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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00004713naa a2200385 4500
001oai:DiVA.org:liu-162197
003SwePub
008191122s2008 | |||||||||||000 ||eng|
024a https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-1621972 URI
024a https://doi.org/10.1523/JNEUROSCI.1654-08.20082 DOI
040 a (SwePub)liu
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Pantazis, Antonios,d 1982-u Department of Physiology, Development, and Neuroscience, University of Cambridge, Cambridge CB2 3DY, United Kingdom4 aut0 (Swepub:liu)antpa45
2451 0a Distinct Roles for Two Histamine Receptors (hclA and hclB) at the Drosophila Photoreceptor Synapse
264 1b Society for Neuroscience,c 2008
338 a print2 rdacarrier
520 a Histamine (HA) is the photoreceptor neurotransmitter in arthropods, directly gating chloride channels on large monopolar cells (LMCs), postsynaptic to photoreceptors in the lamina. Two histamine-gated channel genes that could contribute to this channel in Drosophila are hclA (also known as ort) and hclB (also known as hisCl1), both encoding novel members of the Cys-loop receptor superfamily. Drosophila S2 cells transfected with these genes expressed both homomeric and heteromeric histamine-gated chloride channels. The electrophysiological properties of these channels were compared with those from isolated Drosophila LMCs. HCLA homomers had nearly identical HA sensitivity to the native receptors (EC50 = 25 ÎŒm). Single-channel analysis revealed further close similarity in terms of single-channel kinetics and subconductance states (~25, 40, and 60 pS, the latter strongly voltage dependent). In contrast, HCLB homomers and heteromeric receptors were more sensitive to HA (EC50 = 14 and 1.2 ÎŒm, respectively), with much smaller single-channel conductances (~4 pS). Null mutations of hclA (ortUS6096) abolished the synaptic transients in the electroretinograms (ERGs). Surprisingly, the ERG “on” transients in hclB mutants transients were approximately twofold enhanced, whereas intracellular recordings from their LMCs revealed altered responses with slower kinetics. However, HCLB expression within the lamina, assessed by both a GFP (green fluorescent protein) reporter gene strategy and mRNA tagging, was exclusively localized to the glia cells, whereas HCLA expression was confirmed in the LMCs. Our results suggest that the native receptor at the LMC synapse is an HCLA homomer, whereas HCLB signaling via the lamina glia plays a previously unrecognized role in shaping the LMC postsynaptic response.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Neurovetenskaper0 (SwePub)301052 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Neurosciences0 (SwePub)301052 hsv//eng
700a Segaran, Ashvinau Department of Physiology, Development, and Neuroscience, University of Cambridge, Cambridge CB2 3DY, United Kingdom4 aut
700a Liu, Che-Hsiungu Department of Physiology, Development, and Neuroscience, University of Cambridge, Cambridge CB2 3DY, United Kingdom4 aut
700a Nikolaev, Antonu Department of Biomedical Science, University of Sheffield, Sheffield S10 2TN, United Kingdom4 aut
700a Rister, Jensu Lehrstuhl für Genetik und Neurobiologie, Universität Würzburg, 97074 Würzburg, Germany4 aut
700a Thum, Andreas S.u Lehrstuhl für Genetik und Neurobiologie, Universität Würzburg, 97074 Würzburg, Germany4 aut
700a Roeder, Thomasu Zoologisches Institut, Abteilung Zoophysiologie, Christian-Albrechts-Universität, D-24098 Kiel, Germany4 aut
700a Semenov, Eugeneu Department of Molecular Neurobiology, Drosophila Neurogenetics Laboratory, Institute of Molecular Biology, Bulgarian Academy of Sciences, Sofia 1113, Bulgaria4 aut
700a Juusola, Mikkou Department of Biomedical Science, University of Sheffield, Sheffield S10 2TN, United Kingdom4 aut
700a Hardie, Roger C.u Department of Physiology, Development, and Neuroscience, University of Cambridge, Cambridge CB2 3DY, United Kingdom4 aut
710a Department of Physiology, Development, and Neuroscience, University of Cambridge, Cambridge CB2 3DY, United Kingdomb Department of Biomedical Science, University of Sheffield, Sheffield S10 2TN, United Kingdom4 org
773t Journal of Neuroscienced : Society for Neuroscienceg 28:29, s. 7250-7259q 28:29<7250-7259x 0270-6474x 1529-2401
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-162197
8564 8u https://doi.org/10.1523/JNEUROSCI.1654-08.2008

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