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Veronika Somoza - One of the best experts on this subject based on the ideXlab platform.
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Structure-Dependent Effects of Cinnamaldehyde Derivatives on TRPA1-Induced Serotonin Release in Human Intestinal Cell Models.
Journal of agricultural and food chemistry, 2020Co-Authors: Barbara Lieder, Julia Katharina Hoi, Nathalie Burian, Joachim Hans, Ann-katrin Holik, Leopoldo Raul Beltran Marquez, Jakob Ley, Hanns Hatt, Veronika SomozaAbstract:Activation of the transient receptor potential (TRP) channel TRPA1 by cinnamaldehyde has been shown to stimulate Serotonin Release in enterochromaffin QGP-1 cells. However, the impact of cinnamaldehyde on Serotonin Release in enterocytes is less well understood. In addition, since the neurotransmitter Serotonin plays a regulatory role in a large variety of gastrointestinal and metabolic functions, it is of interest to study which structural characteristics determine cinnamaldehyde-induced Serotonin Release by enterocytes. Thus, the present study analyzed Serotonin Release in differentiated Caco-2 cells as a model for enterocytes in comparison to enterochromaffin QGP-1 cells after stimulation with cinnamaldehyde and 17 naturally occurring structurally related compounds by means of a Serotonin ELISA. Stimulation with cinnamaldehyde induced a dose-dependent increase in Serotonin Release starting from 0.5 mM in both cell lines, with a larger effect size in Caco-2 enterocytes compared to that in QGP-1 enterochromaffin cells. Serotonin Release in Caco-2 cells induced by additional 17 structurally related compounds correlated with Serotonin Release in QGP-1 cells, showing the highest effects for coniferylaldehyde with a 15.84 ± 3.23-fold increase in Caco-2 cells, followed by the parent compound cinnamaldehyde (13.45 ± 2.15), cinnamyl alcohol (6.68 ± 1.08), and α-methyl-cinnamaldehyde (6.59 ± 0.93). Analysis of structural and molecular characteristics that modulate Serotonin Release in Caco-2 enterocytes revealed that the ability of a compound to activate TRPA1, demonstrated by means of HEK293 cells transiently expressing hTRPA1, is a decisive factor to stimulate Serotonin Release in Caco-2 enterocytes, preferring small, electrophilic compounds with a lower polar surface area. In addition, blocking of TRPA1 using 30 μM AP-18 significantly reduced the cinnamaldehyde-induced Serotonin Release by 30.0 ± 5.24%, confirming a TRPA1-dependent component in Serotonin Release by Caco-2 cells.
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Impact of free Nε-carboxymethyllysine, its precursor glyoxal and AGE-modified BSA on Serotonin Release from human parietal cells in culture.
Food & function, 2018Co-Authors: Ann-katrin Holik, Verena Stöger, Kathrin Hölz, Mark M. Somoza, Veronika SomozaAbstract:Advanced glycation end products (AGEs) are frequently encountered in a western diet, in addition to their formation in vivo. N-Epsilon-carboxymethyllysine (CML), one of the chemically diverse compounds formed in the reaction between reducing carbohydrates and amines, is often used as a marker of advanced glycation, and has been shown to stimulate Serotonin Release from cells representing the central (SH-SY5Y cells) and the peripheral (Caco-2 cells) Serotonin system in vitro. Here, we investigated the effect of glyoxal, free CML, and protein-linked AGE-BSA on Serotonin Release from human gastric tumour cells, which originate from an adenocarcinoma of the stomach and have recently been shown to be capable of Serotonin synthesis and Release. Microarray experiments showed both CML and glyoxal to alter genes associated with Serotonin receptors. Furthermore, treatment with glyoxal resulted in a small change in RAGE expression while CML did not alter its expression. On a functional level, treatment with 500 μM CML increased extracellular Serotonin content by 341 ± 241%, while treatment with 1 mg mL−1 AGE-BSA led to a reduction by 49 ± 11% compared to non-treated cells. The CML-induced Serotonin Release was reduced by the HTR3 antagonist granisetron. Incubation with the RAGE antagonist FPS-ZM1 abolished the effect of AGE-BSA on Serotonin Release, while no impact on CML-induced Serotonin Release was observed. Furthermore, treatment with 5 mM CML stimulated proton secretion as a functional outcome measure, assessed using a pH sensitive dye. Taken together, these results indicate a likely HTR3-mediated, RAGE-independent effect of free CML on Serotonin Release and a RAGE-dependent mechanism for the protein linked AGE-BSA.
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the flavanone homoeriodictyol increases sglt 1 mediated glucose uptake but decreases Serotonin Release in differentiated caco 2 cells
PLOS ONE, 2017Co-Authors: Barbara Lieder, Julia Katharina Hoi, Joachim Hans, Ann-katrin Holik, Jakob Ley, Katrin Geissler, Barbara Friedl, Kathrin Liszt, Gerhard Krammer, Veronika SomozaAbstract:Flavanoids and related polyphenols, among them hesperitin, have been shown to modulate cellular glucose transport by targeting SGLT-1 and GLUT-2 transport proteins. We aimed to investigate whether homoeriodictyol, which is structurally related to hesperitin, affects glucose uptake in differentiated Caco-2 cells as a model for the intestinal barrier. The results revealed that, in contrast to other polyphenols, the flavanon homoeriodictyol promotes glucose uptake by 29.0 ± 3.83% at a concentration of 100 μM. The glucose uptake stimulating effect was sensitive to phloridzin, but not to phloretin, indicating an involvement of the sodium-coupled glucose transporter SGLT-1, but not of sodium-independent glucose transporters (GLUT). In addition, in contrast to the increased extracellular Serotonin levels by stimulation with 500 mM D-(+)-glucose, treatment with 100 μM homoeriodictyol decreased Serotonin Release by -48.8 ± 7.57% in Caco-2 cells via a phloridzin-sensitive signaling pathway. Extracellular Serotonin levels were also reduced by -57.1 ± 5.43% after application of 0.01 μM homoeriodictyol to human neural SH-SY5Y cells. In conclusion, we demonstrate that homoeriodictyol affects both the glucose metabolism and the Serotonin system in Caco-2 cells via a SGLT-1-meditated pathway. Furthermore, the results presented here support the usage of Caco-2 cells as a model for peripheral Serotonin Release. Further investigations may address the value of homoeriodictyol in the treatment of anorexia and malnutrition through the targeting of SGLT-1.
Gina L. Forster - One of the best experts on this subject based on the ideXlab platform.
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Chronic amphetamine treatment enhances corticotropin-releasing factor-induced Serotonin Release in the amygdala.
European Journal of Pharmacology, 2010Co-Authors: Jamie L. Scholl, Shawn M Vuong, Gina L. ForsterAbstract:Abstract Amphetamine use is associated with dysphoric states, including heightened anxiety, that emerge within 24 h of withdrawal from the drug. Corticotropin-releasing factor increases Serotonin Release in the central nucleus of the amygdala, and this neurochemical circuitry may play a role in mediating fear and anxiety states. We have previously shown that chronic amphetamine treatment increases corticotropin-releasing factor receptor type-2 levels in the serotonergic dorsal raphe nucleus of the rat. Therefore, we hypothesized that chronic amphetamine treatment would enhance the amygdalar serotonergic response to corticotropin-releasing factor infused into the dorsal raphe nucleus. Male rats were injected once-daily with d-amphetamine (2.5 mg/kg i.p., or saline) for two weeks. Serotonin Release within the central nucleus of the amygdala in response to intra-raphe infusion of corticotropin-releasing factor (100 ng) was measured 24 h after the last treatment in urethane-anesthetized (1.8 mg/kg, i.p.) rats using in vivo microdialysis. Rats pretreated with amphetamine showed significantly enhanced Serotonin Release in the central nucleus of the amygdala in response to corticotropin-releasing factor infusion when compared to saline pretreated rats. Furthermore, this enhanced response was blocked by the corticotropin-releasing factor type-2 receptor antagonist antisauvagine-30 (2 μg) infused into the dorsal raphe nucleus. These results suggest increased sensitivity to corticotropin-releasing factor as mediated by type-2 receptors following chronic amphetamine treatment, which may underlie dysphoric states observed during amphetamine withdrawal.
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Restraint stress increases Serotonin Release in the central nucleus of the amygdala via activation of corticotropin-releasing factor receptors.
Brain research bulletin, 2008Co-Authors: Na Feng, Kenneth J. Renner, Gina L. ForsterAbstract:Abstract Decreases in serotonergic activity in the central nucleus of the amygdala reduce responses to stressors, suggesting an important role for Serotonin in this region of the amygdala in stress reactivity. However, it is not known whether exposure to stressors actually increases Serotonin Release in the central nucleus of the amygdala. The current experiment tested the hypothesis that restraint stress increases extracellular Serotonin within the central nucleus of the amygdala and adjacent medial amygdala using in vivo microdialysis in awake male rats during the dark phase of the light–dark cycle. Serotonin Release in the central nucleus increased immediately in response to restraint stress. In contrast, there was no change in Serotonin Release within the adjacent medial amygdala during or following restraint. Since corticotropin-releasing factor is an important mediator of both responses to stressors and serotonergic activity, subsequent experiments tested the hypothesis that central nucleus serotonergic response to restraint stress is mediated by central corticotropin-releasing factor receptors. Administration of the corticotropin-releasing factor type 1 and 2 receptor antagonist d -Phe-CRF (icv, 10 μg/5 μl) prior to restraint stress suppressed restraint-induced Serotonin Release in the central nucleus. The results suggest that restraint stress rapidly and selectively increases Serotonin Release in the central nucleus of the amygdala by the activation of central corticotropin-releasing factor receptors. Furthermore, the results imply that corticotropin-releasing factor mediated serotonergic activity in central nucleus of the amygdala may be an important component of a stress response.
Michele Vacca - One of the best experts on this subject based on the ideXlab platform.
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glucagon like peptide 1 7 36 amide glp 1 and exendin 4 stimulate Serotonin Release in rat hypothalamus
Peptides, 2008Co-Authors: Luigi Brunetti, Lucia Recinella, Giustino Orlando, Sheila Leone, Claudio Ferrante, Annalisa Chiavaroli, Francesco Lazzarin, Michele VaccaAbstract:Glucagon-like peptide 1 (7-36) amide (GLP-1) and exendin-4 are gastrointestinal hormones as well as neuropeptides involved in glucose homeostasis and feeding regulation, both peripherally and at the central nervous system (CNS), acting through the same GLP-1 receptor. Aminergic neurotransmitters play a role in the modulation of feeding in the hypothalamus and we have previously found that peripheral hormones and neuropeptides, which are known to modulate feeding in the central nervous system, are able to modify catecholamine and Serotonin Release in the hypothalamus. In the present paper we have evaluated the effects of GLP-1 and exendin-4 on dopamine, norepinephrine, and Serotonin Release from rat hypothalamic synaptosomes, in vitro. We found that glucagon-like peptide 1 (7-36) amide and exendin-4 did not modify either basal or depolarization-induced dopamine and norepinephrine Release; on the other hand glucagon-like peptide 1 (7-36) amide and exendin-4 stimulated Serotonin Release, in a dose dependent manner. We can conclude that the central anorectic effects of GLP-1 agonists could be partially mediated by increased Serotonin Release in the hypothalamus, leaving the catecholamine Release unaffected.
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Glucagon-like peptide 1 (7–36) amide (GLP-1) and exendin-4 stimulate Serotonin Release in rat hypothalamus
Peptides, 2008Co-Authors: Luigi Brunetti, Lucia Recinella, Giustino Orlando, Sheila Leone, Claudio Ferrante, Annalisa Chiavaroli, Francesco Lazzarin, Michele VaccaAbstract:Glucagon-like peptide 1 (7-36) amide (GLP-1) and exendin-4 are gastrointestinal hormones as well as neuropeptides involved in glucose homeostasis and feeding regulation, both peripherally and at the central nervous system (CNS), acting through the same GLP-1 receptor. Aminergic neurotransmitters play a role in the modulation of feeding in the hypothalamus and we have previously found that peripheral hormones and neuropeptides, which are known to modulate feeding in the central nervous system, are able to modify catecholamine and Serotonin Release in the hypothalamus. In the present paper we have evaluated the effects of GLP-1 and exendin-4 on dopamine, norepinephrine, and Serotonin Release from rat hypothalamic synaptosomes, in vitro. We found that glucagon-like peptide 1 (7-36) amide and exendin-4 did not modify either basal or depolarization-induced dopamine and norepinephrine Release; on the other hand glucagon-like peptide 1 (7-36) amide and exendin-4 stimulated Serotonin Release, in a dose dependent manner. We can conclude that the central anorectic effects of GLP-1 agonists could be partially mediated by increased Serotonin Release in the hypothalamus, leaving the catecholamine Release unaffected.
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Effects of ghrelin and amylin on dopamine, norepinephrine and Serotonin Release in the hypothalamus.
European journal of pharmacology, 2002Co-Authors: Luigi Brunetti, Lucia Recinella, Giustino Orlando, Barbara Michelotto, Chiara Di Nisio, Michele VaccaAbstract:Ghrelin and amylin are gut-derived hormones that stimulate and inhibit food intake, respectively. Feeding is modulated by aminergic neurotransmitters in the hypothalamus. We have evaluated the effects of ghrelin and amylin on dopamine, norepinephrine and Serotonin Release from rat hypothalamic synaptosomes. We found that ghrelin did not modify dopamine or norepinephrine Release, but inhibited Serotonin Release. On the other hand, amylin inhibited dopamine Release, without affecting norepinephrine or Serotonin. We conclude that the appetite-stimulating activity of ghrelin could be mediated by inhibited Serotonin Release, while the anorectic effects of amylin could involve inhibited Release of dopamine in the hypothalamus.
Rachel F. Tyndale - One of the best experts on this subject based on the ideXlab platform.
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The role of CYP2D in rat brain in methamphetamine-induced striatal dopamine and Serotonin Release and behavioral sensitization
Psychopharmacology, 2021Co-Authors: Marlaina R. Stocco, Ahmed A. El-sherbeni, Bin Zhao, Maria Novalen, Rachel F. TyndaleAbstract:Rationale Cytochrome P450 2D (CYP2D) enzymes metabolize many addictive drugs, including methamphetamine. Variable CYP2D metabolism in the brain may alter CNS drug/metabolite concentrations, consequently affecting addiction liability and neuropsychiatric outcomes; components of these can be modeled by behavioral sensitization in rats. Methods To investigate the role of CYP2D in the brain in methamphetamine-induced behavioral sensitization, rats were pretreated centrally with a CYP2D irreversible inhibitor (or vehicle) 20 h prior to each of 7 daily methamphetamine (0.5 mg/kg subcutaneous) injections. In vivo brain microdialysis was used to assess brain drug and metabolite concentrations, and neurotransmitter Release. Results CYP2D inhibitor (versus vehicle) pretreatment enhanced methamphetamine-induced stereotypy response sensitization. CYP2D inhibitor pretreatment increased brain methamphetamine concentrations and decreased the brain p -hydroxylation metabolic ratio. With microdialysis conducted on days 1 and 7, CYP2D inhibitor pretreatment exacerbated stereotypy sensitization and enhanced dopamine and Serotonin Release in the dorsal striatum. Day 1 brain methamphetamine and amphetamine concentrations correlated with dopamine and Serotonin Release, which in turn correlated with the stereotypy response slope across sessions (i.e., day 1 through day 7), used as a measure of sensitization. Conclusions CYP2D-mediated methamphetamine metabolism in the brain is sufficient to alter behavioral sensitization, brain drug concentrations, and striatal dopamine and Serotonin Release. Moreover, day 1 methamphetamine-induced neurotransmitter Release may be an important predictor of subsequent behavioral sensitization. This suggests the novel contribution of CYP2D in the brain to methamphetamine-induced behavioral sensitization and suggests that the wide variation in human brain CYP2D6 may contribute to differential methamphetamine responses and chronic effects.
Ann-katrin Holik - One of the best experts on this subject based on the ideXlab platform.
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Structure-Dependent Effects of Cinnamaldehyde Derivatives on TRPA1-Induced Serotonin Release in Human Intestinal Cell Models.
Journal of agricultural and food chemistry, 2020Co-Authors: Barbara Lieder, Julia Katharina Hoi, Nathalie Burian, Joachim Hans, Ann-katrin Holik, Leopoldo Raul Beltran Marquez, Jakob Ley, Hanns Hatt, Veronika SomozaAbstract:Activation of the transient receptor potential (TRP) channel TRPA1 by cinnamaldehyde has been shown to stimulate Serotonin Release in enterochromaffin QGP-1 cells. However, the impact of cinnamaldehyde on Serotonin Release in enterocytes is less well understood. In addition, since the neurotransmitter Serotonin plays a regulatory role in a large variety of gastrointestinal and metabolic functions, it is of interest to study which structural characteristics determine cinnamaldehyde-induced Serotonin Release by enterocytes. Thus, the present study analyzed Serotonin Release in differentiated Caco-2 cells as a model for enterocytes in comparison to enterochromaffin QGP-1 cells after stimulation with cinnamaldehyde and 17 naturally occurring structurally related compounds by means of a Serotonin ELISA. Stimulation with cinnamaldehyde induced a dose-dependent increase in Serotonin Release starting from 0.5 mM in both cell lines, with a larger effect size in Caco-2 enterocytes compared to that in QGP-1 enterochromaffin cells. Serotonin Release in Caco-2 cells induced by additional 17 structurally related compounds correlated with Serotonin Release in QGP-1 cells, showing the highest effects for coniferylaldehyde with a 15.84 ± 3.23-fold increase in Caco-2 cells, followed by the parent compound cinnamaldehyde (13.45 ± 2.15), cinnamyl alcohol (6.68 ± 1.08), and α-methyl-cinnamaldehyde (6.59 ± 0.93). Analysis of structural and molecular characteristics that modulate Serotonin Release in Caco-2 enterocytes revealed that the ability of a compound to activate TRPA1, demonstrated by means of HEK293 cells transiently expressing hTRPA1, is a decisive factor to stimulate Serotonin Release in Caco-2 enterocytes, preferring small, electrophilic compounds with a lower polar surface area. In addition, blocking of TRPA1 using 30 μM AP-18 significantly reduced the cinnamaldehyde-induced Serotonin Release by 30.0 ± 5.24%, confirming a TRPA1-dependent component in Serotonin Release by Caco-2 cells.
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Impact of free Nε-carboxymethyllysine, its precursor glyoxal and AGE-modified BSA on Serotonin Release from human parietal cells in culture.
Food & function, 2018Co-Authors: Ann-katrin Holik, Verena Stöger, Kathrin Hölz, Mark M. Somoza, Veronika SomozaAbstract:Advanced glycation end products (AGEs) are frequently encountered in a western diet, in addition to their formation in vivo. N-Epsilon-carboxymethyllysine (CML), one of the chemically diverse compounds formed in the reaction between reducing carbohydrates and amines, is often used as a marker of advanced glycation, and has been shown to stimulate Serotonin Release from cells representing the central (SH-SY5Y cells) and the peripheral (Caco-2 cells) Serotonin system in vitro. Here, we investigated the effect of glyoxal, free CML, and protein-linked AGE-BSA on Serotonin Release from human gastric tumour cells, which originate from an adenocarcinoma of the stomach and have recently been shown to be capable of Serotonin synthesis and Release. Microarray experiments showed both CML and glyoxal to alter genes associated with Serotonin receptors. Furthermore, treatment with glyoxal resulted in a small change in RAGE expression while CML did not alter its expression. On a functional level, treatment with 500 μM CML increased extracellular Serotonin content by 341 ± 241%, while treatment with 1 mg mL−1 AGE-BSA led to a reduction by 49 ± 11% compared to non-treated cells. The CML-induced Serotonin Release was reduced by the HTR3 antagonist granisetron. Incubation with the RAGE antagonist FPS-ZM1 abolished the effect of AGE-BSA on Serotonin Release, while no impact on CML-induced Serotonin Release was observed. Furthermore, treatment with 5 mM CML stimulated proton secretion as a functional outcome measure, assessed using a pH sensitive dye. Taken together, these results indicate a likely HTR3-mediated, RAGE-independent effect of free CML on Serotonin Release and a RAGE-dependent mechanism for the protein linked AGE-BSA.
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the flavanone homoeriodictyol increases sglt 1 mediated glucose uptake but decreases Serotonin Release in differentiated caco 2 cells
PLOS ONE, 2017Co-Authors: Barbara Lieder, Julia Katharina Hoi, Joachim Hans, Ann-katrin Holik, Jakob Ley, Katrin Geissler, Barbara Friedl, Kathrin Liszt, Gerhard Krammer, Veronika SomozaAbstract:Flavanoids and related polyphenols, among them hesperitin, have been shown to modulate cellular glucose transport by targeting SGLT-1 and GLUT-2 transport proteins. We aimed to investigate whether homoeriodictyol, which is structurally related to hesperitin, affects glucose uptake in differentiated Caco-2 cells as a model for the intestinal barrier. The results revealed that, in contrast to other polyphenols, the flavanon homoeriodictyol promotes glucose uptake by 29.0 ± 3.83% at a concentration of 100 μM. The glucose uptake stimulating effect was sensitive to phloridzin, but not to phloretin, indicating an involvement of the sodium-coupled glucose transporter SGLT-1, but not of sodium-independent glucose transporters (GLUT). In addition, in contrast to the increased extracellular Serotonin levels by stimulation with 500 mM D-(+)-glucose, treatment with 100 μM homoeriodictyol decreased Serotonin Release by -48.8 ± 7.57% in Caco-2 cells via a phloridzin-sensitive signaling pathway. Extracellular Serotonin levels were also reduced by -57.1 ± 5.43% after application of 0.01 μM homoeriodictyol to human neural SH-SY5Y cells. In conclusion, we demonstrate that homoeriodictyol affects both the glucose metabolism and the Serotonin system in Caco-2 cells via a SGLT-1-meditated pathway. Furthermore, the results presented here support the usage of Caco-2 cells as a model for peripheral Serotonin Release. Further investigations may address the value of homoeriodictyol in the treatment of anorexia and malnutrition through the targeting of SGLT-1.
