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A role for melanocortin-4 neuropeptide Y, Y1 and Y5 receptors in the hypothalamic circuitry controlling energy homeostasisDempsie, Yvonne January 2003 (has links)
No description available.
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Functional and anatomical properties of brain hypocretin/orexin circuitsSchöne, Cornelia January 2015 (has links)
No description available.
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The electrical activity of lateral hypothalamic neurons and its regulation by nutrients and ethanolVenner, Anne January 2012 (has links)
No description available.
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Cloning and characterization of the first amphibian secretins and secretin receptor functional implication of secretin with orexin in amphibians /Lau, Kwan-wa. January 2009 (has links)
Thesis (M. Phil.)--University of Hong Kong, 2010. / Includes bibliographical references (leaves 131-143). Also available in print.
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Cloning and characterization of the first amphibian secretins and secretin receptor: functional implication ofsecretin with orexin in amphibiansLau, Kwan-wa, 劉君華 January 2009 (has links)
published_or_final_version / Biological Sciences / Master / Master of Philosophy
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Effects of Chronic Sleep and Food Deprivation on In Vivo Levels of Prepro-Hypocretin (PPH)Dunn, Kelly 17 December 2004 (has links)
The hypocretin peptides are two hypothalamic peptides known to be involved in both sleeping and feeding behavior, however their specific roles in these domains are not well understood. The present study sought to determine the effect of chronic (72-hour) sleep deprivation and (48-hour) food deprivation on preprohypocretin (PPH), which is the precursor for the hypocretin peptides. PPH levels were visualized and quantified via in situ hybridization. A three-factor ANOVA ( group x dorsal/ventral x medial/lateral) revealed a significant effect of subregion, specifically dorsal/middle and ventral/medial exhibited elevated PPH levels, however there was no effect of group. A between group one-way ANOVA revealed no effect of group on PPH levels. It is theorized that four possible domains may be responsible for these results: presence of hypothalamic neuronal subpopulations, role of circadian rhythm, role of hypocretins in locomotive behavior and inextricably confounded variables. These are discussed at length.
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Orexin Receptors in Recombinant CHO Cells : Signaling to Short- and Long-Term Cell ResponsesAmmoun, Sylwia January 2005 (has links)
<p>Recently discovered neuropeptides orexins (orexin-A and -B) act as endogenous ligands for G-protein-coupled receptors called OX<sub>1</sub> and OX<sub>2</sub> receptors. Our previous studies have established model systems for investigation of the pharmacology and signaling of these receptors in recombinant CHO cells. OX<sub>1</sub> receptor-expressing CHO cells were mainly utilized in this thesis.</p><p>Orexin-A and -B activate both OX<sub>1</sub> and OX<sub>2</sub> receptors. However, orexin-B is less potent in activating OX<sub>1</sub> receptors than orexin-A, whereas the peptides are equipotent on OX<sub>2</sub> receptors. We have performed mutagenesis on orexin-A to investigate the basis for this selectivity. We show that OX<sub>2</sub> receptor is generally less affected by the mutations and thus OX<sub>2</sub><sup> </sup>receptor appears to have less strict requirements for ligand binding, likely explaining the lack of difference in affinity/potency between orexin-A and orexin-B on OX<sub>2</sub> receptor.</p><p>The other studies focus on orexin receptor signaling. OX<sub>1</sub> receptors are shown to regulate adenylyl cyclase both in positive and negative manner, activate different MAP-kinases (ERK1/2 and p38) and induce cell death after long-lasting stimulation. Adenylyl cyclase regulation occurs likely through three different G-protein families, Gi, Gs and Gq. For ERK1/2, several downstream pathways, such as Ras, Src, PI3-kinase and protein kinase C (PKC) are implicated. OX<sub>1</sub> receptor-mediated activation of ERK is suggested to be cytoprotective whereas p38 MAP-kinase induces programmed cell death. </p><p>Three particularly interesting findings were made. Firstly, novel PKC δ (delta) is suggested to regulate adenylyl cyclase, whereas conventional and atypical PKCs are involved in activation of ERK. Secondly, adenylyl cyclase and ERK activation is fully dependent on extracellular Ca<sup>2+</sup>. Further experiments suggest that the previously discovered receptor-operated Ca<sup>2+</sup> influx is not affecting the downstream effectors of orexin receptors but that it instead enables orexin receptors to couple to several signal cascades. Thirdly, upon inhibition of caspases, classical mediators of programmed cell death, OX<sub>1 </sub>receptor-mediated cell death is not reversed, but instead the pathways to death are altered so de novo gene transcription is no longer required for cell death.</p>
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Orexin Receptors in Recombinant CHO Cells : Signaling to Short- and Long-Term Cell ResponsesAmmoun, Sylwia January 2005 (has links)
Recently discovered neuropeptides orexins (orexin-A and -B) act as endogenous ligands for G-protein-coupled receptors called OX1 and OX2 receptors. Our previous studies have established model systems for investigation of the pharmacology and signaling of these receptors in recombinant CHO cells. OX1 receptor-expressing CHO cells were mainly utilized in this thesis. Orexin-A and -B activate both OX1 and OX2 receptors. However, orexin-B is less potent in activating OX1 receptors than orexin-A, whereas the peptides are equipotent on OX2 receptors. We have performed mutagenesis on orexin-A to investigate the basis for this selectivity. We show that OX2 receptor is generally less affected by the mutations and thus OX2 receptor appears to have less strict requirements for ligand binding, likely explaining the lack of difference in affinity/potency between orexin-A and orexin-B on OX2 receptor. The other studies focus on orexin receptor signaling. OX1 receptors are shown to regulate adenylyl cyclase both in positive and negative manner, activate different MAP-kinases (ERK1/2 and p38) and induce cell death after long-lasting stimulation. Adenylyl cyclase regulation occurs likely through three different G-protein families, Gi, Gs and Gq. For ERK1/2, several downstream pathways, such as Ras, Src, PI3-kinase and protein kinase C (PKC) are implicated. OX1 receptor-mediated activation of ERK is suggested to be cytoprotective whereas p38 MAP-kinase induces programmed cell death. Three particularly interesting findings were made. Firstly, novel PKC δ (delta) is suggested to regulate adenylyl cyclase, whereas conventional and atypical PKCs are involved in activation of ERK. Secondly, adenylyl cyclase and ERK activation is fully dependent on extracellular Ca2+. Further experiments suggest that the previously discovered receptor-operated Ca2+ influx is not affecting the downstream effectors of orexin receptors but that it instead enables orexin receptors to couple to several signal cascades. Thirdly, upon inhibition of caspases, classical mediators of programmed cell death, OX1 receptor-mediated cell death is not reversed, but instead the pathways to death are altered so de novo gene transcription is no longer required for cell death.
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The involvement of the neuropeptides orexins (hypocretins) in fear and anxiety in rats exposed to a single episode of footshocksChen, Xiaoyu 08 1900 (has links)
Post-traumatic stress disorder (PTSD) is a psychiatric condition that can develop when people experience a stressful and life-threatening event. Clinical research indicates that the presence of a state of hyperarousal after a traumatic experience is the best predictor of a subsequent diagnosis of PTSD. The role of arousal peptides called orexins (hypocretins) in a PTSD-like condition produced by exposing rats to a single episode of footshocks (5× 2 s episodes of 1.5 mA) was investigated in this thesis. The first part of my thesis involves the characterization of the footshock model of PTSD and the second part examines the involvement of orexins in this footshock model. The following findings are reported. First, shock rats that exhibited a high level of anxiety to a novel tone (high responders, HR) the day after the footshock exposure subsequently displayed more avoidance when compared to shock rats that exhibited a low level of anxiety (low responders, LR). These results highlight the importance of individual differences in the reaction to a strong fear-inducing experience. Second, the orexin precursor peptide prepro-orexin (ppOX) mRNA was found to be elevated in rats at 6 and 14 days after exposure to footshocks. In addition, ppOX mRNA levels were found to be positively correlated with anxiety at 14 days post-shock. Third, pre-shock injections of the corticotropin releasing factor receptor antagonist antalarmin were found to attenuate the anxiety expressed to the shock chamber and eliminate the correlation between ppOX mRNA levels and anxiety. Fourth, systemic injections of the nonselective orexin receptor antagonist TCS-1102 was found to attenuate the anxiety expressed in rats at 14 days post-shock. Fifth, TCS-1102 was found to have anxiolytic effects that were specific for the HR. The results of these experiments provide evidence linking the orexin system to the anxiety produced by exposure of rats to footshocks. They also provide preclinical evidence in support of the use of orexin antagonists for the treatment of anxiety in PTSD.
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The involvement of the neuropeptides orexins (hypocretins) in fear and anxiety in rats exposed to a single episode of footshocksChen, Xiaoyu 08 1900 (has links)
Post-traumatic stress disorder (PTSD) is a psychiatric condition that can develop when people experience a stressful and life-threatening event. Clinical research indicates that the presence of a state of hyperarousal after a traumatic experience is the best predictor of a subsequent diagnosis of PTSD. The role of arousal peptides called orexins (hypocretins) in a PTSD-like condition produced by exposing rats to a single episode of footshocks (5× 2 s episodes of 1.5 mA) was investigated in this thesis. The first part of my thesis involves the characterization of the footshock model of PTSD and the second part examines the involvement of orexins in this footshock model. The following findings are reported. First, shock rats that exhibited a high level of anxiety to a novel tone (high responders, HR) the day after the footshock exposure subsequently displayed more avoidance when compared to shock rats that exhibited a low level of anxiety (low responders, LR). These results highlight the importance of individual differences in the reaction to a strong fear-inducing experience. Second, the orexin precursor peptide prepro-orexin (ppOX) mRNA was found to be elevated in rats at 6 and 14 days after exposure to footshocks. In addition, ppOX mRNA levels were found to be positively correlated with anxiety at 14 days post-shock. Third, pre-shock injections of the corticotropin releasing factor receptor antagonist antalarmin were found to attenuate the anxiety expressed to the shock chamber and eliminate the correlation between ppOX mRNA levels and anxiety. Fourth, systemic injections of the nonselective orexin receptor antagonist TCS-1102 was found to attenuate the anxiety expressed in rats at 14 days post-shock. Fifth, TCS-1102 was found to have anxiolytic effects that were specific for the HR. The results of these experiments provide evidence linking the orexin system to the anxiety produced by exposure of rats to footshocks. They also provide preclinical evidence in support of the use of orexin antagonists for the treatment of anxiety in PTSD.
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