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Image Search Results
Journal: Neuropharmacology
Article Title: Switch from excitatory to inhibitory actions of ethanol on dopamine levels after chronic exposure: Role of kappa opioid receptors
doi: 10.1016/j.neuropharm.2016.07.022
Figure Lengend Snippet: (A) Schematic of the experimental paradigm. Mice were exposed to three cycles of air or ethanol vapor exposure. Each cycle consisted of 16 hours of air/ethanol vapor exposure followed of 8 hours of room air for four consecutive days, followed by three days of abstinence. This cycle was repeated three times. Microdialysis cannulation surgeries were conducted after termination of cycle two and two days before the beginning of cycle three. Voltammetry and microdialysis experiments were conducted at the cessation of the last 16 hour exposure. (B) Coronal sections showing locations of voltammetric measurements. Blue and red dots represent recording sites in air- and CIE-exposed mice, respectively. (C) Coronal sections showing microdialysis probe locations. Blue and red lines represent probe tracks in air- and CIE-exposed mice, respectively.
Article Snippet: Mice were placed in a
Techniques:
Journal: Neuropharmacology
Article Title: Switch from excitatory to inhibitory actions of ethanol on dopamine levels after chronic exposure: Role of kappa opioid receptors
doi: 10.1016/j.neuropharm.2016.07.022
Figure Lengend Snippet: Voltammetric measurements of baseline stimulated dopamine release and reuptake, and KOR activity. (A) Electrically stimulated baseline dopamine release is significantly lower in CIE (red bar) compared to air (blue bar) exposed mice. (B) The uptake rate of dopamine is faster in CIE (red bar) compared to air (blue bar) exposed animals. (C) Cumulative dose response curve of U69,593, a KOR agonist followed by norBNI, a KOR antagonist mediated reversal. The KOR activation-mediated reduction in electrically stimulated dopamine release was augmented in CIE exposed mice (red circle) in comparison to air exposed mice (blue circle). Bath application of norBNI increased the evoked dopamine release to the baseline levels in both air and CIE exposed mice. (D) In air exposed mice, the comparison between baseline (solid blue bar) and post-norBNI application (shaded blue bar) evoked dopamine release showed no differences. Similarly, in CIE exposed mice evoked dopamine release post-norBNI application (shaded red bar) matched the baseline dopamine release (solid red bar). (E) No differences were observed in baseline dopamine levels in air (blue bar) and CIE (red bar) exposed mice. (F) Saline injection (i.p.) did not increase dopamine levels in air and CIE exposed mice. U69,593 resulted in a significant reduction in dopamine (below baseline) in CIE (red circle) compared to air (blue circles) exposed mice. Voltammetry experimetns: Air (n = 5); Chronic intermittent ethanol (CIE; n = 5). Microdialysis experiments: Air (n = 6); CIE (n = 6). *** p < 0.001; ** p < 0.01; * p < 0.05.
Article Snippet: Mice were placed in a
Techniques: Activity Assay, Activation Assay, Comparison, Saline, Injection
Journal: Neuropharmacology
Article Title: Switch from excitatory to inhibitory actions of ethanol on dopamine levels after chronic exposure: Role of kappa opioid receptors
doi: 10.1016/j.neuropharm.2016.07.022
Figure Lengend Snippet: Microdialysis measurements of baseline and ethanol-induced extracellular levels of dopamine in the absence and presence of norBNI. (A) Baseline extracellular levels of dopamine were not different between air (solid red bar) and CIE (solid blue bar) exposed mice pretreated with saline. Furthermore, administration of norBNI did not alter the dopamine levels in air (shaded red bar) and CIE (shaded blue bar) exposed mice. (B) Acute ethanol administration resulted in the expected increase in dopamine levels in air exposed mice pretreated with saline (solid blue circles). However, in the CIE exposed mice pretreated with saline (solid red circles), ethanol administration resulted in a reduction in dopamine levels compared to baseline. (C) The effect of acute ethanol administration on extracellular dopamine levels was not different in air exposed mice pretreated with saline (solid blue circles) and norBNI (shaded blue circles). (D) NorBNI pretreatment in CIE exposed mice (shaded red circles) reversed the ethanol-mediated reduction in dopamine levels observed in saline pretreated CIE exposed mice (solid red circles). Air-saline (n = 5); Air-norBNI (n = 5); CIE-saline (n = 5); CIE-norBNI (n = 5). ### p < 0.001; ## p < 0.01; comparison of ethanol-induced elevation/reduction in dopamine levels to baseline dopamine levels within a group. Comparison between air exposed and CIE exposed groups. *** p < 0.001; ** p < 0.01; comparison between air exposed and CIE exposed groups.
Article Snippet: Mice were placed in a
Techniques: Saline, Comparison
Journal: Molecules
Article Title: Impact of UV Irradiation on the Chitosan Bioactivity for Biopesticide Applications
doi: 10.3390/molecules28134954
Figure Lengend Snippet: Irradiated-chitosan-induced phosphorylation of MAPKs in grapevine. Activation of two MAPKs detected using immunoblotting with an antibody raised against the human phosphorylated extracellular regulated protein kinase ½ (α-pERK1/2) in grapevine leaf discs treated with non-irradiated or Sun test (Q-Sun XE-1 system)- or UV-box-irradiated chitosan (1 mg/mL) or water (negative control). Homogeneous loading was checked using Ponceau red staining.
Article Snippet: The distance between the lamp and the sample was ~25 cm, the light intensity was 0.25 mW/cm 2 , and the temperature was maintained at 25 °C using a fan. (2) The Petri dishes were covered with a borosilicate lid to protect the
Techniques: Irradiation, Activation Assay, Western Blot, Negative Control, Staining