The Experts below are selected from a list of 12 Experts worldwide ranked by ideXlab platform

B M Salzberg - One of the best experts on this subject based on the ideXlab platform.

  • micromolar 4 aminopyridine enhances invasion of a vertebrate Neurosecretory Terminal arborization optical recording of action potential propagation using an ultrafast photodiode mosfet camera and a photodiode array
    The Journal of General Physiology, 1996
    Co-Authors: A L Obaid, B M Salzberg
    Abstract:

    Modulation of the amount of neuropeptide released from a Neurosecretory tissue may be achieved by different means. These include alterations in the quantity secreted from each active nerve Terminal or in the actual number of Terminals activated. From the vertebrate hypothalamus, magnocellular neurons project their axons as bundles of fibers through the median eminence and infundibular stalk to arborize extensively and terminate in the neurohypophysis, where the neurohypophysial peptides and proteins are released into the circulation by a Ca-dependent mechanism. Elevating [Ca2+]o increases the magnitude of an intrinsic optical change in the neurohypophysial Terminals that is intimately related to the quantity of neuropeptide released. Similarly, the addition of micromolar concentrations of 4-aminopyridine to the bathing solution enhances this change in large angle light scattering. However, we show here that, while these effects are superficially similar, they reflect different mechanisms of action. Evidence from intrinsic optical signals (light scattering) and extrinsic (potentiometric dye) absorption changes suggests that calcium increases the amount of neuropeptide released from each active Terminal in the classical manner, while 4-aminopyridine exerts its secretagogue action by enhancing the invasion of action potentials into the magno-cellular neuron's Terminal arborization, increasing the actual number of Terminals activated. Physiologically, electrical invasion of the complex Terminal arborization in the neurohypophysis may represent an extremely sensitive control point for modulation of peptide secretion. This would be especially effective in a neurohaemal organ like the posterior pituitary, where, in contrast with a collection of presynaptic Terminals, the precise location of release is less important than the quantity released.

A L Obaid - One of the best experts on this subject based on the ideXlab platform.

  • micromolar 4 aminopyridine enhances invasion of a vertebrate Neurosecretory Terminal arborization optical recording of action potential propagation using an ultrafast photodiode mosfet camera and a photodiode array
    The Journal of General Physiology, 1996
    Co-Authors: A L Obaid, B M Salzberg
    Abstract:

    Modulation of the amount of neuropeptide released from a Neurosecretory tissue may be achieved by different means. These include alterations in the quantity secreted from each active nerve Terminal or in the actual number of Terminals activated. From the vertebrate hypothalamus, magnocellular neurons project their axons as bundles of fibers through the median eminence and infundibular stalk to arborize extensively and terminate in the neurohypophysis, where the neurohypophysial peptides and proteins are released into the circulation by a Ca-dependent mechanism. Elevating [Ca2+]o increases the magnitude of an intrinsic optical change in the neurohypophysial Terminals that is intimately related to the quantity of neuropeptide released. Similarly, the addition of micromolar concentrations of 4-aminopyridine to the bathing solution enhances this change in large angle light scattering. However, we show here that, while these effects are superficially similar, they reflect different mechanisms of action. Evidence from intrinsic optical signals (light scattering) and extrinsic (potentiometric dye) absorption changes suggests that calcium increases the amount of neuropeptide released from each active Terminal in the classical manner, while 4-aminopyridine exerts its secretagogue action by enhancing the invasion of action potentials into the magno-cellular neuron's Terminal arborization, increasing the actual number of Terminals activated. Physiologically, electrical invasion of the complex Terminal arborization in the neurohypophysis may represent an extremely sensitive control point for modulation of peptide secretion. This would be especially effective in a neurohaemal organ like the posterior pituitary, where, in contrast with a collection of presynaptic Terminals, the precise location of release is less important than the quantity released.

Jessica C. Nelson - One of the best experts on this subject based on the ideXlab platform.

  • Development/Plasticity/Repair Serotonergic Neurosecretory Synapse Targeting Is Controlled by Netrin-Releasing Guidepost Neurons in
    2016
    Co-Authors: Caenorhabditis Elegans, Jessica C. Nelson, Daniel A. Colón-ramos
    Abstract:

    Neurosecretory release sites lack distinct postsynaptic partners, yet target to specific circuits. This targeting specificity regulates local release of neurotransmitters and modulation of adjacent circuits. How Neurosecretory release sites target to specific regions is not understood.Herewe identify amolecularmechanism that governs the spatial specificity of extrasynaptic Neurosecretory Terminal (ENT) formation in the serotonergic Neurosecretory–motor (NSM) neurons of Caenorhabditis elegans. We show that postembryonic arboriza-tion and Neurosecretory Terminal targeting of the C. elegansNSM neuron is dependent on the Netrin receptor UNC-40/DCC.We observe that UNC-40 localizes to specific Neurosecretory Terminals at the time of axon arbor formation. This localization is dependent on UNC-6/Netrin, which is expressed by nerve ring neurons that act as guideposts to instruct local arbor and release site formation.We find that both UNC-34/Enabled andMIG-10/Lamellipodin are required downstream of UNC-40 to link the sites of ENT formation to nascent axon arbor extensions. Our findings provide a molecular link between release site development and axon arborization and introduce a novel mechanism that governs the spatial specificity of serotonergic ENTs in vivo

  • Serotonergic Neurosecretory synapse targeting is controlled by netrin-releasing guidepost neurons in Caenorhabditis elegans.
    The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013
    Co-Authors: Jessica C. Nelson, Daniel A. Colón-ramos
    Abstract:

    Neurosecretory release sites lack distinct postsynaptic partners, yet target to specific circuits. This targeting specificity regulates local release of neurotransmitters and modulation of adjacent circuits. How Neurosecretory release sites target to specific regions is not understood. Here we identify a molecular mechanism that governs the spatial specificity of extrasynaptic Neurosecretory Terminal (ENT) formation in the serotonergic Neurosecretory-motor (NSM) neurons of Caenorhabditis elegans. We show that postembryonic arborization and Neurosecretory Terminal targeting of the C. elegans NSM neuron is dependent on the Netrin receptor UNC-40/DCC. We observe that UNC-40 localizes to specific Neurosecretory Terminals at the time of axon arbor formation. This localization is dependent on UNC-6/Netrin, which is expressed by nerve ring neurons that act as guideposts to instruct local arbor and release site formation. We find that both UNC-34/Enabled and MIG-10/Lamellipodin are required downstream of UNC-40 to link the sites of ENT formation to nascent axon arbor extensions. Our findings provide a molecular link between release site development and axon arborization and introduce a novel mechanism that governs the spatial specificity of serotonergic ENTs in vivo.

Daniel A. Colón-ramos - One of the best experts on this subject based on the ideXlab platform.

  • Development/Plasticity/Repair Serotonergic Neurosecretory Synapse Targeting Is Controlled by Netrin-Releasing Guidepost Neurons in
    2016
    Co-Authors: Caenorhabditis Elegans, Jessica C. Nelson, Daniel A. Colón-ramos
    Abstract:

    Neurosecretory release sites lack distinct postsynaptic partners, yet target to specific circuits. This targeting specificity regulates local release of neurotransmitters and modulation of adjacent circuits. How Neurosecretory release sites target to specific regions is not understood.Herewe identify amolecularmechanism that governs the spatial specificity of extrasynaptic Neurosecretory Terminal (ENT) formation in the serotonergic Neurosecretory–motor (NSM) neurons of Caenorhabditis elegans. We show that postembryonic arboriza-tion and Neurosecretory Terminal targeting of the C. elegansNSM neuron is dependent on the Netrin receptor UNC-40/DCC.We observe that UNC-40 localizes to specific Neurosecretory Terminals at the time of axon arbor formation. This localization is dependent on UNC-6/Netrin, which is expressed by nerve ring neurons that act as guideposts to instruct local arbor and release site formation.We find that both UNC-34/Enabled andMIG-10/Lamellipodin are required downstream of UNC-40 to link the sites of ENT formation to nascent axon arbor extensions. Our findings provide a molecular link between release site development and axon arborization and introduce a novel mechanism that governs the spatial specificity of serotonergic ENTs in vivo

Daniel A. Colón-ramos - One of the best experts on this subject based on the ideXlab platform.

  • Serotonergic Neurosecretory synapse targeting is controlled by netrin-releasing guidepost neurons in Caenorhabditis elegans.
    The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013
    Co-Authors: Jessica C. Nelson, Daniel A. Colón-ramos
    Abstract:

    Neurosecretory release sites lack distinct postsynaptic partners, yet target to specific circuits. This targeting specificity regulates local release of neurotransmitters and modulation of adjacent circuits. How Neurosecretory release sites target to specific regions is not understood. Here we identify a molecular mechanism that governs the spatial specificity of extrasynaptic Neurosecretory Terminal (ENT) formation in the serotonergic Neurosecretory-motor (NSM) neurons of Caenorhabditis elegans. We show that postembryonic arborization and Neurosecretory Terminal targeting of the C. elegans NSM neuron is dependent on the Netrin receptor UNC-40/DCC. We observe that UNC-40 localizes to specific Neurosecretory Terminals at the time of axon arbor formation. This localization is dependent on UNC-6/Netrin, which is expressed by nerve ring neurons that act as guideposts to instruct local arbor and release site formation. We find that both UNC-34/Enabled and MIG-10/Lamellipodin are required downstream of UNC-40 to link the sites of ENT formation to nascent axon arbor extensions. Our findings provide a molecular link between release site development and axon arborization and introduce a novel mechanism that governs the spatial specificity of serotonergic ENTs in vivo.