high concentrations (10(-4)-10(-3) M). Synaptic responses that were mediated by non-NMDA excitatory amino acid receptors were less affected.(ABSTRACT TRUNCATED AT 250 WORDS)
Estelle B. Gauda - One of the best experts on this subject based on the ideXlab platform.
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Autonomic Ganglion cells: likely source of acetylcholine in the rat carotid body.
Advances in experimental medicine and biology, 2003Co-Authors: Estelle B. Gauda, Reed Cooper, Sheree M. JohnsonAbstract:Peripheral arterial chemoreceptors are essential to respiratory and cardiac homeostasis. Although the components of these chemoreceptors lie within a tiny structure, the carotid body, the physiological affects resulting from activation of the peripheral arterial chemoreceptors have profound effects on arousal responses and cardiorespiratory responses to hypoxia and asphyxia (Gonzalez et αl., 1994). In response to hypoxia, hypercapnia and acidosis the glomus cell within the arterial chemoreceptor depolarizes; intracellular calcium levels rises, and neurotransmitters are released. These neurotransmitters bind to autoreceptors on the glomus cell and postsynaptic receptors on the carotid sinus nerve. Binding of neurotransmitters to autoreceptors on glomus cells regulates further neurotransmitter release, while binding to postsynaptic receptors on chemoafferent nerve fibers results in electrical output through the carotid sinus nerve (for reviews, see Gonzalezet al., 1994; Prabhakar 1994).
