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Jørn Hounsgaard - One of the best experts on this subject based on the ideXlab platform.

  • Roles of ryanodine and inositol triphosphate receptors in regulation of Plateau Potentials in turtle spinal motoneurons
    Neuroscience, 2004
    Co-Authors: S Mejia-gervacio, Jørn Hounsgaard, Mauricio Díaz-muñoz
    Abstract:

    Generation of Plateau Potentials in spinal motoneurons depends on activation of voltage sensitive L-type Ca2+ channels. These channels are facilitated by metabotropic receptors known to promote release of Ca2+ from intracellular stores. The aim of this study is to determine if Ca2+-release receptors in the endoplasmic reticulum (ER) that are sensitive to ryanodine (RyRs) and to inositol triphosphate receptors (IP3Rs) contribute to the generation of Plateau Potentials. The effects of antagonists to RyRs, IP3Rs and phospholipase C (PLC) were tested on discharge patterns associated with Plateau Potentials in motoneurons in slices from the spinal cord of the turtle. Plateau-related discharge patterns, un-facilitated or facilitated by agonists for group I glutamate metabotropic receptors, muscarine-sensitive cholinergic receptors or L-type Ca2+ channels were inhibited by blockade of RyRs. In contrast, antagonists of IP3Rs or PLC preferentially inhibited Plateau-related discharge patterns when facilitated by activation of metabotropic receptors but in only half of the cells when promoted in the absence of metabotropic facilitators. Our findings show that RyRs and IP3Rs regulate the generation of Plateau Potentials in motoneurons and suggest that RyRs may be directly involved with activation of the Plateau potential.

  • Subcellular distribution of L-type Ca2+ channels responsible for Plateau Potentials in motoneurons from the lumbar spinal cord of the turtle.
    The European journal of neuroscience, 2003
    Co-Authors: Magda Simon, Jean-françois Perrier, Jørn Hounsgaard
    Abstract:

    L-type calcium channels mediate the persistent inward current underlying Plateau Potentials in spinal motoneurons. Electrophysiological analysis shows that Plateau Potentials are generated by a persistent inward current mediated by low threshold L-type calcium channels located in the dendrites. As motoneurons express L-type calcium channels of the CaV1.2 and CaV1.3 subtypes, we have investigated the subcellular distribution of these channels using antibody labelling. The Plateau generating a persistent inward current is modulated by the activation of metabotropic receptors. For this reason, we also examined the relationship between CaV1.2 and CaV1.3 subunits in motoneurons and presynaptic terminals labelled with antibodies against synapsin 1a. Motoneurons in the spinal cord of the adult turtle were identified as large neurons, immunopositive for choline acetyltransferase, located in the ventral horn. In these neurons, CaV1.2 subunits were present in the cell bodies and axons. Patches of CaV1.3 subunits were seen in association with the cell membrane of the somata and both the proximal and distal dendrites. Double labelling with an antibody against synapsin 1a showed that CaV1.3 subunits, but not CaV1.2 subunits, were always located at synaptic sites. The distribution of CaV1.2 and CaV1.3 strongly suggests that the persistent inward current underlying Plateau Potentials in spinal motoneurons is mediated by CaV1.3 and not by CaV1.2. Our findings also show that CaV1.3 may be located in the somatic and dendritic membrane adjacent to particular presynaptic terminals.

  • Mechanisms causing Plateau Potentials in spinal motoneurones.
    Advances in experimental medicine and biology, 2002
    Co-Authors: Aidas Alaburda, Jean-françois Perrier, Jørn Hounsgaard
    Abstract:

    Plateau Potentials are generated by a voltage sensitive persistent inward current. In spinal motoneurones this current is predominantly mediated by influx of Ca2+ through L-type Ca2+ channels of the Ca(v)1.3 subtype. Depolarisation-induced facilitation of L-type Ca2+ channels is thought to be the mechanism for delayed activation (wind-up and warm-up) of the Plateau potential and for the hysteresis in firing frequency and I-V relation during triangular depolarisation. L-type Ca2+ channels and Plateau Potentials in spinal motoneurones are facilitated by activation of metabotropic receptors for glutamate, acetylcholine, noradrenaline and serotonin and down regulated by activation of GABA(B) receptors. The facilitation has been shown to depend on activated calmodulin.

  • Facilitation of Plateau Potentials in turtle motoneurones by a pathway dependent on calcium and calmodulin.
    The Journal of Physiology, 2000
    Co-Authors: Jean-françois Perrier, Sheyla Mejia-gervacio, Jørn Hounsgaard
    Abstract:

    1. The involvement of intracellular calcium and calmodulin in the modulation of Plateau Potentials in motoneurones was investigated using intracellular recordings from a spinal cord slice preparation. 2. Chelation of intracellular calcium with BAPTA-AM or inactivation of calmodulin with W-7 or trifluoperazine reduced the amplitude of depolarization-induced Plateau Potentials. Inactivation of calmodulin also inhibited facilitation of Plateau Potentials by activation of group I metabotropic glutamate receptors or muscarinic receptors. 3. In low-sodium medium and in the presence of tetraethylammonium and tetrodotoxin, calcium action Potentials evoked by depolarization were followed by a short hyperpolarization ascribed to the calcium-activated non-selective cationic current (ICAN) and by a dihydropyridine-sensitive afterdepolarization. The amplitude of the afterdepolarization depended on the number of calcium spikes and was mediated by L-type calcium channels. 4. The dihydropyridine-sensitive afterdepolarization induced by calcium spikes was reduced by blockade of calmodulin. 5. It is proposed that Plateau Potentials in spinal motoneurones are facilitated by activation of a calcium-calmodulin-dependent pathway.

  • Local facilitation of Plateau Potentials in dendrites of turtle motoneurones by synaptic activation of metabotropic receptors
    The Journal of Physiology, 1999
    Co-Authors: Rodolfo Delgado-lezama, Jean-françois Perrier, Jørn Hounsgaard
    Abstract:

    1 The spatial distribution of synaptic facilitation of Plateau Potentials in dendrites of motoneurones was investigated in transverse sections of the spinal cord of the turtle using differential polarization by applied electric fields. 2 The excitability of motoneurones in response to depolarizing current pulses was increased following brief activation of either the dorsolateral funiculus (DLF) or the medial funiculus (MF) even when synaptic Potentials were eliminated by antagonists of ionotropic receptors. 3 The medial and lateral compartments of motoneurones were differentially polarized by the electric field generated by passing current between two electrodes on either side of the preparation. In one direction of the field lateral dendrites were depolarized while the cell body and medial dendrites were hyperpolarized (S- configuration). With current in the opposite direction the cell body and medial dendrites were depolarized while lateral dendrites were hyperpolarized (S+ configuration). 4 Following brief activation of the DLF the excitability and the generation of Plateau Potentials were facilitated during differential depolarization of the lateral dendrites but not during differential depolarization of the cell body and medial dendrites. Following brief activation of the MF the excitability and generation of Plateau Potentials were facilitated during differential depolarization of the cell body and medial dendrites but not during differential depolarization of the lateral dendrites. 5 It is concluded that the synaptic facilitation of the dihydropyridine-sensitive response to depolarization is compartmentalized in turtle motoneurones.

David W Tank - One of the best experts on this subject based on the ideXlab platform.

Charles W. Bourque - One of the best experts on this subject based on the ideXlab platform.

  • Autocrine feedback inhibition of Plateau Potentials terminates phasic bursts in magnocellular neurosecretory cells of the rat supraoptic nucleus
    The Journal of Physiology, 2004
    Co-Authors: Colin H. Brown, Charles W. Bourque
    Abstract:

    Phasic activity in magnocellular neurosecretory cells is characterized by alternating periods of activity (bursts) and silence. During phasic bursts, action Potentials are superimposed on Plateau Potentials that are generated by summation of depolarizing after-Potentials. Dynorphin is copackaged in vasopressin neurosecretory vesicles that are exocytosed from magnocellular neurosecretory cell dendrites and terminals, and both peptides have been implicated in the generation of phasic activity. Here we show that somato-dendritic dynorphin release terminates phasic bursts by autocrine inhibition of Plateau Potentials in magnocellular neurosecretory cells recorded intracellularly from hypothalamic explants using sharp electrodes. Conditioning spike trains caused an activity-dependent reduction of depolarizing after-potential amplitude that was partially reversed by α-latrotoxin (which depletes neurosecretory vesicles) and by nor-binaltorphimine (κ-opioid receptor antagonist), but not by an oxytocin/vasopressin receptor antagonist or a μ-opioid receptor antagonist, indicating that activity-dependent inhibition of depolarizing after-Potentials requires exocytosis of an endogenous κ-opioid peptide. κ-Opioid inhibition of depolarizing after-Potentials was not mediated by actions on evoked after-hyperpolarizations since these were not affected by κ-opioid receptor agonists or antagonists. Evoked bursts were prolonged by antagonism of κ-opioid receptors with nor-binaltorphimine and by depletion of neurosecretory vesicles by α-latrotoxin, becoming everlasting in ∼50% of cells. Finally, spontaneously active neurones exposed to nor-binaltorphimine switched from phasic to continuous firing as Plateau Potentials became non-inactivating. Thus, dynorphin coreleased with vasopressin generates phasic activity through activity-dependent feedback inhibition of Plateau Potentials in magnocellular neurosecretory cells.

  • Autocrine feedback inhibition of Plateau Potentials terminates phasic bursts in magnocellular neurosecretory cells of the rat supraoptic nucleus.
    The Journal of physiology, 2004
    Co-Authors: Colin H. Brown, Charles W. Bourque
    Abstract:

    Phasic activity in magnocellular neurosecretory cells is characterized by alternating periods of activity (bursts) and silence. During phasic bursts, action Potentials are superimposed on Plateau Potentials that are generated by summation of depolarizing after-Potentials. Dynorphin is copackaged in vasopressin neurosecretory vesicles that are exocytosed from magnocellular neurosecretory cell dendrites and terminals, and both peptides have been implicated in the generation of phasic activity. Here we show that somato-dendritic dynorphin release terminates phasic bursts by autocrine inhibition of Plateau Potentials in magnocellular neurosecretory cells recorded intracellularly from hypothalamic explants using sharp electrodes. Conditioning spike trains caused an activity-dependent reduction of depolarizing after-potential amplitude that was partially reversed by alpha-latrotoxin (which depletes neurosecretory vesicles) and by nor-binaltorphimine (kappa-opioid receptor antagonist), but not by an oxytocin/vasopressin receptor antagonist or a micro-opioid receptor antagonist, indicating that activity-dependent inhibition of depolarizing after-Potentials requires exocytosis of an endogenous kappa-opioid peptide. kappa-Opioid inhibition of depolarizing after-Potentials was not mediated by actions on evoked after-hyperpolarizations since these were not affected by kappa-opioid receptor agonists or antagonists. Evoked bursts were prolonged by antagonism of kappa-opioid receptors with nor-binaltorphimine and by depletion of neurosecretory vesicles by alpha-latrotoxin, becoming everlasting in approximately 50% of cells. Finally, spontaneously active neurones exposed to nor-binaltorphimine switched from phasic to continuous firing as Plateau Potentials became non-inactivating. Thus, dynorphin coreleased with vasopressin generates phasic activity through activity-dependent feedback inhibition of Plateau Potentials in magnocellular neurosecretory cells.

David J. Bennett - One of the best experts on this subject based on the ideXlab platform.

Ole Kiehn - One of the best experts on this subject based on the ideXlab platform.