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The URI for Queen's University could not be found
To fix, comment below in the following format: MSc http://purl.org/ontology/bibo/degrees/ms
MSc http://purl.org/ontology/bibo/degrees/ms
Record: =LDR 04151cam a2200373 a 4500 =001 3276485 =005 20160427125213.0 =006 m\\f\\d\\\\ =007 he\amu\\bucu =008 090929t20092009kina\\s\\\000\0\eng\d =040 \$aCaOKQ$beng$cCaOKQ =100 1\$aMedeiros, Nancy. =245 10$aSFO neurons are glucose responsive /$cby Nancy Medeiros. =264 \1$aKingston, Ont. :$b[publisher not identified],$c[2009] =264 \4$c©2009 =300 \$axi, 65 leaves :$billustrations =336 \$atext$btxt$2rdacontent =337 \$acomputer$bc$2rdamedia =338 \$aonline resource$bcr$2rdacarrier =502 \$aMaster, Physiology$bQueen's University$c2009 =504 \$aIncludes bibliographical references (leaves 55-65) =520 3\$aGlucose is the primary metabolic signal reflecting the current energy state of the body. Glucose influences the excitability of neurons in the area postrema (AP), a circumventricular organ (CVO), prompting my interest in investigating whether the subfornical organ (SFO), another sensory CVO can also detect glucose. Using patch-clamp electrophysiology, we investigated the influence of changing glucose concentrations on the excitability of SFO neurons. In dissociated SFO neurons, altering the bath concentration of glucose (1mM, 5mM, 10mM) influenced the excitability of 49% of neurons tested (n=67). Glucose-inhibited (GI, hyperpolarized by increased glucose or depolarized by decreased glucose) and glucose-excited (GE, depolarized by increased glucose or hyperpolarized by decreased glucose) neurons were observed. GI neurons (27%, n=18) depolarized in response to decreased glucose (n=10, mean 4.6 ± 1.0 mV) or hyperpolarized in response to increased glucose (n=8, mean -4.4 ± 0.8 mV). In contrast, GE neurons (22%, n=15) depolarized in response to increased glucose (n=9, mean 6.4 ± 0.4) or hyperpolarized in response to decreased glucose (n=6, mean -4.8 ± 0.6 mV). These data show that glucose acts on a subpopulation of SFO neurons to produce both excitatory and inhibitory actions. Using voltage-clamp recordings two groups of SFO neurons were identified: those producing an outward current (GI) and those producing an inward current (GE) in response to increasing concentrations of glucose from 1 to 10 mM (n=23). The mean glucose-induced inward current had a reversal potential of -24 ± 12 mV (mean input resistance 2.0 ± 0.4 GOmega, n= 5), suggesting it may be mediated by a NSCC. The mean glucose-induced outward current (mean input resistance 1.7 ± 0.3 GOmega, n=7) had a mean reversal potential of -78 mV ± 1.2 mV (n = 5), suggesting it may be mediated by an activation of either K+ or Cl-current (ECl = -67 mV, EK = -89 mV). The SFO has projections to the PVN, a regulator of energy balance. I investigated the effects of increasing concentrations of glucose (1 to 10 mM) on the membrane potential of dissociated SFO neurons projecting to the PVN. Thirty percent of SFO-PVN neurons tested (n=10) responded with membrane hyperpolarizations (mean -4.2 ± 0.8 mV, n=3) suggesting a proportion of these cells are GI neurons. These data indicate that SFO neurons are glucose-responsive, which supports a role for the SFO as a regulator of energy balance. =533 \$aCopy 2, microfiche.$bOttawa :$cNational Library of Canada,$d[2010] --$e1 microfiches ; 11 x 15 cm. --$f(Canadian theses = Thèses canadiennes) =538 \$aMode of access: World Wide Web. =540 \$aThis publication is made available by the authority of the copyright owner solely for the purpose of private study and research and may not be copied or reproduced except as permitted by the copyright laws without written authority from the copyright owner. =500 \$aGMD: electronic resource. =653 \$aGlucose-responsiveness. =653 \$aSubfornical organ. =653 \$aCircumventricular organs. =653 \$aElectrophysiology. =710 2\$aQueen's University (Kingston, Ont.).$bDepartment of Physiology. =710 2\$aQueen's University (Kingston, Ont.).$tTheses (Queen's University (Kingston, Ont.)) =830 \0$aCanadian theses. =902 \$aMARCIVE2013
Record File: fe9cd75570efc370fac9c3eb2d1e7526.mrc
The URI for Queen's University could not be found
To fix, comment below in the following format:
MSc http://purl.org/ontology/bibo/degrees/msRecord: =LDR 04151cam a2200373 a 4500 =001 3276485 =005 20160427125213.0 =006 m\\f\\d\\\\ =007 he\amu\\bucu =008 090929t20092009kina\\s\\\000\0\eng\d =040 \$aCaOKQ$beng$cCaOKQ =100 1\$aMedeiros, Nancy. =245 10$aSFO neurons are glucose responsive /$cby Nancy Medeiros. =264 \1$aKingston, Ont. :$b[publisher not identified],$c[2009] =264 \4$c©2009 =300 \$axi, 65 leaves :$billustrations =336 \$atext$btxt$2rdacontent =337 \$acomputer$bc$2rdamedia =338 \$aonline resource$bcr$2rdacarrier =502 \$aMaster, Physiology$bQueen's University$c2009 =504 \$aIncludes bibliographical references (leaves 55-65) =520 3\$aGlucose is the primary metabolic signal reflecting the current energy state of the body. Glucose influences the excitability of neurons in the area postrema (AP), a circumventricular organ (CVO), prompting my interest in investigating whether the subfornical organ (SFO), another sensory CVO can also detect glucose. Using patch-clamp electrophysiology, we investigated the influence of changing glucose concentrations on the excitability of SFO neurons. In dissociated SFO neurons, altering the bath concentration of glucose (1mM, 5mM, 10mM) influenced the excitability of 49% of neurons tested (n=67). Glucose-inhibited (GI, hyperpolarized by increased glucose or depolarized by decreased glucose) and glucose-excited (GE, depolarized by increased glucose or hyperpolarized by decreased glucose) neurons were observed. GI neurons (27%, n=18) depolarized in response to decreased glucose (n=10, mean 4.6 ± 1.0 mV) or hyperpolarized in response to increased glucose (n=8, mean -4.4 ± 0.8 mV). In contrast, GE neurons (22%, n=15) depolarized in response to increased glucose (n=9, mean 6.4 ± 0.4) or hyperpolarized in response to decreased glucose (n=6, mean -4.8 ± 0.6 mV). These data show that glucose acts on a subpopulation of SFO neurons to produce both excitatory and inhibitory actions. Using voltage-clamp recordings two groups of SFO neurons were identified: those producing an outward current (GI) and those producing an inward current (GE) in response to increasing concentrations of glucose from 1 to 10 mM (n=23). The mean glucose-induced inward current had a reversal potential of -24 ± 12 mV (mean input resistance 2.0 ± 0.4 GOmega, n= 5), suggesting it may be mediated by a NSCC. The mean glucose-induced outward current (mean input resistance 1.7 ± 0.3 GOmega, n=7) had a mean reversal potential of -78 mV ± 1.2 mV (n = 5), suggesting it may be mediated by an activation of either K+ or Cl-current (ECl = -67 mV, EK = -89 mV). The SFO has projections to the PVN, a regulator of energy balance. I investigated the effects of increasing concentrations of glucose (1 to 10 mM) on the membrane potential of dissociated SFO neurons projecting to the PVN. Thirty percent of SFO-PVN neurons tested (n=10) responded with membrane hyperpolarizations (mean -4.2 ± 0.8 mV, n=3) suggesting a proportion of these cells are GI neurons. These data indicate that SFO neurons are glucose-responsive, which supports a role for the SFO as a regulator of energy balance. =533 \$aCopy 2, microfiche.$bOttawa :$cNational Library of Canada,$d[2010] --$e1 microfiches ; 11 x 15 cm. --$f(Canadian theses = Thèses canadiennes) =538 \$aMode of access: World Wide Web. =540 \$aThis publication is made available by the authority of the copyright owner solely for the purpose of private study and research and may not be copied or reproduced except as permitted by the copyright laws without written authority from the copyright owner. =500 \$aGMD: electronic resource. =653 \$aGlucose-responsiveness. =653 \$aSubfornical organ. =653 \$aCircumventricular organs. =653 \$aElectrophysiology. =710 2\$aQueen's University (Kingston, Ont.).$bDepartment of Physiology. =710 2\$aQueen's University (Kingston, Ont.).$tTheses (Queen's University (Kingston, Ont.)) =830 \0$aCanadian theses. =902 \$aMARCIVE2013
Record File: fe9cd75570efc370fac9c3eb2d1e7526.mrc