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Selective serotonin reuptake inhibitors (SSRIs) are drugs that can alleviate symptoms of depression by blocking the reuptake of serotonin (5-HT) from the synaptic cleft, thereby increasing the amount of time that 5-HT remains active. Elevated levels of 5-HT within the synapse are associated with feelings of well-being; conversely, low levels of 5-HT are correlated with depressive symptoms. Recent studies have shown that SSRIs can also mediate their antidepressant effects by increasing brain levels of certain cytokines, including interferon gamma (IFNY). IFNY directly induces the expression of the protein p11 in neighboring neurons, which then interacts with 5-HTR4, a 5-HT transmembrane receptor. Figures 1 and 2 provide information about this interaction. 5-HTR4 protein ression (% of WT) 120T 100- 80- 60- 40+ WT ☐KO

Selective serotonin reuptake inhibitors (SSRIs) are drugs that can alleviate symptoms of depression by blocking the reuptake of serotonin (5-HT) from the synaptic cleft, thereby increasing the amount of time that 5-HT remains active. Elevated levels of 5-HT within the synapse are associated with feelings of well-being; conversely, low levels of 5-HT are correlated with depressive symptoms. Recent studies have shown that SSRIs can also mediate their antidepressant effects by increasing brain levels of certain cytokines, including interferon gamma (IFNY). IFNY directly induces the expression of the protein p11 in neighboring neurons, which then interacts with 5-HTR4, a 5-HT transmembrane receptor. Figures 1 and 2 provide information about this interaction. 5-HTR4 protein ression (% of WT) 120T 100- 80- 60- 40+ WT ☐KO

Chemistry
Chemistry
10th Edition
ISBN:9781305957404
Author:Steven S. Zumdahl, Susan A. Zumdahl, Donald J. DeCoste
Publisher:Steven S. Zumdahl, Susan A. Zumdahl, Donald J. DeCoste
Chapter1: Chemical Foundations
Section: Chapter Questions
Problem 1RQ: Define and explain the differences between the following terms. a. law and theory b. theory and...
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Selective serotonin reuptake inhibitors (SSRIs) are drugs that can alleviate symptoms of depression by blocking the reuptake of serotonin (5-HT) from the synaptic cleft, thereby increasing the amount of time that 5-HT remains active. Elevated levels of 5-HT within the synapse are associated with feelings of well-being; conversely, low levels of 5-HT are correlated with depressive symptoms. Recent studies have shown that SSRIs can also mediate their antidepressant effects by increasing brain levels of certain cytokines, including interferon gamma (IFNY). IFNY directly induces the expression of the protein p11 in neighboring neurons, which then interacts with 5-HTR4, a 5-HT transmembrane receptor. Figures 1 and 2 provide information about this interaction. 5-HTR4 protein expression (% of WT) CAMP levels (% change control) from MEM TOT Figure 1 5-HTR4 protein expression in plasma membrane-enriched fraction (MEM) of hippocampal lysate and in total hippocampal lysate (TOT) from p11 wild-type (WT) or p11 knockout (KO) mice 120T 100+ 80+ 60+ 40+ 20+ 0- p11 expression (% control) 120T 100+ 80+ 60+ 40+ 20- Figure 2 Effect of 5-HT on cAMP levels in cells transfected with 5-HTR4 and/or p11 Studies have shown that analgesics, such as ibuprofen (IBU), inhibit the behavioral antidepressant responses normally observed in mice undergoing chronic SSRI administration. Figure 3 shows the effect of citalopram (CIT), an SSRI, and IBU on IFNY expression in mice. Figure 4 shows the effect of IBU on p11 expression in the presence and absence of treatment with CIT. In both figures, VEHI represents the group given the control solution. 1.0T 300- 250- 200+ 150+ 100- 50- 0 Control p11 5-HTR4 5-HTR4 +p11 OA protein kinase OD OB. tyrosine kinase receptor. OC. ligand-gated ion channel. IFNY (fold change) G protein-coupled receptor. Figure 3 Effect of citalopram and ibuprofen on IFNY levels in the mouse frontal cortex # 0.8+ 0.6- According to the data presented in the passage, 5-HTR4 is a: O A. Histidine O B. Proline 0.4+ 0.2+ НО. O C. Tyrosine O D. Tryptophan ofI VEH IBU Figure 4 Effect of ibuprofen on p11 expression in the brain in the presence and absence of citalopram treatment -0.2- VEH WT око CIT IBU IBU + CIT 5-HT is synthesized from a single amino acid by a short metabolic pathway consisting of a hydroxylation reaction followed by a decarboxylation reaction. The chemical structure of 5-HT is shown. NH₂2 ■VEH □CIT From which amino acid is 5-HT synthesized? O A. Normal mice treated with an SSRI O B. Depressed mice treated with IBU OC. Normal mice treated with a placebo O D. Depressed mice treated with cytokines In an experiment in which IBU alone was administered to normal mice in order to determine whether long-term treatment with the analgesic can cause behavioral symptoms of depression, what would be the appropriate control group? Which comparison best determines whether IFNY is necessary for antidepressant-induced increases in the expression of p11? Expression levels of p11 in: O A. wild-type mice versus IFNY knockout mice, both treated with p11 O B. wild-type mice versus IFNY knockout mice, both treated with an SSRI OC. wild-type mice treated with IFNY versus wild-type mice treated with an SSRI OD. wild-type mice treated with IFNY versus wild-type mice treated with ibuprofen
Transcribed Image Text:Selective serotonin reuptake inhibitors (SSRIs) are drugs that can alleviate symptoms of depression by blocking the reuptake of serotonin (5-HT) from the synaptic cleft, thereby increasing the amount of time that 5-HT remains active. Elevated levels of 5-HT within the synapse are associated with feelings of well-being; conversely, low levels of 5-HT are correlated with depressive symptoms. Recent studies have shown that SSRIs can also mediate their antidepressant effects by increasing brain levels of certain cytokines, including interferon gamma (IFNY). IFNY directly induces the expression of the protein p11 in neighboring neurons, which then interacts with 5-HTR4, a 5-HT transmembrane receptor. Figures 1 and 2 provide information about this interaction. 5-HTR4 protein expression (% of WT) CAMP levels (% change control) from MEM TOT Figure 1 5-HTR4 protein expression in plasma membrane-enriched fraction (MEM) of hippocampal lysate and in total hippocampal lysate (TOT) from p11 wild-type (WT) or p11 knockout (KO) mice 120T 100+ 80+ 60+ 40+ 20+ 0- p11 expression (% control) 120T 100+ 80+ 60+ 40+ 20- Figure 2 Effect of 5-HT on cAMP levels in cells transfected with 5-HTR4 and/or p11 Studies have shown that analgesics, such as ibuprofen (IBU), inhibit the behavioral antidepressant responses normally observed in mice undergoing chronic SSRI administration. Figure 3 shows the effect of citalopram (CIT), an SSRI, and IBU on IFNY expression in mice. Figure 4 shows the effect of IBU on p11 expression in the presence and absence of treatment with CIT. In both figures, VEHI represents the group given the control solution. 1.0T 300- 250- 200+ 150+ 100- 50- 0 Control p11 5-HTR4 5-HTR4 +p11 OA protein kinase OD OB. tyrosine kinase receptor. OC. ligand-gated ion channel. IFNY (fold change) G protein-coupled receptor. Figure 3 Effect of citalopram and ibuprofen on IFNY levels in the mouse frontal cortex # 0.8+ 0.6- According to the data presented in the passage, 5-HTR4 is a: O A. Histidine O B. Proline 0.4+ 0.2+ НО. O C. Tyrosine O D. Tryptophan ofI VEH IBU Figure 4 Effect of ibuprofen on p11 expression in the brain in the presence and absence of citalopram treatment -0.2- VEH WT око CIT IBU IBU + CIT 5-HT is synthesized from a single amino acid by a short metabolic pathway consisting of a hydroxylation reaction followed by a decarboxylation reaction. The chemical structure of 5-HT is shown. NH₂2 ■VEH □CIT From which amino acid is 5-HT synthesized? O A. Normal mice treated with an SSRI O B. Depressed mice treated with IBU OC. Normal mice treated with a placebo O D. Depressed mice treated with cytokines In an experiment in which IBU alone was administered to normal mice in order to determine whether long-term treatment with the analgesic can cause behavioral symptoms of depression, what would be the appropriate control group? Which comparison best determines whether IFNY is necessary for antidepressant-induced increases in the expression of p11? Expression levels of p11 in: O A. wild-type mice versus IFNY knockout mice, both treated with p11 O B. wild-type mice versus IFNY knockout mice, both treated with an SSRI OC. wild-type mice treated with IFNY versus wild-type mice treated with an SSRI OD. wild-type mice treated with IFNY versus wild-type mice treated with ibuprofen
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