LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 10 of total 18

Search options

  1. Article: Oxytocin-secreting neurons: A physiological model of morphological neuronal and glial plasticity in the adult hypothalamus.

    Theodosis, Dionysia T

    Frontiers in neuroendocrinology

    2002  Volume 23, Issue 1, Page(s) 101–135

    Abstract: Oxytocin-secreting neurons of the hypothalamoneurohypophysial system undergo reversible morphological changes whenever they are strongly stimulated. In the hypothalamus, such structural plasticity is represented by modifications in the size and shape of ... ...

    Abstract Oxytocin-secreting neurons of the hypothalamoneurohypophysial system undergo reversible morphological changes whenever they are strongly stimulated. In the hypothalamus, such structural plasticity is represented by modifications in the size and shape of their somata and dendrites, in the extent to which their surfaces are covered by glia, and in the density of their synapses. In the neurohypophysis, there is a parallel reduction in glial (pituicyte) coverage of their axons together, with retraction of pituicyte processes from the perivascular basal lamina and an increase in the number and size of their terminals. These changes occur rapidly, within a few hours. On the other hand, the system returns to its prestimulated condition on arrest of stimulation at a rate that depends on the length of time it has remained activated. Such neuronal-glial changes have several functional consequences. In the hypothalamic nuclei, reduction in astrocytic coverage of oxytocinergic neurons and their synapses modifies extracellular ionic homeostasis and glutamate clearance and, therefore, their overall excitability. Since it results in extensive dendritic bundling, it may also lead to ephaptic interactions and may facilitate dendritic electrotonic coupling. A most important indirect effect may be to permit synaptic remodeling that occurs concomitantly and that results in significant increases in the number of excitatory and inhibitory synapses driving their activity. In the stimulated neurohypophysis, glial retraction results in increased levels of extracellular K+ which can enhance neurohormone release while an enlarged neurovascular contact zone may facilitate diffusion of neurohormone into the circulation. Ongoing work aims to unravel the cell mechanisms and factors underlying such plasticity and has revealed that neurons and glia of the hypothalamoneurohypophysial system continue to express juvenile molecular features associated with similar neuronglial interactions and synaptic events during development and regeneration. They include strong expression of cell surface adhesion molecules like F3/contactin and polysialylated neural cell adhesion molecule, extracellular matrix glycoproteins like tenascin C, and cytoskeletal proteins like vimentin and microtubule-associated protein 1D. Some of these molecules reach the cell surface constitutively while others follow the activity-dependent regulated pathway. We consider many of these molecular features permissive, allowing oxytocin neurons and their glia to undergo morphological remodeling throughout life, provided the proper stimulus intervenes. In the hypothalamic nuclei, one such stimulus is centrally released oxytocin; in the neurohypophysis, an adrenergic, cAMP-mediated mechanism appears responsible.
    MeSH term(s) Animals ; Humans ; Hypothalamus/cytology ; Hypothalamus/metabolism ; Neuroglia/metabolism ; Neuroglia/ultrastructure ; Neuronal Plasticity/physiology ; Neurons/metabolism ; Neurons/ultrastructure ; Oxytocin/secretion ; Synapses/physiology
    Chemical Substances Oxytocin (50-56-6)
    Language English
    Publishing date 2002-01
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 390985-2
    ISSN 1095-6808 ; 0091-3022 ; 0532-7466
    ISSN (online) 1095-6808
    ISSN 0091-3022 ; 0532-7466
    DOI 10.1006/frne.2001.0226
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  2. Article ; Online: Polysialic acid and activity-dependent synapse remodeling.

    Bonfanti, Luca / Theodosis, Dionysia T

    Cell adhesion & migration

    2009  Volume 3, Issue 1, Page(s) 43–50

    Abstract: Polysialic acid (PSA) is a large carbohydrate added post-translationally to the extracellular domain of the Neural Cell Adhesion Molecule (NCAM) that influences its adhesive and other functional properties. PSA-NCAM is widely distributed in the ... ...

    Abstract Polysialic acid (PSA) is a large carbohydrate added post-translationally to the extracellular domain of the Neural Cell Adhesion Molecule (NCAM) that influences its adhesive and other functional properties. PSA-NCAM is widely distributed in the developing nervous system where it promotes dynamic cell interactions, like those responsible for axonal growth, terminal sprouting and target innervation. Its expression becomes restricted in the adult nervous system where it is thought to contribute to various forms of neuronal and glial plasticity. We here review evidence, obtained mainly from hypothalamic neuroendocrine centers and the olfactory system, that it intervenes in structural synaptic plasticity and accompanying neuronal-glial transformations, making possible the formation and elimination of synapses that occur under particular physiological conditions. While the mechanism of action of this complex sugar is unknown, it is now clear that it is a necessary molecular component of various cell transformations, including those responsible for activity-dependent synaptic remodeling.
    MeSH term(s) Animals ; Axons/metabolism ; Humans ; Neural Cell Adhesion Molecule L1/chemistry ; Neural Cell Adhesion Molecule L1/metabolism ; Neuronal Plasticity ; Olfactory Pathways/metabolism ; Sialic Acids/chemistry ; Sialic Acids/metabolism ; Synapses/metabolism
    Chemical Substances Neural Cell Adhesion Molecule L1 ; Sialic Acids ; polysialic acid ; polysialyl neural cell adhesion molecule
    Language English
    Publishing date 2009-01-23
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2268518-2
    ISSN 1933-6926 ; 1933-6918
    ISSN (online) 1933-6926
    ISSN 1933-6918
    DOI 10.4161/cam.3.1.7258
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  3. Article: Activity-dependent structural and functional plasticity of astrocyte-neuron interactions.

    Theodosis, Dionysia T / Poulain, Dominique A / Oliet, Stéphane H R

    Physiological reviews

    2008  Volume 88, Issue 3, Page(s) 983–1008

    Abstract: Observations from different brain areas have established that the adult nervous system can undergo significant experience-related structural changes throughout life. Less familiar is the notion that morphological plasticity affects not only neurons but ... ...

    Abstract Observations from different brain areas have established that the adult nervous system can undergo significant experience-related structural changes throughout life. Less familiar is the notion that morphological plasticity affects not only neurons but glial cells as well. Yet there is abundant evidence showing that astrocytes, the most numerous cells in the mammalian brain, are highly mobile. Under physiological conditions as different as reproduction, sensory stimulation, and learning, they display a remarkable structural plasticity, particularly conspicuous at the level of their lamellate distal processes that normally ensheath all portions of neurons. Distal astrocytic processes can undergo morphological changes in a matter of minutes, a remodeling that modifies the geometry and diffusion properties of the extracellular space and relationships with adjacent neuronal elements, especially synapses. Astrocytes respond to neuronal activity via ion channels, neurotransmitter receptors, and transporters on their processes; they transmit information via release of neuroactive substances. Where astrocytic processes are mobile then, astrocytic-neuronal interactions become highly dynamic, a plasticity that has important functional consequences since it modifies extracellular ionic homeostasis, neurotransmission, gliotransmission, and ultimately neuronal function at the cellular and system levels. Although a complete picture of intervening cellular mechanisms is lacking, some have been identified, notably certain permissive molecular factors common to systems capable of remodeling (cell surface and extracellular matrix adhesion molecules, cytoskeletal proteins) and molecules that appear specific to each system (neuropeptides, neurotransmitters, steroids, growth factors) that trigger or reverse the morphological changes.
    MeSH term(s) Animals ; Astrocytes/physiology ; Cell Communication ; Cell Shape ; Humans ; Nervous System Diseases/pathology ; Nervous System Diseases/physiopathology ; Neuronal Plasticity ; Neurons/physiology ; Signal Transduction
    Language English
    Publishing date 2008-07
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 209902-0
    ISSN 1522-1210 ; 0031-9333
    ISSN (online) 1522-1210
    ISSN 0031-9333
    DOI 10.1152/physrev.00036.2007
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  4. Article ; Online: Kainate receptor-induced retrograde inhibition of glutamatergic transmission in vasopressin neurons.

    Bonfardin, Valérie D J / Theodosis, Dionysia T / Konnerth, Arthur / Oliet, Stéphane H R

    The Journal of neuroscience : the official journal of the Society for Neuroscience

    2012  Volume 32, Issue 4, Page(s) 1301–1310

    Abstract: Presynaptic kainate receptors (KARs) exert a modulatory action on transmitter release. We here report that applications of agonists of GluK1-containing KARs in the rat supraoptic nucleus has an opposite action on glutamatergic transmission according to ... ...

    Abstract Presynaptic kainate receptors (KARs) exert a modulatory action on transmitter release. We here report that applications of agonists of GluK1-containing KARs in the rat supraoptic nucleus has an opposite action on glutamatergic transmission according to the phenotype of the postsynaptic neuron. Whereas glutamate release was facilitated in oxytocin (OT) neurons, it was inhibited in vasopressin (VP) cells. Interestingly, an antagonist of GluK1-containing KARs caused an inhibition of glutamate release in both OT and VP neurons, revealing the existence of tonically activated presynaptic KARs that are positively coupled to transmitter release. We thus postulated that the inhibition of glutamate release observed with exogenous applications of GluK1 agonists on VP neurons could be indirect. In agreement with this hypothesis, we first showed that functional GluK1-containing KARs were present postsynaptically on VP neurons but not on OT cells. We next showed that the inhibitory effect induced by exogenous GluK1 receptor agonist was compromised when BAPTA was added in the recording pipette to buffer intracellular Ca2+ and block the release of a putative retrograde messenger. Under these conditions, GluK1-containing KAR agonist facilitates glutamatergic transmission in VP neurons in a manner similar to that observed for OT neurons and that resulted from the activation of presynaptic GluK1 receptors. GluK1-mediated inhibition of glutamate release in VP neurons was also blocked by a κ-opioid receptor antagonist. These findings suggest that activation of postsynaptic GluK1-containing KARs on VP neurons leads to the release of dynorphin, which in turn acts on presynaptic κ-opioid receptors to inhibit glutamate release.
    MeSH term(s) Animals ; Excitatory Postsynaptic Potentials/physiology ; Glutamic Acid/metabolism ; Male ; Neural Inhibition/physiology ; Neurons/metabolism ; Rats ; Rats, Wistar ; Receptors, Kainic Acid/physiology ; Synaptic Transmission/physiology ; Vasopressins/physiology
    Chemical Substances Gluk1 kainate receptor ; Receptors, Kainic Acid ; Vasopressins (11000-17-2) ; Glutamic Acid (3KX376GY7L)
    Language English
    Publishing date 2012-01-25
    Publishing country United States
    Document type Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 604637-x
    ISSN 1529-2401 ; 0270-6474
    ISSN (online) 1529-2401
    ISSN 0270-6474
    DOI 10.1523/JNEUROSCI.3017-11.2012
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  5. Article: Remodeling of astrocytes, a prerequisite for synapse turnover in the adult brain? Insights from the oxytocin system of the hypothalamus.

    Theodosis, Dionysia T / Trailin, Andrei / Poulain, Dominique A

    American journal of physiology. Regulatory, integrative and comparative physiology

    2006  Volume 290, Issue 5, Page(s) R1175–82

    Abstract: Neurons, including their synapses, are generally ensheathed by fine processes of astrocytes, but this glial coverage can be altered under different physiological conditions that modify neuronal activity. Changes in synaptic connectivity accompany ... ...

    Abstract Neurons, including their synapses, are generally ensheathed by fine processes of astrocytes, but this glial coverage can be altered under different physiological conditions that modify neuronal activity. Changes in synaptic connectivity accompany astrocytic transformations so that an increased number of synapses are associated with reduced astrocytic coverage of postsynaptic elements, whereas synaptic numbers are reduced on reestablishment of glial coverage. A system that exemplifies activity-dependent structural synaptic plasticity in the adult brain is the hypothalamo-neurohypophysial system, and in particular, its oxytocin component. Under strong, prolonged activation (parturition, lactation, chronic dehydration), extensive portions of somatic and dendritic surfaces of magnocellular oxytocin neurons are freed of intervening astrocytic processes and become directly juxtaposed. Concurrently, they are contacted by an increased number of inhibitory and excitatory synapses. Once stimulation is over, astrocytic processes again cover oxytocinergic surfaces and synaptic numbers return to baseline levels. Such observations indicate that glial ensheathment of neurons is of consequence to neuronal function, not only directly, for example by modifying synaptic transmission, but indirectly as well, by preparing neuronal surfaces for synapse turnover.
    MeSH term(s) Animals ; Astrocytes/physiology ; Brain/cytology ; Brain/physiology ; Brain Chemistry ; Humans ; Hypothalamus/physiology ; Neuronal Plasticity/physiology ; Oxytocin/physiology ; Synapses/physiology
    Chemical Substances Oxytocin (50-56-6)
    Language English
    Publishing date 2006-04-07
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 603839-6
    ISSN 1522-1490 ; 0363-6119
    ISSN (online) 1522-1490
    ISSN 0363-6119
    DOI 10.1152/ajpregu.00755.2005
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  6. Article ; Online: Glia-dependent switch of kainate receptor presynaptic action.

    Bonfardin, Valérie D J / Fossat, Pascal / Theodosis, Dionysia T / Oliet, Stéphane H R

    The Journal of neuroscience : the official journal of the Society for Neuroscience

    2010  Volume 30, Issue 3, Page(s) 985–995

    Abstract: Presynaptic kainate receptors (KARs) exert a modulatory action on transmitter release. This effect can be switched from facilitation to inhibition by an increased concentration of KAR agonists. We here report that activation of presynaptic GluK1- ... ...

    Abstract Presynaptic kainate receptors (KARs) exert a modulatory action on transmitter release. This effect can be switched from facilitation to inhibition by an increased concentration of KAR agonists. We here report that activation of presynaptic GluK1-containing KARs facilitates GABA release on oxytocin and vasopressin neurons in the supraoptic nucleus of the hypothalamus. Increase in ambient levels of glutamate associated with the physiological reduction of astrocytic coverage of oxytocin neurons in lactating rats switches this KAR-mediated facilitation to inhibition of GABAergic transmission. This effect was reproduced in both oxytocin and vasopressin neurons of virgin rats when glutamate transporters were blocked pharmacologically, thereby establishing that enhanced levels of extracellular glutamate induce the switch in KAR-mediated action. The facilitation of GABA release was inhibited with philanthotoxin, a Ca(2+)-permeable KAR antagonist, suggesting that this effect was associated with an ionotropic mode of action. Conversely, KAR-mediated inhibition was compromised in the presence of U73122, a phospholipase C inhibitor, in agreement with the involvement of a metabotropic pathway. We thus reveal that physiological astrocytic plasticity modifies the mode of action of presynaptic KARs, thereby inversing their coupling with GABA release.
    MeSH term(s) Animals ; Electric Stimulation/methods ; Excitatory Amino Acid Agonists/pharmacology ; Excitatory Amino Acid Antagonists/pharmacology ; Glutamic Acid/metabolism ; In Vitro Techniques ; Inhibitory Postsynaptic Potentials/drug effects ; Inhibitory Postsynaptic Potentials/physiology ; Kainic Acid/pharmacology ; Lysine/analogs & derivatives ; Lysine/metabolism ; Neuroglia/drug effects ; Neuroglia/physiology ; Neurons/cytology ; Patch-Clamp Techniques/methods ; Presynaptic Terminals/drug effects ; Presynaptic Terminals/metabolism ; Rats ; Rats, Wistar ; Receptors, Kainic Acid/agonists ; Receptors, Kainic Acid/antagonists & inhibitors ; Receptors, Kainic Acid/metabolism ; Suprachiasmatic Nucleus/cytology ; gamma-Aminobutyric Acid/metabolism
    Chemical Substances Excitatory Amino Acid Agonists ; Excitatory Amino Acid Antagonists ; Gluk1 kainate receptor ; Receptors, Kainic Acid ; Glutamic Acid (3KX376GY7L) ; gamma-Aminobutyric Acid (56-12-2) ; biocytin (G6D6147J22) ; Lysine (K3Z4F929H6) ; Kainic Acid (SIV03811UC)
    Language English
    Publishing date 2010-01-20
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 604637-x
    ISSN 1529-2401 ; 0270-6474
    ISSN (online) 1529-2401
    ISSN 0270-6474
    DOI 10.1523/JNEUROSCI.3389-09.2010
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  7. Article: Induction of rapid, activity-dependent neuronal-glial remodelling in the adult rat hypothalamus in vitro.

    Langle, Sarah L / Poulain, Dominique A / Theodosis, Dionysia T

    The European journal of neuroscience

    2003  Volume 18, Issue 1, Page(s) 206–214

    Abstract: The hypothalamic oxytocinergic system offers a remarkable model of morphological plasticity in the adult because its neurons and astrocytes undergo mutual remodelling in relation to differing physiological conditions. Among various factors involved in ... ...

    Abstract The hypothalamic oxytocinergic system offers a remarkable model of morphological plasticity in the adult because its neurons and astrocytes undergo mutual remodelling in relation to differing physiological conditions. Among various factors involved in such plasticity, oxytocin (OT) itself appears of primary importance as its central administration resulted in morphological changes similar to those brought on by physiological stimuli. In the present study, we applied OT on acute hypothalamic slices from adult rats that included the supraoptic nucleus. Using ultrastructural morphometric analyses, we found that it induced a significant reduction of astrocytic coverage of OT neurons, leaving their surfaces directly juxtaposed, to an extent similar to that detected in vivo under conditions like lactation. These neuronal-glial changes were rapid and reversible, occurring within a few hours, and specifically mediated via OT receptors. They were potentiated by oestrogen and depended on calcium mobilization and de novo protein synthesis. Moreover, they depended on concurrent neuronal activation brought on by hyperosmotic stimulation or blockade of inhibitory GABAergic neurotransmission; they were inhibited by blockade of glutamatergic receptors. Taken together, our observations show that intrahypothalamic release of OT affects not only neuronal activation of the OT system but its morphological plasticity as well. Moreover, the activity dependence of the OT-induced changes strongly suggests that astrocytes can sense the level of activity of adjacent neurons and/or afferent input and this can subsequently act as a signal to bring on the neuronal and glial conformational changes.
    MeSH term(s) Animals ; Calcium Signaling/drug effects ; Calcium Signaling/physiology ; Estrogens/pharmacology ; Female ; Hypothalamus/cytology ; Hypothalamus/physiology ; Immunohistochemistry ; In Vitro Techniques ; Microscopy, Electron ; Nerve Tissue Proteins/biosynthesis ; Neuroglia/physiology ; Neuroglia/ultrastructure ; Neuronal Plasticity/drug effects ; Neuronal Plasticity/physiology ; Neurons/physiology ; Neurons/ultrastructure ; Oxytocin/pharmacology ; Pregnancy ; Rats ; Rats, Wistar ; Supraoptic Nucleus/cytology ; Supraoptic Nucleus/drug effects ; Supraoptic Nucleus/physiology ; Synapses/drug effects ; Synapses/physiology
    Chemical Substances Estrogens ; Nerve Tissue Proteins ; Oxytocin (50-56-6)
    Language English
    Publishing date 2003-06-09
    Publishing country France
    Document type Journal Article
    ZDB-ID 645180-9
    ISSN 1460-9568 ; 0953-816X
    ISSN (online) 1460-9568
    ISSN 0953-816X
    DOI 10.1046/j.1460-9568.2003.02741.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  8. Article: Neuronal-glial remodeling: a structural basis for neuronal-glial interactions in the adult hypothalamus.

    Langle, Sarah L / Poulain, Dominique A / Theodosis, Dionysia T

    Journal of physiology, Paris

    2002  Volume 96, Issue 3-4, Page(s) 169–175

    Abstract: Increasing evidence is establishing that adult neurons and their associated glia can undergo state-dependent changes in their morphology and in consequence, in their relationships and functional interactions. A neuronal system that illustrates this kind ... ...

    Abstract Increasing evidence is establishing that adult neurons and their associated glia can undergo state-dependent changes in their morphology and in consequence, in their relationships and functional interactions. A neuronal system that illustrates this kind of neuronal-glial plasticity in an exemplary fashion is that responsible for the secretion of the neurohormone oxytocin (OT). As shown by comparative ultrastructural analysis, during physiological conditions like lactation and dehydration, which result in enhanced peripheral and central release of the peptide, astrocytic coverage of OT neurons is markedly reduced and their surfaces are left directly juxtaposed. Such reduced glial coverage is of consequence to neuronal activity since it modifies extracellular ionic homeostasis and glutamate neurotransmission. In addition, it is probably prerequisite to the synaptic remodeling that occurs concurrently, and results in an enhanced number of inhibitory (GABAergic) and excitatory (glutamatergic, noradrenergic) synapses, thus further affecting neuronal function. The neuronal-glial and synaptic changes occur rapidly, within a matter of hours, and are reversible with termination of stimulation. The adult OT system retains many juvenile molecular features that may allow such plasticity, including expression of cell adhesion molecules implicated in neuronal-glial interactions during development, like polysialylated NCAM, F3/contactin and its ligand, the matrix glycoprotein, tenascin-C. On the other hand, OT itself can induce the changes since in vivo (ventricular microinfusion) or in vitro (on acute hypothalamic slices) application leads to glial and neuronal transformations similar to those induced by physiological stimuli.
    MeSH term(s) Age Factors ; Animals ; Cell Communication/physiology ; Hypothalamus/cytology ; Hypothalamus/physiology ; Neuroglia/cytology ; Neuronal Plasticity/physiology ; Neurons/cytology
    Language English
    Publishing date 2002-11-25
    Publishing country France
    Document type Journal Article ; Review
    ZDB-ID 1141200-8
    ISSN 1769-7115 ; 0928-4257
    ISSN (online) 1769-7115
    ISSN 0928-4257
    DOI 10.1016/s0928-4257(02)00003-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  9. Article: Polysialic acid is required for active phases of morphological plasticity of neurosecretory axons and their glia.

    Monlezun, Stéphanie / Ouali, Saliha / Poulain, Dominique A / Theodosis, Dionysia T

    Molecular and cellular neurosciences

    2005  Volume 29, Issue 4, Page(s) 516–524

    Abstract: The morphology of axons and astrocytes in the neurohypophysis changes considerably during physiological stimulation, increasing neurovascular contact and facilitating neurosecretion. We here assessed the contribution of alpha2, 8-linked polysialic acid ( ... ...

    Abstract The morphology of axons and astrocytes in the neurohypophysis changes considerably during physiological stimulation, increasing neurovascular contact and facilitating neurosecretion. We here assessed the contribution of alpha2, 8-linked polysialic acid (PSA), which intervenes in axonal changes during development and covers all neurohypophysial axon and glial surfaces. Using an in vitro model, we first analyzed neurohypophysial ultrastructure under different conditions of plasticity. After 2 h incubation in hyperosmotic medium or with the beta-adrenergic agonist, isoprenaline, neurovascular contact significantly increased, due essentially to an enhanced number of terminals, and gliovascular contact decreased correspondingly. This morphology was maintained during 22 h exposure to isoprenaline and reversed 2 h after agonist washout. Removal of PSA from cell surfaces with endoneurominidase prevented stimulation-related induction and reversal of axon and glial changes but had no effect once remodeling had occurred. PSA, therefore, by promoting dynamic cell interactions, is necessary for plasticity of axons and their associated glia.
    MeSH term(s) Adrenergic beta-Agonists/pharmacology ; Animals ; Axons/metabolism ; Axons/secretion ; Axons/ultrastructure ; Blood-Brain Barrier/drug effects ; Blood-Brain Barrier/physiology ; Blood-Brain Barrier/ultrastructure ; Cell Communication/drug effects ; Cell Communication/physiology ; Cell Membrane/drug effects ; Cell Membrane/metabolism ; Endothelial Cells/physiology ; Endothelial Cells/ultrastructure ; Glycoside Hydrolases/pharmacology ; Hypertonic Solutions/pharmacology ; Intercellular Junctions/drug effects ; Intercellular Junctions/physiology ; Intercellular Junctions/ultrastructure ; Male ; Microscopy, Electron, Transmission ; Neuroglia/metabolism ; Neuroglia/ultrastructure ; Neuronal Plasticity/physiology ; Organ Culture Techniques ; Pituitary Gland, Posterior/metabolism ; Pituitary Gland, Posterior/secretion ; Pituitary Gland, Posterior/ultrastructure ; Rats ; Rats, Wistar ; Sialic Acids/metabolism ; Water-Electrolyte Balance/drug effects ; Water-Electrolyte Balance/physiology
    Chemical Substances Adrenergic beta-Agonists ; Hypertonic Solutions ; Sialic Acids ; polysialic acid ; Glycoside Hydrolases (EC 3.2.1.-) ; endo-alpha-sialidase (EC 3.2.1.129)
    Language English
    Publishing date 2005-08
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1046640-x
    ISSN 1095-9327 ; 1044-7431
    ISSN (online) 1095-9327
    ISSN 1044-7431
    DOI 10.1016/j.mcn.2005.04.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  10. Article: Glial modulation of synaptic transmission: Insights from the supraoptic nucleus of the hypothalamus.

    Oliet, Stéphane H R / Piet, Richard / Poulain, Dominique A / Theodosis, Dionysia T

    Glia

    2004  Volume 47, Issue 3, Page(s) 258–267

    Abstract: Astrocytes clear synaptically released glutamate from the extracellular space through high-affinity transporters present on their plasma membrane. By controlling the extracellular level of the main excitatory transmitter in the central nervous system, ... ...

    Abstract Astrocytes clear synaptically released glutamate from the extracellular space through high-affinity transporters present on their plasma membrane. By controlling the extracellular level of the main excitatory transmitter in the central nervous system, astrocytes thus contribute prominently to the regulation of overall cellular excitability and synaptic information processing. We recently investigated the influence of the glial environment on glutamatergic and GABAergic neurotransmission in the supraoptic nucleus of the rat hypothalamus under physiological conditions such as lactation that significantly reduce astrocytic coverage of its neurons. By performing electrophysiological analyses on this unique model of dynamic neuronal-glial interactions, we have been able to show that the fine astrocytic processes normally enwrapping synapses serve two important functions. First, they govern the level of activation of presynaptic metabotropic glutamate receptors on glutamatergic terminals, thereby regulating synaptic efficacy at excitatory synapses. Second, they act as a physical and functional barrier to diffusion in the extracellular space, limiting spillover of glutamate and other neuroactive substances and therefore contributing to the regulation of heterosynaptic transmission and intercellular communication.
    MeSH term(s) Animals ; Astrocytes/physiology ; Astrocytes/ultrastructure ; Cell Communication/physiology ; Extracellular Space/metabolism ; Glutamic Acid/metabolism ; Humans ; Receptors, Metabotropic Glutamate/metabolism ; Supraoptic Nucleus/physiology ; Supraoptic Nucleus/ultrastructure ; Synapses/physiology ; Synapses/ultrastructure ; Synaptic Transmission/physiology ; gamma-Aminobutyric Acid/metabolism
    Chemical Substances Receptors, Metabotropic Glutamate ; Glutamic Acid (3KX376GY7L) ; gamma-Aminobutyric Acid (56-12-2)
    Language English
    Publishing date 2004-06-17
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 639414-0
    ISSN 1098-1136 ; 0894-1491
    ISSN (online) 1098-1136
    ISSN 0894-1491
    DOI 10.1002/glia.20032
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

To top