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  • 1
    Online Resource
    Online Resource
    Temporal dependence of shifts in mu opioid receptor mobility at the cell surface after agonist binding observed by single-particle tracking
    Springer Science and Business Media LLC ; 2019
    In:  Scientific Reports Vol. 9, No. 1 ( 2019-05-13)
    Details
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 9, No. 1 ( 2019-05-13)
    Abstract: Agonist binding to the mu opioid receptor (MOR) results in conformational changes that allow recruitment of G-proteins, activation of downstream effectors and eventual desensitization and internalization, all of which could affect receptor mobility. The present study employed single particle tracking (SPT) of quantum dot labeled FLAG-tagged MORs to examine shifts in MOR mobility after agonist binding. FLAG-MORs on the plasma membrane were in both mobile and immobile states under basal conditions. Activation of FLAG-MORs with DAMGO caused an acute increase in the fraction of mobile MORs, and free portions of mobile tracks were partially dependent on interactions with G-proteins. In contrast, 10-minute exposure to DAMGO or morphine increased the fraction of immobile FLAG-MORs. While the decrease in mobility with prolonged DAMGO exposure corresponded to an increase in colocalization with clathrin, the increase in colocalization was present in both mobile and immobile FLAG-MORs. Thus, no single mobility state of the receptor accounted for colocalization with clathrin. These findings demonstrate that SPT can be used to track agonist-dependent changes in MOR mobility over time, but that the mobility states observed likely arise from a diverse set of interactions and will be most informative when examined in concert with particular downstream effectors.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    URL: Article
    DOI: 10.1038/s41598-019-43657-x
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2019
    detail.hit.zdb_id: 2615211-3
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  • 2
    Online Resource
    Online Resource
    Ventral tegmental area glutamate neurons mediate nonassociative consequences of stress
    Springer Science and Business Media LLC ; 2022
    In:  Molecular Psychiatry
    Details
    In: Molecular Psychiatry, Springer Science and Business Media LLC
    Type of Medium: Online Resource
    ISSN: 1359-4184 , 1476-5578
    URL: Article
    DOI: 10.1038/s41380-022-01858-3
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 1502531-7
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  • 3
    Online Resource
    Online Resource
    Separate GABA Afferents to Dopamine Neurons Mediate Acute Action of Opioids, Development of Tolerance, and Expression of Withdrawal
    Elsevier BV ; 2014
    In:  Neuron Vol. 82, No. 6 ( 2014-06), p. 1346-1356
    Details
    In: Neuron, Elsevier BV, Vol. 82, No. 6 ( 2014-06), p. 1346-1356
    Type of Medium: Online Resource
    ISSN: 0896-6273
    URL: Article
    DOI: 10.1016/j.neuron.2014.04.030
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2014
    detail.hit.zdb_id: 2001944-0
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    Ovarian Dependence for Pituitary Tumorigenesis in D2 Dopamine Receptor-Deficient Mice
    The Endocrine Society ; 2002
    In:  Endocrinology Vol. 143, No. 12 ( 2002-12), p. 4536-4543
    Details
    In: Endocrinology, The Endocrine Society, Vol. 143, No. 12 ( 2002-12), p. 4536-4543
    Type of Medium: Online Resource
    ISSN: 0013-7227 , 1945-7170
    URL: Article
    DOI: 10.1210/en.2002-220421
    Language: English
    Publisher: The Endocrine Society
    Publication Date: 2002
    detail.hit.zdb_id: 2011695-0
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  • 5
    Online Resource
    Online Resource
    Differential Regulation of Synaptic Inputs by Constitutively Released Endocannabinoids and Exogenous Cannabinoids
    Society for Neuroscience ; 2005
    In:  The Journal of Neuroscience Vol. 25, No. 42 ( 2005-10-19), p. 9746-9751
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 25, No. 42 ( 2005-10-19), p. 9746-9751
    Abstract: Endocannabinoid release from a single neuron has been shown to cause presynaptic inhibition of transmitter release at many different sites. Here, we demonstrate that hypothalamic proopiomelanocortin (POMC) neurons release endocannabinoids continuously under basal conditions, unlike other release sites at which endocannabinoid production must be stimulated. The basal endocannabinoid release selectively inhibited GABA release onto POMC neurons, although exogenous administration of cannabinoid agonists also inhibited glutamate release. The CB1 cannabinoid receptor antagonist AM 251 [ N -(piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1 H -pyrazole-3-carboxamide] blocked endocannabinoid-mediated inhibition of GABA release without affecting excitatory synaptic currents, whereas the CB1 receptor agonist WIN 55,212-2 [ R -(+)-(2,3-dihydro-5-methyl-3-[(4-morpholinyl)methyl]pyrol [1,2,3-de] -1,4-benzoxazin-6-yl)(1-naphthalenyl) methanone monomethanesulfonate] inhibited both inhibitory and excitatory synaptic currents in POMC neurons. These data demonstrate that endogenously released cannabinoids and exogenously applied CB1 receptor agonists can have markedly different effects on synaptic inputs. Furthermore, the data suggest a novel form of endocannabinoid-mediated retrograde inhibition, whereby the regulation of a subset of inputs requires either the removal of tonic presynaptic inhibition caused by endocannabinoids or the engagement of a mechanism that actively inhibits endocannabinoid production.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.2769-05.2005
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2005
    detail.hit.zdb_id: 1475274-8
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  • 6
    Online Resource
    Online Resource
    Proopiomelanocortin Expression in both GABA and Glutamate Neurons
    Society for Neuroscience ; 2009
    In:  The Journal of Neuroscience Vol. 29, No. 43 ( 2009-10-28), p. 13684-13690
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 29, No. 43 ( 2009-10-28), p. 13684-13690
    Abstract: Proopiomelanocortin (POMC) neurons have been intensively studied because of their essential role in regulating energy balance and body weight. Many effects of POMC neurons can be attributed to their release of cognate neuropeptides from secretory granules in axon terminals. However, these neurons also synaptically release non-peptide neurotransmitters. The aim of this study was to settle the controversy whether there are separate populations of POMC neurons that release GABA or glutamate. Transgenic mice expressing a red fluorescent protein [Discosoma red (DsRed)] driven by Pomc neuronal regulatory elements (POMC–DsRed) were crossed to mice that expressed green fluorescent protein (gfp) in GABAergic neurons (GAD67–gfp). Approximately 40% of POMC neurons in the arcuate nucleus of the double-transgenic mice expressed the GAD67–gfp transgene. In vitro neurotransmitter release was detected using whole-cell electrophysiologic recordings in cultured GAD67–gfp-positive and GAD67–gfp-negative POMC neurons that had formed recurrent synapses (autapses). Autapses from GAD67–gfp-positive neurons were uniformly GABAergic. In contrast, autapses from the GAD67–gfp-negative POMC neurons exclusively exhibited postsynaptic currents mediated by glutamate. Together, these results indicate that there are two subpopulations of POMC neurons in the arcuate nucleus differentiated by their amino acid neurotransmitter phenotype. Whole-cell voltage-clamp recordings from POMC neurons in live brain slices indicated that GABAergic and glutamatergic POMC neurons are under similar presynaptic and postsynaptic regulation, although the GABAergic POMC neurons are smaller and have higher input resistance. GABAergic and glutamatergic POMC neurons may mediate distinct aspects of POMC neuron function, including the regulation of energy homeostasis.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.3770-09.2009
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2009
    detail.hit.zdb_id: 1475274-8
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  • 7
    Online Resource
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    GABAergic Inputs to POMC Neurons Originating from the Dorsomedial Hypothalamus Are Regulated by Energy State
    Society for Neuroscience ; 2019
    In:  The Journal of Neuroscience Vol. 39, No. 33 ( 2019-08-14), p. 6449-6459
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 39, No. 33 ( 2019-08-14), p. 6449-6459
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.3193-18.2019
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2019
    detail.hit.zdb_id: 1475274-8
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  • 8
    Online Resource
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    Desensitization-resistant and -sensitive GPCR-mediated inhibition of GABA release occurs by Ca 2+ -dependent and -independent mechanisms at a hypothalamic synapse
    American Physiological Society ; 2016
    In:  Journal of Neurophysiology Vol. 115, No. 5 ( 2016-05-01), p. 2376-2388
    Details
    In: Journal of Neurophysiology, American Physiological Society, Vol. 115, No. 5 ( 2016-05-01), p. 2376-2388
    Abstract: Whereas the activation of Gα i/o -coupled receptors commonly results in postsynaptic responses that show acute desensitization, the presynaptic inhibition of transmitter release caused by many Gα i/o -coupled receptors is maintained during agonist exposure. However, an exception has been noted where GABA B receptor (GABA B R)-mediated inhibition of inhibitory postsynaptic currents (IPSCs) recorded in mouse proopiomelanocortin (POMC) neurons exhibit acute desensitization in ∼25% of experiments. To determine whether differential effector coupling confers sensitivity to desensitization, voltage-clamp recordings were made from POMC neurons to compare the mechanism by which μ-opioid receptors (MORs) and GABA B Rs inhibit transmitter release. Neither MOR- nor GABA B R-mediated inhibition of release relied on the activation of presynaptic K + channels. Both receptors maintained the ability to inhibit release in the absence of external Ca 2+ or in the presence of ionomycin-induced Ca 2+ influx, indicating that inhibition of release can occur through a Ca 2+ -independent mechanism. Replacing Ca 2+ with Sr 2+ to disrupt G-protein-mediated inhibition of release occurring directly at the release machinery did not alter MOR- or GABA B -mediated inhibition of IPSCs, suggesting that reductions in evoked release can occur through the inhibition of Ca 2+ channels. Additionally, both receptors inhibited evoked IPSCs in the presence of selective blockers of N- or P/Q-type Ca 2+ channels. Altogether, the results show that MORs and GABA B Rs can inhibit transmitter release through the inhibition of calcium influx and by direct actions at the release machinery. Furthermore, since both the desensitizing and nondesensitizing presynaptic receptors are similarly coupled, differential effector coupling is unlikely responsible for differential desensitization of the inhibition of release.
    Type of Medium: Online Resource
    ISSN: 0022-3077 , 1522-1598
    URL: Article
    DOI: 10.1152/jn.00535.2015
    RVK:
    XA 10000 ; XA 552555
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2016
    detail.hit.zdb_id: 80161-6
    detail.hit.zdb_id: 1467889-5
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  • 9
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    Online Resource
    Disruption of GABA or glutamate release from POMC neurons in the adult mouse does not affect metabolic end points
    American Physiological Society ; 2020
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 319, No. 5 ( 2020-11-01), p. R592-R601
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 319, No. 5 ( 2020-11-01), p. R592-R601
    Abstract: Proopiomelanocortin (POMC) neurons contribute to the regulation of many physiological processes; the majority of which have been attributed to the release of peptides produced from the POMC prohormone such as α-MSH, which plays key roles in food intake and metabolism. However, it is now clear that POMC neurons also release amino acid transmitters that likely contribute to the overall function of POMC cells. Recent work indicates that constitutive deletion of these transmitters can affect metabolic phenotypes, but also that the expression of GABAergic or glutamatergic markers changes throughout development. The goal of the present study was to determine whether the release of glutamate or GABA from POMC neurons in the adult mouse contributes notably to energy balance regulation. Disturbed release of glutamate or GABA specifically from POMC neurons in adult mice was achieved using a tamoxifen-inducible Cre construct ( Pomc-CreER T2 ) expressed in mice also carrying floxed versions of Slc17a6 (vGlut2) or Gad1 and Gad2, encoding the vesicular glutamate transporter type 2 and GAD67 and GAD65 proteins, respectively. All mice in the experiments received tamoxifen injections, but control mice lacked the tamoxifen-inducible Cre sequence. Body weight was unchanged in Gad1- and Gad2- or vGlut2-deleted female and male mice. Additionally, no significant differences in glucose tolerance or refeeding after an overnight fast were observed. These data collectively suggest that the release of GABA or glutamate from POMC neurons in adult mice does not significantly contribute to the metabolic parameters tested here. In light of prior work, the data also suggest that amino acid transmitter release from POMC cells may contribute to separate functions in the adult versus the developing mouse.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.00180.2020
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2020
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 10
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    Online Resource
    A Transgenic Marker for Newly Born Granule Cells in Dentate Gyrus
    Society for Neuroscience ; 2004
    In:  The Journal of Neuroscience Vol. 24, No. 13 ( 2004-03-31), p. 3251-3259
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 24, No. 13 ( 2004-03-31), p. 3251-3259
    Abstract: Neurogenesis in the dentate gyrus continues into adulthood, yet little is known about the function of newly born neurons or how they integrate into an existing network of mature neurons. We made transgenic mice that selectively and transiently express enhanced green fluorescent protein (EGFP) in newly born granule cells of the dentate gyrus under the transcriptional control of proopiomelanocortin (POMC) genomic sequences. Analysis of transgenic pedigrees with truncation or deletion mutations indicated that EGFP expression in the dentate gyrus required cryptic POMC promoter regions dispensable for arcuate hypothalamic or pituitary expression. Unlike arcuate neurons, dentate granule cells did not express the endogenous POMC gene. EGFP-positive neurons had immature properties, including short spineless dendrites and small action potentials. Colocalization with bromodeoxyuridine indicated that EGFP-labeled granule cells were ∼2 weeks postmitotic. EGFP-labeled cells expressed markers for immature granule cells but not the glial marker GFAP. The number of EGFP-labeled neurons declined with age and increased with exercise, paralleling neurogenesis. Our results indicate that POMC-EGFP marks immature granule cells and that adult-generated granule cells integrate quite slowly into the hippocampal circuitry.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.5173-03.2004
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2004
    detail.hit.zdb_id: 1475274-8
    SSG: 12
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