Relevant bibliographies by topics / Connexin-36

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Academic literature on the topic 'Connexin-36'

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Published: 4 June 2021
Last updated: 13 February 2022

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Journal articles on the topic "Connexin-36"

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SITARAMAYYA, ARI, JOHN W. CRABB, DIANE F. MATESIC, ALEXANDER MARGULIS, VINITA SINGH, SADHONA PULUKURI, and LOAN DANG. "Connexin 36 in bovine retina: Lack of phosphorylation but evidence for association with phosphorylated proteins." Visual Neuroscience 20, no. 4 (July 2003): 385–95. http://dx.doi.org/10.1017/s0952523803204041.

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In vertebrate retina interneuronal communication through gap junctions is involved in light adaptation and in the transfer of visual information from the rod pathway to the cone pathway. Reports over the last two decades have indicated that these gap junctions are regulated by cyclic nucleotide-dependent protein kinases suggesting that the gap junction proteins, connexins, are phosphorylated. Though all the connexins involved in light adaptation and information transfer from rod to cone pathway are not yet known, connexin 36 has been shown to be definitively involved in the latter process. We have therefore attempted to investigate the cyclic nucleotide-dependent phosphorylation of this connexin in bovine retina. We found several soluble and membrane proteins in bovine retina whose phosphorylation was regulated by cyclic nucleotides. However, no protein of about 36 kDa with cyclic nucleotide-regulated phosphorylation was found in gap junction-enriched membrane preparations. A 36-kDa phosphorylated protein was found in gap junction-enriched membranes phosphorylated in the presence of calcium. However, this protein was not immunoprecipitated by anti-connexin 36 antibodies indicating that it was not connexin 36 in spite of its similarity in molecular weight. Immunoprecipitation did reveal phosphorylated proteins coimmunoprecipitated with connexin 36. Two of these proteins were identified as beta and alpha tubulin subunits. Though cyclic GMP and calcium did not greatly influence the association of these proteins with connexin 36, the results suggest the possibility of connexin 36 associating with other proteins. Together, these observations indicate that interneuronal communication at gap junctions made by connexin 36 may not be regulated by direct phosphorylation of connexin 36, but possibly by phosphorylation of associated proteins.
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Alonso, Angelika, Eileen Reinz, Jürgen W. Jenne, Marc Fatar, Hannah Schmidt-Glenewinkel, Michael G. Hennerici, and Stephen Meairs. "Reorganization of Gap Junctions after Focused Ultrasound Blood–Brain Barrier Opening in the Rat Brain." Journal of Cerebral Blood Flow & Metabolism 30, no. 7 (March 24, 2010): 1394–402. http://dx.doi.org/10.1038/jcbfm.2010.41.

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Ultrasound-induced opening of the blood–brain barrier (BBB) is an emerging technique for targeted drug delivery to the central nervous system. Gap junctions allow transfer of information between adjacent cells and are responsible for tissue homeostasis. We examined the effect of ultrasound-induced BBB opening on the structure of gap junctions in cortical neurons, expressing Connexin 36, and astrocytes, expressing Connexin 43, after focused 1-MHz ultrasound exposure at 1.25 MPa of one hemisphere together with intravenous microbubble (Optison, Oslo, Norway) application. Quantification of immunofluorescence signals revealed that, compared with noninsonicated hemispheres, small-sized Connexin 43 and 36 gap-junctional plaques were markedly reduced in areas with BBB breakdown after 3 to 6 hours (34.02±6.04% versus 66.49±2.16%, P=0.02 for Connexin 43; 33.80±1.24% versus 36.77±3.43%, P=0.07 for Connexin 36). Complementing this finding, we found significant increases in large-sized gap-junctional plaques (5.76±0.96% versus 1.02±0.84%, P=0.05 for Connexin 43; 5.62±0.22% versus 4.65±0.80%, P=0.02 for Connexin 36). This effect was reversible at 24 hours after ultrasound exposure. Western blot analyses did not show any change in the total connexin amount. These results indicate that ultrasound-induced BBB opening leads to a reorganization of gap-junctional plaques in both neurons and astrocytes. The plaque-size increase may be a cellular response to imbalances in extracellular homeostasis after BBB leakage.
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Song, Ji-Hoon, Yongfu Wang, Joseph D. Fontes, and Andrei B. Belousov. "Regulation of connexin 36 expression during development." Neuroscience Letters 513, no. 1 (March 2012): 17–19. http://dx.doi.org/10.1016/j.neulet.2012.01.075.

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Gonzalez-Nieto, D., J. M. Gomez-Hernandez, B. Larrosa, C. Gutierrez, M. D. Munoz, I. Fasciani, J. O'Brien, A. Zappala, F. Cicirata, and L. C. Barrio. "Regulation of neuronal connexin-36 channels by pH." Proceedings of the National Academy of Sciences 105, no. 44 (October 28, 2008): 17169–74. http://dx.doi.org/10.1073/pnas.0804189105.

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Barrio, Luis C., Daniel González-Nieto, Juan Gómez-Hernández, Bélen Larrosa, Cristina Gutièrrez, Ilaria Fasciani, María D. Muñoz, John O'Brien, Agata Zappala, and Federico Cicirata. "Regulation Of Neuronal Connexin-36 Channels by pH." Biophysical Journal 96, no. 3 (February 2009): 285a. http://dx.doi.org/10.1016/j.bpj.2008.12.1412.

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Nevin, Remington L. "Mefloquine Blockade of Connexin 36 and Connexin 43 Gap Junctions and Risk of Suicide." Biological Psychiatry 71, no. 1 (January 2012): e1-e2. http://dx.doi.org/10.1016/j.biopsych.2011.07.026.

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Mills, Stephen L., Jennifer J. O'Brien, Wei Li, John O'Brien, and Stephen C. Massey. "Rod pathways in the mammalian retina use connexin 36." Journal of Comparative Neurology 436, no. 3 (2001): 336–50. http://dx.doi.org/10.1002/cne.1071.

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Bargiotas, Panagiotis, Sajjad Muhammad, Mahbubur Rahman, Nurith Jakob, Raimund Trabold, Elke Fuchs, Lothar Schilling, Nikolaus Plesnila, Hannah Monyer, and Markus Schwaninger. "Connexin 36 promotes cortical spreading depolarization and ischemic brain damage." Brain Research 1479 (October 2012): 80–85. http://dx.doi.org/10.1016/j.brainres.2012.08.046.

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Le Gurun, Sabine, David Martin, Andrea Formenton, Pierre Maechler, Dorothée Caille, Gérard Waeber, Paolo Meda, and Jacques-Antoine Haefliger. "Connexin-36 Contributes to Control Function of Insulin-producing Cells." Journal of Biological Chemistry 278, no. 39 (May 22, 2003): 37690–97. http://dx.doi.org/10.1074/jbc.m212382200.

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Hartfield, Elizabeth M., Federica Rinaldi, Colin P. Glover, Liang-Fong Wong, Maeve A. Caldwell, and James B. Uney. "Connexin 36 Expression Regulates Neuronal Differentiation from Neural Progenitor Cells." PLoS ONE 6, no. 3 (March 9, 2011): e14746. http://dx.doi.org/10.1371/journal.pone.0014746.

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Dissertations / Theses on the topic "Connexin-36"

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McKenna, James. "Sensitivity to Dopamine D1/D2 Receptor Stimulation in Mice Lacking Connexin-32 or Connexin-36." ScholarWorks@UNO, 2004. http://scholarworks.uno.edu/td/91.

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Previous work has shown D1/D2 requisite synergism can still occur in the striatum in the absence of action potentials. Some nonclassical communication such as gap junctions may be allowing the segregated dopamine (DA) receptors to interact to produce stereotyped motor activity. Connexin-32 (Cx32) and connexin-36 (Cx36) were targeted for study due to their abundance in neural tissues and presence in the striatum. Mice lacking either the Cx32 or Cx36 gene and their respective wildtype littermates were compared on a climbing behavior task used to gauge their dopaminergic activity after receiving either saline, D1 agonist, D2 agonist, or both D1 and D2 agonists. The results showed that D1/D2 requisite synergism was still intact in both strains of mice. The Cx32 WT mice displayed significantly greater scores than the KO mice in the D1/D2 treatment. The Cx36 mice did not display a significant genotype difference, but a trend was observed with the KO females having larger scores relative to WT females or to males of either genotype.
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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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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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Hartfield, Elizabeth Margaret. "Viral-mediated molecular and electrophysiological studies of connexin-36 function in models of neuronal connectivity." Thesis, University of Bristol, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.526016.

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Pistorius, Stephanie Suzette. "Chemogenetic Stimulation of Electrically Coupled Midbrain GABA Neurons in Alcohol Reward and Dependence." BYU ScholarsArchive, 2017. https://scholarsarchive.byu.edu/etd/6813.

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The prevailing view is that enhancement of dopamine (DA) transmission in the mesolimbic system leads to the rewarding properties of alcohol. The mesolimbic DA system, which plays an important role in regulating reward and addiction, consists of DA neurons in the midbrain ventral tegmental area (VTA) that innervate the nucleus accumbens (NAc). It is believed that VTA DA neurons are inhibited by local gamma-aminobutyric acid (GABA) interneurons that express connexin-36 (Cx36) gap junctions (GJs). We have previously demonstrated that blocking Cx36 GJs suppresses electrical coupling between VTA GABA neurons and reduces ethanol intoxication and consumption suggesting that electrical coupling between mature VTA GABA neurons underlies the rewarding properties of ethanol. The aim of this study was to further investigate the role of VTA GABA neurons expressing Cx36 GJs in regulating DA neuron activity and release and mediating ethanol effects on VTA GABA neurons. To this end, we customized a Designer Receptor Exclusively Activated by Designer Drugs (DREADDs) viral vector to target VTA GABA neurons expressing Cx36 GJs in order to chemogenetically modulate their activity. In order to more conclusively demonstrate the role of this sub population of VTA GABA neurons in regulating DA neural activity and release we used electrophysiology to characterize the electrical changes that occur in VTA DA and GABA neurons when Cx36-expressing VTA GABA cells were selectively activated. In addition, we evaluated the effects of activation of VTA GABA neurons on brain stimulation reward and alcohol consumption in ethanol naive and dependent mice. Results indicate that there are two populations of GABA neurons in the VTA, one that is GAD65+/Cx36+ and one that is GAD67+/Cx36-. Activation of Cx36+ VTA GABA neurons by clozapine-n-oxide (CNO) in mice injected with Gq DREADD activated VTA DA neurons and subsequent DA release in the NAc, suggesting that Cx36-containing GABA neurons are inhibiting non-Cx36 GABA neurons to disinhibit DA neurons. In hM3Dq animals, CNO administration provided a rewarding stimulus in the conditioned pace preference paradigm, and reduced consumption in the drink-in-the-dark ethanol consumption paradigm in dependent and naïve mice. A better understanding of the circuitry of the mesolimbic DA system is key to understanding the mechanisms that lead to addiction and may ultimately lead to improved therapies for substance abuse.
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Brunal-Brown, Alyssa Alexandra. "Effects of constitutive and acute Connexin 36 deficiency on brain-wide susceptibility to PTZ-induced neuronal hyperactivity." Diss., Virginia Tech, 2020. http://hdl.handle.net/10919/100748.

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Connexins are transmembrane proteins that form hemichannels allowing the exchange of molecules between the extracellular space and the cell interior. Two hemichannels from adjacent cells dock and form a continuous gap junction pore, thereby permitting direct intercellular communication. Connexin 36 (Cx36), expressed primarily in neurons, is involved in the synchronous activity of neurons and may play a role in aberrant synchronous firing, as seen in seizures. To understand the reciprocal interactions between Cx36 and seizure-like neural activity, we examined three questions: a) does Cx36 deficiency affect seizure susceptibility, b) does seizure-like activity affect Cx36 expression patterns, and c) does acute blockade of Cx36 conductance increase seizure susceptibility. We utilize the zebrafish pentylenetetrazol (PTZ; a GABA(A) receptor antagonist) induced seizure model, taking advantage of the compact size and optical translucency of the larval zebrafish brain to assess how PTZ affects brain-wide neuronal activity and Cx36 protein expression. We exposed wild-type and genetic Cx36-deficient (cx35.5-/-) zebrafish larvae to PTZ and subsequently mapped neuronal activity across the whole brain, using phosphorylated extracellular-signal-regulated kinase (pERK) as a proxy for neuronal activity. We found that cx35.5-/- fish exhibited region-specific susceptibility and resistance to PTZ-induced hyperactivity compared to wild-type controls, suggesting that genetic Cx36 deficiency may affect seizure susceptibility in a region-specific manner. Regions that showed increased PTZ sensitivity include the dorsal telencephalon, which is implicated in human epilepsy, and the lateral hypothalamus, which has been underexplored. We also found that PTZ-induced neuronal hyperactivity resulted in a rapid reduction of Cx36 protein levels within. 30 minutes and one-hour exposure to 20 mM PTZ significantly reduced the expression of Cx36. This Cx36 reduction persists after one-hour of recovery but recovered after 3-6 hours. This acute downregulation of Cx36 by PTZ is likely maladaptive, as acute pharmacological blockade of Cx36 by mefloquine results in increased susceptibility to PTZ-induced neuronal hyperactivity. Together, these results demonstrate a reciprocal relationship between Cx36 and seizure-associated neuronal hyperactivity: Cx36 deficiency contributes region-specific susceptibility to neuronal hyperactivity, while neuronal hyperactivity-induced downregulation of Cx36 may increase the risk of future epileptic events.
Doctor of Philosophy
Within the brain, cells (neurons) communicate with each other to pass along information. This communication is important for normal functions of the brain such as learning and memory, muscle movement, etc. Epilepsy is a disease of the brain that is caused by rapid over synchronized communication between cells. This leads to seizures which can include convulsions, loss of attention, and much more. Currently, 30% of patients suffering from epilepsy do not have a treatment option that works for them, it is, therefore, imperative to investigate new targets for treatment in this disease. Connexin36 is a protein in the brain that directly connects cells so they can pass information quickly between them. Connexin36, therefore, might make a good target for treatment. Previous work has aimed to understand this relationship but has been limited in their ability to look at the entire brain at any one time. The goal of this study was to understand the relationship between connexin 36 and brain hyperactivity across the whole brain simultaneously. To understand this relationship, we first determined what happened to brain activity if the protein was missing entirely after exposure to a seizure causing drug. We were asking: How does connexin 36 affect hyperactivity. We found that different regions of the brain responded differently without the connexin 36 protein. This suggests that one size does not fit all, and one must look at the whole brain to understand the effects of the connexin 36 protein. Next, we asked a similar question, but in the opposite direction, how does hyperactivity affect connexin 36? We found, in the short-term, hyperactivity reduced the amount of connexin 36 present in certain regions of the brain. This continued until 3 hours following exposure to the seizure causing drug Pentylenetetrazol (PTZ). Lastly, to determine if this short-term reduction in connexin 36 meant that an individual was more likely to experience hyperactivity. To do this, we used a connexin 36 blocking drug, then introduced the seizure causing drug at different concentrations. We found, at all concentrations, the connexin 36 blocking drug caused significant changes in neuronal activity, depending on the brain regions. Overall, our results showed that connexin 36 plays an important role in hyperactivity and that a short-term reduction in connexin 36 is detrimental, and may contribute to an increase in the possibility of subsequent hyperactivity.
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Akintürk, Sulhiye Serra [Verfasser], Rolf [Gutachter] Dermietzel, and Michael [Gutachter] Hollmann. "Interaction of the neuronal gap junction protein Connexin 36 with alpha Calcium/Calmodulin-dependent protein Kinase II / Sulhiye Serra Akintürk ; Gutachter: Rolf Dermietzel, Michael Hollmann." Bochum : Ruhr-Universität Bochum, 2013. http://d-nb.info/1131354621/34.

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Allison, David Wilbanks. "Cocaine and Mefloquine-induced Acute Effects in Ventral Tegmental Area Dopamine and GABA Neurons." BYU ScholarsArchive, 2009. https://scholarsarchive.byu.edu/etd/2362.

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The aim of the two studies presented here was to evaluate the effects of cocaine and mefloquine (MFQ) on γ-aminobutyric acid (GABA) and dopamine (DA) neurons in the ventral tegmental area (VTA). Cocaine: In vivo, lower doses of intravenous cocaine (0.25-0.5 mg/kg), or methamphetamine (METH), enhanced VTA GABA neuron firing rate via D2/D5 receptor activation. Higher cocaine doses (1.0-2.0 mg/kg) inhibited their firing rate. Cocaine and lidocaine inhibited the firing rate and spike discharges induced by stimulation of the internal capsule (ICPSDs) at dose levels 0.25-2 mg/kg (IC50 1.2 mg/kg), but neither DA nor METH reduced ICPSDs. In VTA GABA neurons in vitro, cocaine reduced (IC50 13 µM) current-evoked spikes and sodium currents in a use-dependent manner. In VTA DA neurons, cocaine reduced IPSCs (IC50 13 µM), increased IPSC paired-pulse facilitation, and decreased sIPSC frequency, without affecting mIPSC frequency or amplitude. These findings suggest cocaine reduces activity-dependent GABA release on DA neurons in the VTA, and that cocaine's use-dependent blockade of VTA GABA neuron voltage-sensitive sodium channels (VSSCs) may synergize with its DAT inhibiting properties to enhance mesolimbic DA transmission implicated in cocaine reinforcement. Mefloquine: Mefloquine (MFQ) is an anti-malarial agent, Connexin-36 (Cx36) gap junction blocker, 5-HT3 antagonist, and calcium ionophore. Mounting evidence of a Cx36-mediated VTA GABA neuron syncytium suggests MFQ-related dysphoria may attribute to its gap junction blocking effects on VTA synaptic homeostasis. We observed that MFQ (25 µM) increased DA neuron spontaneous IPSC frequency 6 fold, and mIPSC 3 fold. Carbenoxolone (CBX, 100 µM) only increased sIPSC frequency 2 fold, and did not affect DA mIPSC frequency. Ondansetron did not mimic MFQ. Additionally, MFQ did not affect VTA DA evoked IPSC paired pulse ratio (PPR). However, Mefloquine did induce a 3.5 fold increase in bath-applied GABA current. Remarkably, MFQ did not affect VTA GABA neuron inhibition. At VTA DA neuron excitatory synapses MFQ increased sEPSC frequency in-part due to an increase in the AMPA/NMDA ratio. These finding suggest MFQ alters VTA synapses differentially depending on neuron and synapse type, and that these alterations appear to involve MFQ's gap junction blocking and calcium ionophore actions.
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Hales, Kimberly. "Neuronal and Molecular Adaptations of GABA Neurons in the Ventral Tegmental Area to Chronic Alcohol." Diss., CLICK HERE for online access, 2007. http://contentdm.lib.byu.edu/ETD/image/etd2182.pdf.

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Melo, Edgard Julian Osuna. "Expressão de conexina 36 e conexina 43 em células do gânglio da raiz dorsal e seu envolvimento na nocicepção." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/42/42136/tde-11062014-165139/.

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Os canais de junções comunicantes (gap junctions, JC) são formados por subunidades chamadas de conexinas (Cx). Estas proteínas têm papel relevante no acoplamento celular, participando da condutância de células nervosas ou gliais e modulando vários processos fisiológicos e fisiopatológicos. O objetivo deste trabalho é avaliar o envolvimento das conexinas na nocicepção aguda, por meio de ensaios comportamentais e estudos de mapeamento da sua expressão em células do gânglio da raiz dorsal de ratos. Para tanto, foi analisado o efeito de carbenoxolone (CBX) e quinina (bloqueadores de JCs), assim como de oligonucleotídeos antisense para conexinas 36 e 43 na indução e manutenção de hiperalgesia induzida por carragenina em ratos. Os resultados mostraram que a carragenina induz uma diminuição do limiar nociceptivo em ratos e que esse efeito hiperalgésico da carragenina foi bloqueado pelo tratamento com carbenoxolone (nas doses 20-50mg) e significantemente inibido por quinina (nas doses 20-50mg), sugerindo uma participação das junções comunicantes (JC) no processo.
Gap junctions channels (GJ) are formed by proteic subunits called connexins (Cx). These proteins have an important role in cellular coupling, participating in the conductance of glial and nerve cells or modulating various physiological and pathophysiological processes. The aim of this study is to evaluate Cx36 and Cx43 involvement in acute nociception through behavioral assays, mapping studies of its expression in rat dorsal root ganglion cells. For this purpose, we analyzed the effect of intrathecal treatment with carbenoxolone (CBX) and quinine (GJs blockers), as well as antisense oligonucleotides for connexins 36 and 43 in the induction and maintenance of carrageenan-induced hyperalgesia in rats. The results show that carrageenan induces a nociceptive threshold decrease in rats. The hyperalgesic effect was blocked by treatment with carbenoxolone (20-50mg doses), Cx43 antisense and inhibited significantly by quinine (at doses 20 -50mg) but no with Cx36 antisense, suggesting an involvement of gap junctions (JC) in the process.
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