The Experts below are selected from a list of 321 Experts worldwide ranked by ideXlab platform
Mitchell F. Roitman - One of the best experts on this subject based on the ideXlab platform.
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the aversive agent Lithium Chloride suppresses phasic dopamine release through central glp 1 receptors
Neuropsychopharmacology, 2016Co-Authors: Samantha M Fortin, Elena H Chartoff, Mitchell F. RoitmanAbstract:Unconditioned rewarding stimuli evoke phasic increases in dopamine concentration in the nucleus accumbens (NAc) while discrete aversive stimuli elicit pauses in dopamine neuron firing and reductions in NAc dopamine concentration. The unconditioned effects of more prolonged aversive states on dopamine release dynamics are not well understood and are investigated here using the malaise-inducing agent Lithium Chloride (LiCl). We used fast-scan cyclic voltammetry to measure phasic increases in NAc dopamine resulting from electrical stimulation of dopamine cell bodies in the ventral tegmental area (VTA). Systemic LiCl injection reduced electrically evoked dopamine release in the NAc of both anesthetized and awake rats. As some behavioral effects of LiCl appear to be mediated through glucagon-like peptide-1 receptor (GLP-1R) activation, we hypothesized that the suppression of phasic dopamine by LiCl is GLP-1R dependent. Indeed, peripheral pretreatment with the GLP-1R antagonist exendin-9 (Ex-9) potently attenuated the LiCl-induced suppression of dopamine. Pretreatment with Ex-9 did not, however, affect the suppression of phasic dopamine release by the kappa-opioid receptor agonist, salvinorin A, supporting a selective effect of GLP-1R stimulation in LiCl-induced dopamine suppression. By delivering Ex-9 to either the lateral or fourth ventricle, we highlight a population of central GLP-1 receptors rostral to the hindbrain that are involved in the LiCl-mediated suppression of NAc dopamine release.
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the aversive agent Lithium Chloride suppresses phasic dopamine release through central glp 1 receptors
Neuropsychopharmacology, 2016Co-Authors: Samantha M Fortin, Elena H Chartoff, Mitchell F. RoitmanAbstract:Unconditioned rewarding stimuli evoke phasic increases in dopamine concentration in the nucleus accumbens (NAc) while discrete aversive stimuli elicit pauses in dopamine neuron firing and reductions in NAc dopamine concentration. The unconditioned effects of more prolonged aversive states on dopamine release dynamics are not well understood and are investigated here using the malaise-inducing agent Lithium Chloride (LiCl). We used fast-scan cyclic voltammetry to measure phasic increases in NAc dopamine resulting from electrical stimulation of dopamine cell bodies in the ventral tegmental area (VTA). Systemic LiCl injection reduced electrically evoked dopamine release in the NAc of both anesthetized and awake rats. As some behavioral effects of LiCl appear to be mediated through glucagon-like peptide-1 receptor (GLP-1R) activation, we hypothesized that the suppression of phasic dopamine by LiCl is GLP-1R dependent. Indeed, peripheral pretreatment with the GLP-1R antagonist exendin-9 (Ex-9) potently attenuated the LiCl-induced suppression of dopamine. Pretreatment with Ex-9 did not, however, affect the suppression of phasic dopamine release by the kappa-opioid receptor agonist, salvinorin A, supporting a selective effect of GLP-1R stimulation in LiCl-induced dopamine suppression. By delivering Ex-9 to either the lateral or fourth ventricle, we highlight a population of central GLP-1 receptors rostral to the hindbrain that are involved in the LiCl-mediated suppression of NAc dopamine release.
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c fos induction in rat brainstem in response to ethanol and Lithium Chloride induced conditioned taste aversions
Alcoholism: Clinical and Experimental Research, 1996Co-Authors: Todd E Thiele, Mitchell F. Roitman, Llene L BernsteinAbstract:When consumption of a novel taste (conditioned stimulus; CS) is followed by exposure to a toxin, organisms will avoid consumption of that taste in the future. This learned response, known as a conditioned taste aversion (CTA), can be demonstrated using a variety of drugs, including Lithium Chloride (LiCl) and ethanol. c-Fos immunohistochemistry was used to examine neural activation in the rat brainstem associated with drug administration and with a CS taste previously paired with these drugs. Relative to saline controls, animals injected with either LiCl (76 mg/kg) or ethanol (3.5 g/kg) displayed greater c-Fos expression in area postrema, nucleus of the solitary tract (NTS), and lateral parabrachial nucleus. At these doses, LiCl- and ethanol-injected groups did not differ from each other. For establishing a CTA, intraoral infusion of a 0.15% saccharin solution was followed by injection of either LiCl or ethanol. Both LiCl and ethanol produced quantitatively similar CTAs. Relative to unpaired control groups, saccharin paired with either drug induced significant c-Fos expression in NTS. Thus, like LiCl, ethanol and tastes that have become aversive by virtue of their association with ethanol activate brainstem regions hypothesized to play a role in CTA learning.
Thore S. Berntsson - One of the best experts on this subject based on the ideXlab platform.
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Viscosity and density of aqueous solutions of Lithium bromide, Lithium Chloride, zinc bromide, calcium Chloride and Lithium nitrate. 2. Two-salt solutions
Journal of Chemical & Engineering Data, 1994Co-Authors: J. Martin Wimby, Thore S. BerntssonAbstract:New experimental data for the viscosity and density of the binary systems Lithium Chloride+water, Lithium bromide+water, calcium Chloride+water, Lithium nitrate+water, and zinc bromide+water are presented. Densities are presented in tabular form and as 10-parameter correlations, while Cinematic and dynamic viscosities are presented in tabular form. Data are presented in the concentration range from intermediate dilution to close to room temperature crystallization concentration. The temperature ranges are 20-70 o C for density and 25-90 o C for viscosity. When available, literature data are compared with the new data, and some disagreement is found
Samantha M Fortin - One of the best experts on this subject based on the ideXlab platform.
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the aversive agent Lithium Chloride suppresses phasic dopamine release through central glp 1 receptors
Neuropsychopharmacology, 2016Co-Authors: Samantha M Fortin, Elena H Chartoff, Mitchell F. RoitmanAbstract:Unconditioned rewarding stimuli evoke phasic increases in dopamine concentration in the nucleus accumbens (NAc) while discrete aversive stimuli elicit pauses in dopamine neuron firing and reductions in NAc dopamine concentration. The unconditioned effects of more prolonged aversive states on dopamine release dynamics are not well understood and are investigated here using the malaise-inducing agent Lithium Chloride (LiCl). We used fast-scan cyclic voltammetry to measure phasic increases in NAc dopamine resulting from electrical stimulation of dopamine cell bodies in the ventral tegmental area (VTA). Systemic LiCl injection reduced electrically evoked dopamine release in the NAc of both anesthetized and awake rats. As some behavioral effects of LiCl appear to be mediated through glucagon-like peptide-1 receptor (GLP-1R) activation, we hypothesized that the suppression of phasic dopamine by LiCl is GLP-1R dependent. Indeed, peripheral pretreatment with the GLP-1R antagonist exendin-9 (Ex-9) potently attenuated the LiCl-induced suppression of dopamine. Pretreatment with Ex-9 did not, however, affect the suppression of phasic dopamine release by the kappa-opioid receptor agonist, salvinorin A, supporting a selective effect of GLP-1R stimulation in LiCl-induced dopamine suppression. By delivering Ex-9 to either the lateral or fourth ventricle, we highlight a population of central GLP-1 receptors rostral to the hindbrain that are involved in the LiCl-mediated suppression of NAc dopamine release.
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the aversive agent Lithium Chloride suppresses phasic dopamine release through central glp 1 receptors
Neuropsychopharmacology, 2016Co-Authors: Samantha M Fortin, Elena H Chartoff, Mitchell F. RoitmanAbstract:Unconditioned rewarding stimuli evoke phasic increases in dopamine concentration in the nucleus accumbens (NAc) while discrete aversive stimuli elicit pauses in dopamine neuron firing and reductions in NAc dopamine concentration. The unconditioned effects of more prolonged aversive states on dopamine release dynamics are not well understood and are investigated here using the malaise-inducing agent Lithium Chloride (LiCl). We used fast-scan cyclic voltammetry to measure phasic increases in NAc dopamine resulting from electrical stimulation of dopamine cell bodies in the ventral tegmental area (VTA). Systemic LiCl injection reduced electrically evoked dopamine release in the NAc of both anesthetized and awake rats. As some behavioral effects of LiCl appear to be mediated through glucagon-like peptide-1 receptor (GLP-1R) activation, we hypothesized that the suppression of phasic dopamine by LiCl is GLP-1R dependent. Indeed, peripheral pretreatment with the GLP-1R antagonist exendin-9 (Ex-9) potently attenuated the LiCl-induced suppression of dopamine. Pretreatment with Ex-9 did not, however, affect the suppression of phasic dopamine release by the kappa-opioid receptor agonist, salvinorin A, supporting a selective effect of GLP-1R stimulation in LiCl-induced dopamine suppression. By delivering Ex-9 to either the lateral or fourth ventricle, we highlight a population of central GLP-1 receptors rostral to the hindbrain that are involved in the LiCl-mediated suppression of NAc dopamine release.
T K Gogoi - One of the best experts on this subject based on the ideXlab platform.
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multi objective optimization of double effect series and parallel flow water Lithium Chloride and water Lithium bromide absorption refrigeration systems
Energy Conversion and Management, 2019Co-Authors: D Konwar, T K GogoiAbstract:Abstract In this study, multi-objective optimization of the series and parallel flow type double effect absorption refrigeration systems is presented. Genetic algorithm is used to find the optimal solutions and the Pareto-optimal fronts. First, a thermodynamic model is developed to simulate the double effect series and parallel flow configurations with water–Lithium Chloride and water–Lithium bromide solution pairs. Energy and exergy balances are applied to evaluate coefficient of performance, exergy efficiency and irreversible losses in the system components separately for the two working fluid pairs. Next, optimization is done considering coefficient of performance, exergy efficiency and the total system irreversibility rate as objective functions. The low and high pressure generator temperatures are taken as decision variables in the series configuration while for the parallel system; additionally the distribution ratio is also taken as a decision parameter. The optimization is done for four different cases of fixed evaporator, absorber and condenser temperatures. For each case, the optimal decision parameter values are determined for both the water–Lithium Chloride and water–Lithium bromide operated double effect series and parallel configurations. The optimized coefficients of performance were found slightly lower for water–Lithium Chloride. Contrary to this, the optimal exergy efficiencies were more and the total system irreversibility were less for water–Lithium Chloride. Further, the optimal performances of the double effect water–Lithium Chloride systems were obtained comparatively at lower generator temperatures than those of the water–Lithium bromide systems.
Elena H Chartoff - One of the best experts on this subject based on the ideXlab platform.
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the aversive agent Lithium Chloride suppresses phasic dopamine release through central glp 1 receptors
Neuropsychopharmacology, 2016Co-Authors: Samantha M Fortin, Elena H Chartoff, Mitchell F. RoitmanAbstract:Unconditioned rewarding stimuli evoke phasic increases in dopamine concentration in the nucleus accumbens (NAc) while discrete aversive stimuli elicit pauses in dopamine neuron firing and reductions in NAc dopamine concentration. The unconditioned effects of more prolonged aversive states on dopamine release dynamics are not well understood and are investigated here using the malaise-inducing agent Lithium Chloride (LiCl). We used fast-scan cyclic voltammetry to measure phasic increases in NAc dopamine resulting from electrical stimulation of dopamine cell bodies in the ventral tegmental area (VTA). Systemic LiCl injection reduced electrically evoked dopamine release in the NAc of both anesthetized and awake rats. As some behavioral effects of LiCl appear to be mediated through glucagon-like peptide-1 receptor (GLP-1R) activation, we hypothesized that the suppression of phasic dopamine by LiCl is GLP-1R dependent. Indeed, peripheral pretreatment with the GLP-1R antagonist exendin-9 (Ex-9) potently attenuated the LiCl-induced suppression of dopamine. Pretreatment with Ex-9 did not, however, affect the suppression of phasic dopamine release by the kappa-opioid receptor agonist, salvinorin A, supporting a selective effect of GLP-1R stimulation in LiCl-induced dopamine suppression. By delivering Ex-9 to either the lateral or fourth ventricle, we highlight a population of central GLP-1 receptors rostral to the hindbrain that are involved in the LiCl-mediated suppression of NAc dopamine release.
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the aversive agent Lithium Chloride suppresses phasic dopamine release through central glp 1 receptors
Neuropsychopharmacology, 2016Co-Authors: Samantha M Fortin, Elena H Chartoff, Mitchell F. RoitmanAbstract:Unconditioned rewarding stimuli evoke phasic increases in dopamine concentration in the nucleus accumbens (NAc) while discrete aversive stimuli elicit pauses in dopamine neuron firing and reductions in NAc dopamine concentration. The unconditioned effects of more prolonged aversive states on dopamine release dynamics are not well understood and are investigated here using the malaise-inducing agent Lithium Chloride (LiCl). We used fast-scan cyclic voltammetry to measure phasic increases in NAc dopamine resulting from electrical stimulation of dopamine cell bodies in the ventral tegmental area (VTA). Systemic LiCl injection reduced electrically evoked dopamine release in the NAc of both anesthetized and awake rats. As some behavioral effects of LiCl appear to be mediated through glucagon-like peptide-1 receptor (GLP-1R) activation, we hypothesized that the suppression of phasic dopamine by LiCl is GLP-1R dependent. Indeed, peripheral pretreatment with the GLP-1R antagonist exendin-9 (Ex-9) potently attenuated the LiCl-induced suppression of dopamine. Pretreatment with Ex-9 did not, however, affect the suppression of phasic dopamine release by the kappa-opioid receptor agonist, salvinorin A, supporting a selective effect of GLP-1R stimulation in LiCl-induced dopamine suppression. By delivering Ex-9 to either the lateral or fourth ventricle, we highlight a population of central GLP-1 receptors rostral to the hindbrain that are involved in the LiCl-mediated suppression of NAc dopamine release.