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Dissertations / Theses on the topic 'Gap junctions'

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Author: Grafiati

Published: 4 June 2021

Last updated: 10 March 2023

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1

Sheela, Thomas Vinaya. "Regulation of Connexin40 Gap Junctions." Digital Archive @ GSU, 2008. http://digitalarchive.gsu.edu/biology_diss/55.

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Gap junctions provide direct electrical and biochemical communication between cardiomyocytes in the heart. Connexin40 (Cx40) is the major connexin in the atria of the heart and little is known regarding its regulation. Thus, the goal was to investigate the regulation of Cx40 in both physiological and pathophysiological conditions. The first objective of this thesis was to determine whether Cx40 gap junctions were regulated by â-adrenergic receptor activation. Cx40 has previously been shown to be acutely activated by cAMP, this cAMP-induced increase in Cx40-mediated cell-to-cell dye transfer has been shown to be effected through the â-adrenergic receptor-adenylyl cyclase- Protein Kinase A (PKA) pathway in Cx40-transfected HeLa cells. The second objective of this thesis was to determine whether Cx40 gap junctions were regulated by intracellular Ca2+ concentration ([Ca2+]i ). [Ca2+]i was increased by addition of the ionophore ionomycin and elevating extracellular calcium [Ca2+]o from 1.8 mM to 21.8 mM. This resulted in an elevation of [Ca2+]i and effected an inhibition of Cx40-mediated cell-to-cell dye transfer (IC50 of 500 ± 0.72 nM) which was Calmodulin-dependent. The third objective of this thesis was to determine whether Cx40 gap junctions were regulated by ischemia. Inducing ischemia chemically by inhibiting the electron transport chain with sodium cyanide and glycolysis with iodoacetate and 2-deoxyglucose effected an inhibition of Cx40-mediated cell-to-cell dye transfer that was shown to be Calmodulin dependent. The main conclusions of this thesis were: (1) â-adrenergic receptor activation increases Cx40-mediated cell-to-cell dye transfer which requires the activation of PKA; (2) A sustained elevation in [Ca2+]i causes a partial inhibition of Cx40 gap junction-mediated cell-to-cell dye transfer which was Ca2+-and Calmodulin dependent; (3) Chemical ischemia causes a partial inhibition of Cx40 gap junction-mediated cell-to-cell dye transfer which was shown to be Calmodulin-dependent.

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2

Carolan, E. J. "Gap junctions in lymphocyte ontogeny." Thesis, University of Glasgow, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233181.

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3

Nishimura, Tamiko. "Gap junctions in early human placental development." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/MQ63198.pdf.

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4

Ko, Yu-Shien. "Connexin heterogeneity in vascular cell gap junctions." Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.393781.

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5

Pintsch, Monika. "Cx37 abhängige Calciumsignalausbreitung durch myoendotheliale Gap Junctions." Diss., Ludwig-Maximilians-Universität München, 2015. http://nbn-resolving.de/urn:nbn:de:bvb:19-182614.

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Eine effektive Regulation der Gewebedurchblutung erfordert eine Koordination der Reaktion einzelner Gefäßzellen bzw. verschiedener Gefäßabschnitte. Der zur Koordination erforderliche interzelluläre Signalaustausch kann zumindest teilweise über Gap Junction-Kanäle erfolgen, die als interzelluläre Verbindungen den Austausch von elektrischen und chemischen Signalstoffen zwischen benachbarten Zellen ermöglichen. Dieser Austausch kann über die Modulation der Permeabilität von Gap Junction-Kanälen reguliert werden. Aus Untersuchungen an Modellzellen (HeLA-Zellen) war bereits bekannt dass NO eine solche Modulatorwirkung ausübt, wenn die Gap Junctions nur Connexin 37 (Cx37) enthalten während kein Effekt von NO auf Gap Junctions zu beobachtet war, wenn Gap Junctions aus Cx43 oder Cx40 gebildet wurden. Da Endothelzellen normalerweise alle drei Connexine exprimieren, sollte in der vorliegenden Arbeit untersucht werden, inwieweit NO in diesen Zellen überhaupt eine nachweisbare Wirkung auf die Gap Junction Permeabilität und damit auf den Signalaustausch entfaltet. Als Modell des Signalaustauschs wurde die Ausbreitung von Calciumwellen jeweils zwischen Endothelzellen oder glatten Muskelzellen allein oder zwischen beiden Zelltypen untersucht. Nach Auslösung von interzellulären Calciumwellen als Folge einer mechanischen Stimulation von einzelnen Zellen konnte zunächst gezeigt werden, dass die interzelluläre Ausbreitung von Calcium unter den gewählten Versuchsbedingungen über Gap Junctions-erfolgte. Im Gegensatz zum Modellsystem der HeLa Zellen, in denen nur Cx37 exprimiert war, zeigte NO in den Endothelzellen (humane Nabelschnur, alle drei Connexine exprimiert) abgesehen von einer geringradigen Verzögerung keinen Hemmeffekt auf die Gap Junction-abhängige Ausbreitung von Calcium-Signalen. Wurde jedoch Cx43 durch Behandlung mit siRNA herunterreguliert, führte NO auch in den Endothelzellen zu einer Hemmung der interzellulären Calciumwellenausbreitung. Auch in intakten Endothelzellen, die mit glatten Muskelzellen kokultiviert wurden, ließ sich bei genauerer Analyse ein Hemmeffekt von NO nachweisen. Dieser war jedoch auf die Zellbereiche beschränkt, in denen Endothelzellen und glatte Muskelzellen unmittelbar benachbart waren (myoendotheliale Junctions). In diesen myoendo-thelialen Gap Junctions, fanden wir auf der Endothelseite immunhistochemisch überwiegend Cx37 exprimiert. Aufgrund dieser präferentiellen Lokalisation von Cx37 scheint daher NO eine besondere Rolle bei der Modulation des Calciumaustauschs (und potentiell auch anderer Signalmoleküle wie IP3 oder cyclische Nukleotide) zu spielen. Die Kontrolle des Calciumaustauschs könnte funktionell eine calciumabhängige glattmuskuläre Kontraktion bei Endothelstimulation verhindern und somit die endothelabhängige Dilatation verstärken. Diese bisher unbekannte NO-Wirkung auf Cx37-exprimierende Gap Junctions könnte einen weiteren Mechanismus der Gefäßtonusregulation darstellen.

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6

Rahman, Salman. "Biochemical and immunological studies on gap junctions." Thesis, University College London (University of London), 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266786.

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7

Kalapothakis, Evanguedes. "Expression and biomolecular assembly of gap junctions." Thesis, Open University, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.332822.

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8

Calkins, Travis L. "Gap Junctions in the Mosquito, Aedes aegypti." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu149217328492135.

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9

Gakhar, Gunjan. "Role of gap junctions in breast cancer." Diss., Manhattan, Kan. : Kansas State University, 2009. http://hdl.handle.net/2097/2228.

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10

Moore, Lisa Karen. "Regulation of gap junctions in vascular smooth muscle." Diss., The University of Arizona, 1993. http://hdl.handle.net/10150/186240.

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Gap junctions form low resistance pathways between neighboring cells and thereby provide for coordination of tissue function. In vascular smooth muscle these channels are believed to be important in maintenance of and coordination of changes in vessel tone. In this study we demonstrate that vascular smooth muscle cells from vessels of different origin and species differ in the connexin protein expressed as well as in the size of the channel formed by these proteins. We have shown that pig coronary and rat mesentery express mRNA for Cx43 and exhibit a single channel conductance of 60 or 80 pS respectively. We have determined the A7r5 express Cx40 in the form of a 70 pS channel and Cx43 as 108 and 141 pS channel. And finally we show that human coronary appear to express Cx40 exclusively, yet have two channel sizes with conductances of 52 and 104 pS. We further demonstrate that the effect of oleic acid (OA), the predominant fatty acid found in the cell membrane differs in its effect on the A7r5 vs. heart cells. The A7r5 cells responded with a rapid uncoupling to ∼50% at low dose, and did not further uncouple with increasing concentrations. Single channel analysis suggests the 70 pS channel was very sensitive to OA. The 140 pS channel appeared to be insensitive to OA. Lastly, we examined the effect of the monoamine, serotonin on gap junctions from vessel beds known to differ in their regulation. Junctional conductance and dye-coupling was increased on both long- and short-term exposure to 1,5, or 10 μM doses in all cell types. In the pig coronary cells and the rat mesentery, no change in unitary conductance was observed. The relative frequencies of the channel populations were shifted in both the A7r5 and the human coronary cells. These data support the conclusion that multiple strategies exist for gap junction regulation.

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11

Heyman, Nathanael Stanlee. "Selectivity of Connexin43 and Connexin40 Comprised Gap Junctions." Diss., The University of Arizona, 2007. http://hdl.handle.net/10150/196060.

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Gap junctions are aggregates of intercellular channels each formed of protein subunits termed connexins (Cx). Recently published data show that junctional dye permeability relative to conductance (permselectivity) varies across several orders of magnitude for Cx43 junctions, suggesting variable selectivity of the comprising Cx43 channels. Logical candidates for this variable selectivity are variability in charge or size selectivity. Consequently, junctional charge and size selectivities were determined in the current study by simultaneous measurement of junctional permeance to dyes of differing size or charge.The results show that for a number of dyes differing in size, charge, chemical composition, and structure the primary determinant for selectivity through Cx43 gap junctions was the size of the dye permeant with this selectivity showing essentially no variability beyond that seen between incompletely divided cells, presumably representing the variability inherent to the measurement. As such, selectivity of dye-permeable Cx43 channels is well described by the physical dimensions of the channel pore acting essentially as a simple molecular sieve. The seemingly disparate dye selectivity and permselectivity results can be reconciled by the variable presence of a dye-impermeable but electrically conductive channel conformation for Cx43 channels, affording a possible mechanism for independent regulation of diffusion of larger molecules versus electrical conductance to smaller ions.Cx40 junctions, known to be cation selective, also showed minimal variability in charge selectivity indicating that Cx40 charge selectivity is also an essentially fixed parameter. Co-expression of Cx40 and Cx43 lead to charge selectivities ranging from Cx43 to Cx40 with an average intermediate between the two. Activation of PKC leads to an increase in cationic selectivity of Cx40/Cx43 composed junctions by specifically reducing permeability through non-selective Cx43 channels favoring permeation through cation-selective Cx40 channels, allowing for junctional charge selectivity regulation.The combined data suggest that selectivity properties for dye permeable channels composed of Cx43 or Cx40 are essentially fixed parameters of the channel pore. Only upon co-expression of these connexins is significant variability in selectivity seen. The differential effects of PKC-mediated phosphorylation on permeability of Cx43 and Cx40 channels then allows for regulation of junctional charge selectivity but only in cells expressing both connexins.

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12

Harfst, Elizabeth. "A biochemical and immunological study of cardiac gap junctions." Thesis, Imperial College London, 1990. http://hdl.handle.net/10044/1/46332.

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13

Doble, Bradley Wayne. "Cardiac gap junctions, a target of growth factor signaling." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ57507.pdf.

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14

Thomas-Brown, Terri Petrese. "Natural Retinoid Modulation of Epiderman gap junctions and differentiation." DigitalCommons@Robert W. Woodruff Library, Atlanta University Center, 1987. http://digitalcommons.auctr.edu/dissertations/1185.

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Modulation of mouse epidermal gap junctions and differentiation in response to a natural retinoid, retinyl palmitate (RP), was evaluated. This is the first report of gap junction isolation and partial protein characterization from normal or retinoid-treated epidermis. Adult male Swiss Webster mice received parenteral injections of 13,750 International Units (IU) of RP for 12 days. Skin specimens were excised and analyzed by transmission electron microscopy (TEM) for morphologic changes in gap junctions and the epidermis. Gap junction proteins were isolated by discontinuous sucrose gradient centrifugation, following suspension in sodium bicarbonate buffer and, subsequent, solubilization in sarkosyl. Samples were analyzed by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE). Verification of the reliability of the epidermal gap junction isolation procedure was ascertained in corollary liver studies using the standard protocol. Each isolation step was monitored by TEM. The ultrastructural results revealed an increase in the number of gap junctions in retinoid-treated epidermal specimens. Keratinization and keratinocyte differentiation were inhibited as reflected in. a decrease in the number of tonofilaments in keratinocytes and the subsequent suppression of stratum corneum formation. Analyses of isolated epidermal gap junction proteins by SDS-PAGE indicate four distinct bands ranging in molecular weight of 30-20 kilodaltons. Retinyl palmitate-treated samples are distinguished by enhanced gel profiles. Isolated epidermal connexin has a relative molecular weight of 30,000 daltons in samples from both treated and control specimens. The data suggest a positive role of gap junctions in retinoid-directed metabolic cooperation in the regulation of epidermal differentiation. These studies will form the basis for further investigations to determine if the intercellularly exchanged molecules, retinoids,induce requisite molecular alterations in gap junctions during epidermal differentiation. An understanding will be gained of the independent and/or collaborative mechanism(s) of action of retinoids and gap junctions in epithelia.

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15

Tearle, Adam William. "Structural and functional aspects of gap junctions in invertebrates." Thesis, University of Sussex, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.395011.

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16

Wang, Chiuhui Mary. "The role of gap junctions in diabetic wound healing." Thesis, University College London (University of London), 2008. http://discovery.ucl.ac.uk/1446186/.

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The process of wound healing is slow in diabetes, often resulting in infection or chronic wounds that can lead to amputation. Cell-cell communication through the gap junction protein connexin 43 (Cx43) and the dynamic regulation of Cx43 expression play pivotal roles in the wound healing process. Acute streptozotocin-induced diabetes in rats altered connexin expression in uninjured back skin, decreasing Cx26, Cx30 and Cx43 protein and gap junctional communication in the epidermis and increasing Cx43 protein and communication in the dermis. Diabetes was also found to alter the dynamic changes of connexins associated with the wound healing response. Within 24 hours, Cx43 was upregulated in a thickened bulb of keratinocytes at the wound edge (rather than downregulated, as in controls which formed a thin process of migratory cells). Cx43 protein reduction was delayed until 48 hours when re-epithelialisation then began. Although Cx26 protein was upregulated as usual in diabetes, its distribution at the wound edge was abnormal, being more widespread. Preventing the abnormal upregulation of Cx43 expression in wound edge keratinocytes with Cx43 specific antisense oligodeoxynucleotides doubled the rate of re-epithelialisation to control levels and above. Other subsequent events of wound healing including the inflammatory response and granulation tissue maturation were also greatly improved. These results imply that diabetes-induced changes in connexin expression dynamics contribute to delayed wound healing and that targeting Cx43 expression is of potential therapeutic value in diabetic wound healing. A pilot study showed that Cx43 plays a role in the early activation of endothelial cells during inflammation. The data in this thesis provide further evidence for the central roles of connexins in the homeostasis of skin and response to injury. In particular, its role in the coordination of inflammatory response can have a pivotal impact on the quality of cutaneous wound repair.

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17

Lazzaro, Massimo. "Potential involvement of gap junctions in pathology of addiction." Doctoral thesis, Università di Catania, 2013. http://hdl.handle.net/10761/1341.

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Cocaine abuse represents a huge social problem for the widespread in the world and for the many health risks associated. Moreover, a significative percentage of cocaine users develop an addiction with loss of control on drug intake. Several molecular modifications occurs with cocaine use, some of which seem occur only in addicted individuals. Gap junctions (GJs) allow cellular communication, indeed they are fundamental to regulate cellular synchronization, cellular growth and metabolic coordination in tissues. We analyzed the role of GJs proteins in the cocaine s mechanism of action and furthermore we verified the potential role of GJs in addiction. Our experiments show several modifications occurring at early and after prolonged cocaine exposure. In addition are shown differential alterations depending by addiction-like behaviour in animals, suggesting a potential involvement of GJs in transition to addiction.

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18

Li, Wing-man Michelle, and 李穎雯. "Gap junction regulates the blood-testis barrier dynamics during spermatogenesis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45450225.

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19

Butkevich, Eugenia. "Submembrane cytoskeleton-regulated assembly and functional activity of gap junctions." Doctoral thesis, [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=972736174.

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20

Edwards, Jill Carole. "Gap junctions and connexin expression in the mouse inner ear." Thesis, University College London (University of London), 2004. http://discovery.ucl.ac.uk/1446883/.

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Gap junctions are sites of direct communication between adjacent cells where clusters of channels in the membrane of one cell contact clusters of channels in the membrane of the neighbouring cell. Six constituent proteins, known as connexins (Cx), make up each hemi-channel. The channels allow the passage of small metabolites (up to 1200 Daltons in size), ions, and second messengers between cells, coupling them both electrically and chemically. This provides a means for signalling between the cells that enables co-ordinated activity of cells in a tissue and may permit one cell to trigger a response in its neighbour. Mutations of several connexin genes have been associated with deafness and the inner ear is richly endowed with gap junctions. A review of freeze fracture replicas, obtained from various species, illustrates the unusually large size and number of gap junction plaques throughout cells of the inner ear. A comprehensive analysis of the gap junctions and connexin expression in the inner ear has been performed. Using a variety of techniques these communication channels have been observed and their constituent protein isoforms characterised. Initial screening of cochlear and vestibular tissue with rt-PCR primers established which connexin isoforms might be present; immunohistochemical follow-up with an array of antibodies enabled spatial and temporal localisation of the proteins. It has been established that Cx26 and Cx30 are the major isoforms expressed in mature inner ear whilst isofoms Cx31, Cx43, Cx45 and Cx50 play a role in development of the cochlea. Isoforms Cx26 and Cx30 appear to be co-localised within the same junctional plaques and may form heteromeric gap junctions unique to the inner ear.

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21

Bani-Yaghoub, Mahmud. "The role of gap junctions in neuronal and astroglial differentiation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0013/NQ42495.pdf.

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22

Eloff, Benjamin Charles. "ROLE OF GAP JUNCTIONS IN THE GENESIS OF CARDIAC ARRHYTHMIAS." Case Western Reserve University School of Graduate Studies / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=case1106579517.

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23

Hinley, Jennifer Susan. "Cx32 gap junctions in human urothelial barrier generation and restitution." Thesis, University of York, 2015. http://etheses.whiterose.ac.uk/13003/.

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The ability of the urothelium to act as a urinary barrier is afforded by two key features: 1) It has the tightest barrier function of any epithelium, generated by tight junctions which assemble upon differentiation; 2) In response to damage, the quiescent urothelium can rapidly switch to a regenerative phenotype to enable regeneration and restitution of barrier function. Central to repair is the ability for the urothelium to sense damage; a process hypothesised to involve cell-cell communication. Direct cell-cell communication occurs through gap junctions, channels comprising connexin (Cx) proteins which allow for the passage of signalling molecules. Cxs have been linked to wound healing, as well as to maintenance of polarity and homeostasis in other epithelia, by both communication-dependent and independent mechanisms. A systematic characterisation of Cx expression has not been performed in urothelium and the significance of specific Cxs to urothelial physiology is not understood. This study aimed to investigate whether specific Cx proteins contribute to the regulation of barrier maintenance and restitution in human urothelium. Analysis of Cx transcripts identified Cx32, which was expressed in situ and highly induced upon in vitro differentiation of normal human urothelial (NHU) cells using two independent methods. In differentiated NHU cells, Cx32 proteins assembled into functional gap junction channels at cell borders, co-localising with the barrier defining tight junction proteins occludin and ZO-2. shRNA studies demonstrated that normal tight junction development and barrier function were dependent on the presence of intercellular Cx32, but not gap junction communication. In wound-healing experiments, intercellular communication through Cx32 channels inhibited urothelial cell migration and proliferation, in a process which involved suppression of activated SMAD3. Together the evidence presented here supports an unanticipated central role for Cx32 in orchestrating the homeostasis between barrier function and repair in human urothelium.

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24

Holzbecher, André Jörg. "Function of interneuronal gap junctions in hippocampal sharp wave-ripples." Doctoral thesis, Humboldt-Universität zu Berlin, 2018. http://dx.doi.org/10.18452/19364.

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Eine einzigartige experimentelle Beobachtung, welche die Basis für eine ganzheitliche, neurowissentschafliche Theorie für Gedächtnis darstellen könnte, sind sharp wave-ripples (SWRs). SWRs werden in lokalen Neuronennetzwerken erzeugt und sind wichtig für Gedächtniskonsolidierung; SWRs sind charakteristische Ereignisse der lokalen Feldpotentiale im Hippocampus des Säugetiers, die in Phasen von Schlaf und Ruhe vorkommen. Eine SWR besteht aus einer sharp wave, einer ≈ 100 ms langen Auslenkung des Feldpotentials, welche mit ripples, 110–250 Hz Oszillationen, überlagert ist. Jüngste Experimente bekräftigen die Theorie, dass ripples in Netzwerken inhibitorischer Interneurone (INT-INT) erzeugt werden, die aus parvalbumin-positive basket cells (PV+BCs) bestehen. PV+BCs sind untereinander über rekurrente inhibitorische Synapsen und Gap Junctions (GJs) gekoppelt. In dieser Arbeit untersuche ich die spezifische Funktion von interneuronalen Gap Junctions in ripples. Im Hauptteil dieser Arbeit demonstriere ich, dass GJs in INT-INT Netzwerken die neuronale Synchronität und die Feuerrate während ripples erhöhen, die ripple-Frequenz sich hingegen nur leicht verändert. Zusätzlich zeige ich, dass diese rippleunterstützenden Effekte nur dann auftreten, wenn die GJ-Transmission schnell genug ist (≈< 0.5 ms), was wiederum somanahe Kopplung voraussetzt (≈< 100 µm). Darüber hinaus zeige ich, dass GJs die oszillatorische Stärke der ripples erhöhen und so die minimale für ripples notwendige Netzwerkgröße verringern. Abschließend zeige ich, dass ausschließlich mit Gap Junctions gekoppelte INT-INT Netzwerke zwar mit ripple Frequenz oszillieren können, aber wahrscheinlich nicht der Erzeuger von experimentell beobachteten ripple-artigen Oszillationen sind. Zusammengenommen zeigen meine Resultate, dass schnelle Gap Junction-Kopplung von Interneuronen die Entstehung von ripples begünstigt und somit SWRs unterstützt, welche einen wichtigen Beitrag zur Bildung unserers Gedächtnisses leisten.
A unique experimental observation that opens ways for a holistic, bottom-up theory for memory generation are sharp-wave ripples (SWRs). SWRs are generated in local neuronal networks and are important for memory consolidation. SWRs are prominent features of the extracellular field potentials in the mammalian hippocampus that occur during rest and sleep; they are characterized by sharp waves, ≈ 100 ms long voltage deflections, that are accompanied by ripples, i.e., 110–250 Hz oscillations. Recent experiments support the view that ripples are clocked by recurrent networks of inhibitory interneurons (INT-INT), which are likely constituted by networks of parvalbumin-positive basket cells (PV+BCs). PV+BCs are not only recurrently coupled by inhibition but also by gap junctions (GJs). In this thesis, I investigate the specific function of interneuronal GJs in hippocampal ripples. Consequently, I simulate INT-INT networks and demonstrate that gap junctions increase the neuronal synchrony and firing rates during ripple oscillations, while the ripple frequency is only affected mildly. I further show that GJs only have these supporting effects on ripples when they are sufficiently fast (≈< 0.5 ms), which requires proximal GJ coupling (≈< 100 µm). Additionally, I find that gap junctions increase the oscillatory power of ripple oscillations and by this means reduce the minimal network size required for INT-INT networks to generate ripple oscillations. Finally, I demonstrate that exclusively GJ-coupled INT-INT networks can oscillate at ripple frequency, however, are unlikely the generator of experimentally observed ripple-like oscillations. In sum, my results show that fast interneuronal gap junction coupling promotes the emergence of ripples and hereby supports SWRs, which are important for the formation of memory.

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25

Neef, Martin. "Expression der Connexine 40, 43 und 45 unter chronischer Stimulation durch Insulin und die Wachstumsfaktoren IGF-1, VEGF, TGF-β und FGF-2 bei neonatalen Rattenkardiomyozyten." Doctoral thesis, Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-209143.

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Gap Junctions als wichtigste Elemente der Zelle zur Ermöglichung einer interzellulären Kommunikation erlauben eine koordinierte Antwort auf externe und interne Stimuli und somit ein Zusammenspiel von Zellgruppen und Organen im Gesamtorganismus. In der vorliegenden Arbeit wurde der Einfluss einer mittelfristigen und chronischen Stimulation neonataler Rattenkardiomyozyten durch Insulin und den Wachstumsfaktoren Insulin-like Growth Factor-1 (IGF-1), Vascular Endothelial Growth Factor (VEGF), Transforming Growth Factor-β (TGF-β) und Fibroblast Growth Factor-2 (FGF-2) auf die Expression der Connexine 40, 43 und 45 untersucht. Dabei zeigte sich unter der Insulin-Stimulation eine konzentrationsabhängige Regulation der Connexin 43 (Cx43) Expression. Die Exposition gegenüber IGF-1 hatte einen signifikanten Anstieg der Cx43 Proteinmenge zur Folge. Unter 24stündiger VEGF- oder FGF-2-Stimulation fand sich dagegen diesbezüglich kein relevanter Unterschied. Die Analysen nach langfristiger Exposition gegebenüber TGF-β zeigten eine signifikante Abnahme der Cx43 Proteinmenge bei unveränderter Cx43 mRNA. Zur Erfassung mittelfristiger Veränderungen wurden die Kardiomyozyten jeweils 3 Stunden mit den Wachstumsfaktoren VEGF und TGF-β inkubiert. Dabei zeigte sich jeweils eine signifikante Zunahme der Cx43 Proteinmenge und –mRNA. Die Connexine 40 und 45 waren in den ventrikulären Kardiomyozyten nur spärlich nachweisbar und durch keinen der untersuchten Faktoren signifikant induzierbar.

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26

Giessmann, Daniel. "Funktionelle Korrelation von Zytoskelett und gap junctions am Modell der Linsenepithelzelle." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=968700454.

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27

Khandoga, Natascha. "Einfluss von oxLDL auf die Apoptoseinduktion und Zellkopplung über Gap Junctions." Diss., lmu, 2007. http://nbn-resolving.de/urn:nbn:de:bvb:19-74235.

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28

Lall, Varinder Kaur. "The influence of connexin 36 containing gap junctions on autonomic activity." Thesis, University of Leeds, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.595850.

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Gap junctions (GJ) connect the cytoplasm of two adjacent cells and have two probable functions, synchronisation of networks by direct electrical communication and allowing. the passage of small molecules. This thesis examines the distribution patterns and physiological roles of the neuronal GJ sub unit connexin 36 (Cx36) in autonomic and respiratory control. Using the working heart brainstem preparation of the rat and mouse recordings were made during baseline and during peripheral chemoreceptor and baroreceptor stimulation. Central sympathetic drive was attenuated with the addition of 1 μM of mefloquine (M F) to the perfusate. MF (which blocks Cx36 containing GJs) induced a resting bradycardia, attenuated the amplitude of respiratory related sympathetic bursts, attenuated chemoreceptor-induced sympathoexcitation and increased heart rate recovery time after chemoreceptor stimulation. Attenuated respiratory responses to autonomic reflex stimulation were observed with MF, no significant alterations in baroreflex sensitivity were observed. Studies in Cx36 knockout mice were analogous to data obtained with MF. Telemetric probes inserted in free running wild type and Cx36 knockout mice which continually recorded heart rate and arterial pressure revealed significantly augmented variations in resting heart rate and arterial pressure in Cx36 knockout mice in comparison to wild type mice. Autonomic reflexes examined in anaesthetised Cx36 knockout mice revealed attenuated heart rate changes in response to chemoreceptor stimulation. Cx36 immunoreactivity and Cx36 cyan fluorescent protein expression was reported at various brainstem and spinal cord sites involved in autonomic function including, the nucleus of the solitary tract and sympathetic preganglionic neurones (SPNs). The results revealed that Cx36, at the level of the SPNs, plays important roles in regulating sympathetic outflow. This may have important clinical implications as an imbalance in the sympathetic and parasympathetic outflow to the heart for example, underlies various maladies from hypertension to cardiac arrhythmias

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29

Dietze, Anna. "Die Wirkung von Desipramin an kardialen Gap Junctions unter ischämischen Bedingungen." Doctoral thesis, Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-216543.

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Kardiovaskuläre Erkrankungen in Deutschland führen die Todesursachenstatistik an (19,1 % 2013) und verursachen die höchsten Krankheitskosten (14,5 % 2008) (Statistisches Bundesamt, 2015a,b). Im Rahmen von ischämischen Ereignissen am Herzen kann es zu Rhythmusstörungen kommen. In der Therapie dieser Störungen werden traditionell klassische Antiarrhythmika mit Wirkort Ionenkanal eingesetzt, welche jedoch stets ein proarrhythmisches Potenzial aufweisen. Im Fokus der Forschung der letzten Jahre stehen deswegen Peptide wie AAP10 (Antiarrhythmisches Peptid 10), welche direkt an den Gap Junctions ansetzen. In Radioligandenbindungsstudien konnte gezeigt werden, dass Desipramin AAP10 von seinem Rezeptor verdrängen kann. In der vorliegenden Arbeit wurde der Einfluss von Desipramin auf die Gap Junction-Leitfähigkeit in adulten humanen atrialen Kardiomyozyten bestimmt (Jozwiak 2012). Die Bestimmung der Leitfähigkeit erfolgte durch die Technik des Double-Cell-Voltage-Clamp. Es konnte gezeigt werden, dass Desipramin die elektrische Kopplung in humanen Kardiomyozyten, welche vorab durch CO2-induzierte Azidose partiell entkoppelt wurden, erhöht. Weiterhin wurde in der Mapping-Analyse mit dem Langendorff-System gezeigt, dass Desipramin in ischämischen Gebieten am ganzen Kaninchenherzen eine Reduktion der Homogenität und eine Steigerung der Dispersion verhindern kann. In anschließend hergestellten Western Blots aus Gewebeproben derselben Kaninchenherzen ließ sich eine verminderte Dephosphorylierung von Connexin 43 in ischämischen Gebieten unter Desipramin nachweisen. Ebenso vermag Desipramin eine Lateralisierung des Connexin 43 entlang der Zellmembran zu verhindern. Die Ergebnisse zeigen, dass Desipramin die Wahrscheinlichkeit für das Auftreten von Herzrhythmusstörungen unter ischämischen Bedingungen signifikant verringern und damit möglicherweise zur Senkung der Morbidität und Mortalität von Herzkreislauferkrankungen beitragen kann.

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30

Cao, Jiexin. "The Circadian Rhythm of Gap Junctions between photoreceptors in Goldfish retina." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1468761145.

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31

Elias, Laura Allyn Barker. "The role of gap junctions in the development of the neocortex." Diss., Search in ProQuest Dissertations & Theses. UC Only, 2008. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3311338.

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32

Ale-Agha, Niloofar. "Untersuchungen zum Einfluss von Retinoiden, Flavonoiden und Menadion auf interzelluläre Kommunikation über gap junctions." [S.l. : s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=968651534.

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Chandrasekhar, Anjana. "Insights into the mechanisms of growth suppression by connexins in model systems : a dissertation /." San Antonio : UTHSC, 2007. http://proquest.umi.com/pqdweb?did=1375515321&sid=1&Fmt=2&clientId=70986&RQT=309&VName=PQD.

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34

Morrow, Dympna Mary Paula. "Tumour promotion : mechanisms of action and modes of prevention." Thesis, University of Ulster, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322414.

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35

Striedinger, Katharine. "Degeneration and regeneration of the retina after trauma: emphasis on gap junctions." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=973201126.

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Schügner, Ricarda. "Synthese von Retinoiden zur Untersuchung der Zell-Zell-Kommunikation via gap junctions." [S.l. : s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=968931367.

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37

Pintsch, Monika [Verfasser], and Ulrich [Akademischer Betreuer] Pohl. "Cx37 abhängige Calciumsignalausbreitung durch myoendotheliale Gap Junctions / Monika Pintsch. Betreuer: Ulrich Pohl." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2015. http://d-nb.info/1073825760/34.

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38

Strom, Maria. "Targeting Gap Junctions as a Mechanism and Potential Treatment of Cardiac Arrhythmias." Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1262100592.

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39

Dilger, Nadine Saskia [Verfasser]. "Regulation von Ionenkanälen und Gap Junctions während der Zellentwicklung / Nadine Saskia Dilger." Hannover : Gottfried Wilhelm Leibniz Universität Hannover, 2020. http://d-nb.info/1212582489/34.

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40

Bradley, Kathryn Diane. "The Role of Connexin-36 Gap Junctions in Alcohol Intoxication and Reward." BYU ScholarsArchive, 2009. https://scholarsarchive.byu.edu/etd/2055.

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The purpose of this thesis project was to examine the function of connexin-36 (Cx36) gap junctions (GJs) in producing alcohol's intoxicating and rewarding effects. GABA neurons are thought to inhibit dopamine (DA) neurotransmission in the mesocorticolimbic system, which originates in the midbrain ventral tegmental area (VTA) and projects to limbic structures such as the nucleus accumbens (NAcc). The mesolimbic DA system is believed to be the neural substrate of alcohol intoxication and addiction (Tepper, Paladini, & Celada, 1998). Alcohol suppresses the firing rate of GABA neurons in the VTA (Gallegos, Criado, Lee, Henriksen, & Steffensen, 1999) and presumably disinhibits DA neurons thereby resulting in enhanced release of DA in the NAcc. Interestingly, VTA GABA neurons appear to form part of a larger syncytium of GABA neurons in the reticular formation that are linked by electrical synapses via Cx36 GJs (Allison, et al., 2006; Stobbs, et al., 2004; Lassen, et al., 2007). Gap junction blockers, including the Cx36-selective antagonist mefloquine, also suppress the excitability and electrical coupling of VTA GABA neurons (Stobbs, et al., 2004). Thus, I hypothesized that Cx36 GJs cause synchrony in VTA GABA neurons which alcohol blocks to cause intoxication and reward. To accomplish these studies I compared the effects of intoxicating doses of ethanol in Cx36 knockout (KO) mice and mefloquine-treated mice and their wild-type (WT) controls with two tests that index ataxia, an open field activity system and the fixed-speed rotarod apparatus, as well as with ethanol self-administration. I found that Cx36 KO and mefloquine-treated mice exhibit significantly more ethanol-induced loss of movement in the open field test, a paradigm which indexes gross motor activity and tremor, but less ataxia than their WT controls in the rotarod paradigm, a paradigm which indexes balance and coordination. Most importantly, both Cx36 KO and mefloquine-treated mice consumed less ethanol than their controls. These findings provide evidence in support of the hypothesis that Cx36 GJs are important targets for ethanol effects in the mesolimbic system.

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Mok, Wing-yee Bobo. "Expression of Gap-junctional connexin 31 in rat testis /." Hong Kong : University of Hong Kong, 1999. http://sunzi.lib.hku.hk/hkuto/record.jsp?B21254084.

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42

莫穎兒 and Wing-yee Bobo Mok. "Expression of Gap-junctional connexin 31 in rat testis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B31223205.

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Daubrawa, Felicitas Ulrike. "Effekte von Astaxanthin und Canthaxanthin auf die Zell-Zell-Kommunikation über Gap Junctions." [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=979445736.

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Hundhausen, Christina. "Einfluß der endothelialen Autakoide NO und PGI2 auf die Permeabilität endothelialer Gap Junctions." Diss., lmu, 2003. http://nbn-resolving.de/urn:nbn:de:bvb:19-12703.

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45

Yeh, Hung-I. "Vascular cell gap junctions : diversity of connexin expression in healthy and injured artery." Thesis, Imperial College London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265945.

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46

Salvage, Samantha. "Modulation of gap junctions and the intracellular resistance pathway in guinea-pig myocardium." Thesis, University of Surrey, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.604348.

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Myocardial intracellular communication via gap junctions (GJ) is fundamental to action potential (AP) propagation facilitating ordered atrial and ventricular contraction. Cardiac arrhythmias can be initiated by increased intracellular (Ca2+), and are associated with abnormal AP conduction due to increased intracellular resistivity (RI) and, specifically, gap junction resistivity (Rj), Recent evidence suggested the Ca2+/calmodulin (CaM)-dependent protein phosphatase calcineurin (Cn) slowed conduction, possibly through increasing RI. This work aimed to demonstrate the role of Cn-dependent pathways in modulating RJ when intracellular [(a2+] was raised, any role of CaMkinase-1I (CaMKII) was also assessed. Rj was measured by longitudinal impedance measurements using atrial and ventricular guinea-pig preparations in control and low-Na Tyrode's solutions, with or without the Cn inhibitors cyclosporin-A (5 IlM) and calcineurin auto-inhibitory peptide (50IlM). CaMKl1 was also assessed by using its inhibitor KN-93. Western blot and immunohistochemical confocal analyses, with Cx40, total Cx43 and phospho-specific Cx43 antibodies, were performed to quantify alterations in GJ abundance, localisation and phosphorylation state. The study established that a raised intracellular {Ca 2+J increased RJ by a CnA-dependent pathway, but CaMKII had no role. In atrial tissue RJ increase was associated with a Cn-dependent increase of Cx43-S368 phosphorylation in addition to a Cn-independent increase of Cx40 abundance. By contrast, ventricular myocardium showed an overall increase of de phosphorylated Cx43 typical of increased Ri and GJ uncoupling. These novel findings identify a potential pathway for investigation and clinical manipulation in cardiac pathologies consequent on an elevated intracellular [Ca 2+].

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47

Bennett, Peter. "Intrinsic Connectivity of the Claustrum : Gap Junctions Demonstrated by Immunohistochemistry and Electron Microscopy." Thesis, Norges teknisk-naturvitenskapelige universitet, Institutt for nevromedisin, 2014. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-26190.

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The claustrum is a much neglected nucleus in the brain, whose fuction remains unknown to date. Yet, based on the extensive reciprocal connections it shares with virtually all functional regions of cortex, it most likely serves a far from meaningless purpose. Current hypotheses propose a role in perceptual binding by synchronization of cortical activity. These hypotheses come with a number of assumptions, such as a wide network of connections intrinsic to the claustrum. In this context, gap junctions have been suggested as a means to interconnect portions of the claustrim and to synchronize incoming cortical activity. Neuronal gap junctions have been shown to be involved in supporting synchronous activity and oscillations in areas such as the hippocampus, making them a feasible candidate for such a mechanism in the claustrum. While gap junctions have been described in many areas of the brain, they have not been observed in the claustrum prior to the present study. Set aginst this background, the presence of gap junctions in the claustrum was investigated in this thesis. To this end, an immunohistochemical approach was first used to localize the gap junction protein connexin 36. Once a protocol was established, a small population of connexin 36 expressin neurons was identified in the posterior half of the dorsomedial aspect of the ventral claustrum (also known as the endopiriform nucleus). However, no further labeling was observed throughout the rest of the claustrum. These results were supported by electron microscopy, as putative gap junctions were exclusively observed in an area corresponding to where connexin 36 expression was found. These results represent the first steps in confirming the presenceof the hypothesized gap junction network in the claustrum. Yet, it could be argued that their limited occurrence in both number and location are not entirely in line with current hypotheses predicting a wide gap junction network common to the entire claustrum.

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Greer, Claire Elizabeth. "A role for gap junctions in the growth and development of Drosophila melanogaster." Thesis, University of Sussex, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.409962.

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49

Nickel, Regina. "An exploration of the role of gap junctions in the avian inner ear." Thesis, University College London (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.412533.

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50

Recktenwald, Johanna Christina [Verfasser]. "Hyperosmolare Sucrose-Lösung induziert ultrastrukturelle Veränderungen in astrozytären Gap Junctions / Johanna Christina Recktenwald." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2020. http://d-nb.info/1229435891/34.

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