40. Use the diagram below for this question. In this research study, Jager et al. (Frontiers Psychiatry, 2019) used the elevated-plus maze test in mice to examine the effects of increasing doses of the psychostimulant known as methylphenidate (MPH). From the pictures and graph provided, what could they conclude? Elevated-plus maze test after acute treatment with methylphenidate (MPH) Time in Open Arms Venice Contra MPH 3 mg/kg MPH 10 mak a. MPH significantly augmented anxiety in a dose-dependent manner. b. MPH significantly reduced anxiety in a dose-dependent manner. c. MPH significantly augmented depression in a dose-dependent manner. d. MPH significantly reduced depression in a dose-dependent manner. Neng TotalTime urine

40. Use the diagram below for this question. In this research study, Jager et al. (Frontiers Psychiatry, 2019) used the elevated-plus maze test in mice to examine the effects of increasing doses of the psychostimulant known as methylphenidate (MPH). From the pictures and graph provided, what could they conclude? Elevated-plus maze test after acute treatment with methylphenidate (MPH) Time in Open Arms Venice Contra MPH 3 mg/kg MPH 10 mak a. MPH significantly augmented anxiety in a dose-dependent manner. b. MPH significantly reduced anxiety in a dose-dependent manner. c. MPH significantly augmented depression in a dose-dependent manner. d. MPH significantly reduced depression in a dose-dependent manner. Neng TotalTime urine

An Illustrated Guide To Vet Med Term

4th Edition

ISBN:9781305465763

Author:ROMICH

Publisher:ROMICH

Chapter13: Nerves Of Steel

Section: Chapter Questions

Problem 6CTE

See similar textbooks

Similar questions

Link: https://doi.org/10.1186/s12868-022-00692-1 A. In the effect of mitoxantrone on histopathological changes in the brain section of the results section the authors wrote “In Fig. 4, the demyelination of (A-C) the cerebellum and (F-H) brain stem was evaluated using LFB staining and median scored 2.5 in both sedentary and exercised untreated EAE rats indicating extensive demyelination.” Why was demyelination evaluated in this study? B. In the effect of mitoxantrone on histopathological changes in the brain section of the results section the authors wrote “Post-administration of mitoxantrone to sedentary and exercised groups smaller patches of demyelination with microcyst formation and lymphocytic infiltrates were seen; and bare unmyelinated axons were fewer (Figs. 3D, E, I, J and 4D, E, I, J).” Based on this quote, what is mitoxantrone doing exactly/directly?
A consumer survey has highlighted a major increase in the use of Pregabalin, an authorised antiepileptic drug. The working hypothesis is that this drug is being used in other pathologies, such as to treat neuropathic pain. What sort of indicators could we use to obtain information that might enable us to test this hypothesis? Select one: O a. The conducting of a controlled clinical trial enabling us to assess the efficacy of Pregabalin in neuropathic pain. O b. The construction of drug-indication indicators (studying consumption in terms of the indication for which it is prescribed). O c. The construction of indicators that relate the drug to the indication and the treatment outcome. O d. A comparison between the consumption of Pregabalin in defined daily doses per 1000 inhabitants per day and the diagnosed prevalence of epilepsy.
In the experiment of the impacts of sedative and hypnotic acivities in MEJP leaves, does the different behavioral models in mice are the independent variables while the amount of dosage is the dependent variables?
Aducanumab is a human antibody treatment strategy currently undergoing phase III clinical trials in Alzheimer’s disease. This acts by: (choose all that apply) increasing cholinergic stimulation selectively inhibiting serotonin stimulating dopamine receptors reducing the production of Aβ plaques promoting neurogenesis reducing neurofibrillary tangles
Looking at Fig. 3a and 3b, how do you know that 3a has a significant difference and that Fig. 3b does not? In the euthyroid HT induces ultrastructure changes in frontal synapses section of the results section the authors wrote “Quantitatively, the ultrastructure of the frontal lobe neurons revealed lower synaptic density (Fig. 5c), fewer presynaptic vesicles (Fig. 5d), shorter active zone length (Fig. 5e), thinner postsynaptic densities (Fig. 5g), and decreased synaptic curvature (Fig. 5h) in the HT mice compared with those in the Con mice.” Based on this quote would you expect nerve transmission to be faster or slower in HT mice?
Please answer the question based on on the following article.(The article is a systematic review and the question come from my systematic review critique paper) Article: "Optimal nonpharmacological management of agitation in Alzheimer’s disease: challenges and solutions" by José Carlos Millán-Calenti,1 Laura Lorenzo-López,1 Begoña Alonso-Búa,1 Carmen de Labra,2 Isabel González-Abraldes,1 and Ana Maseda1 Questions: Credibility: for the following questions provide a brief rationale or explanation for your answers. Yes, No or Not Clear is not sufficient. How did the authors address the quality of the studies they included? What criteria were used to assess the quality?
Seasonal affective disorder (SAD) is a mood disordercharacterized by, among other symptoms, increasedappetite, sluggishness, and increased sleepiness. It occursmost commonly during the winter months, especially inregions with long winter nights. Propose a role formelatonin in SAD and a possible non-drug therapy.
Part 2: Please read the following scenarios. For each scenario, identify the confound and suggest how it might be removed in a follow-up experiment. McCann and Holmes (1984) tested the hypothesis that exercise reduces depression. They randomly assigned depressed undergraduate women either to an exercise condition (attending an aerobics class a couple of times a week for ten weeks) or to a relaxation training condition (the individuals relaxed at home by watching a videotape over the same period of time). Although the results showed that the exercise group reported less depression at the end of the ten-week period than did the relaxation group, why can't the researchers conclude that exercise reduces depression?
3) Where is TTX obtained from? 4) What was the effect of Lidocaine? 5) Relate 4 above to Lidocaine's clinical use Activity 5: Measuring Refractory Periods of Neurons: this simulation you will gradually decrease the time between successive stimuli until: d. A stronger stimulus is required to generate a 2nd AP (relative refractory period) of b. A second AP cannot be produced at all (absolute refractory period). Use your data from Chart 5 to answer the questions below: 1) What interval between stimuli initially prevented a second AP? 2) Was this the relative or absolute refractory period? 3) What was the minimum interval for relative refractory period (hint: minimum interval where you could still generate a second AP with a stronger stimulus? 4) What interval completely prevented a second AP? 5) Is this relative or absolute RP? ME Activity 6: The "Language" of the nervous system: Frequency of Aps. Use your data from Chart 6 to answer the questions below: 1) What is the effect of…
The receptor or drug target in this case was the rat GABAA receptor obtained from homogenised rat brain cortical tissue. Using the same radioligand binding technique, what other way could you look at ligand affinity to GABAA receptors without using GABAA receptors derived from homogenised tissue and What are the advantages/disadvantages to each strategy?
Why is experimental design the best study for fentanyl exposure in the brain.
Kirsch (2010) argues that in double-blind clinical trials to test the effects of antidepressants, a large fraction of patients figure out whether they have been given the antidepressant or the placebo by noticing the presence or absence of known side effects of the antidepressant. Doctors evaluating the patients are also able to determine which treatment patients are receiving. How might this situation affect the results of the clinical trial? Specifically, is the treatment effect (difference between the means of the antidepressant and placebo treatments) likely to be overestimated, underestimated, or unaffected by this knowledge?