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Questions related to Behavioral Pharmacology
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I'm looking for protocols that mimic clinically relevant the exposure to oral methylphenidate in mice. More specifically, I'm looking for the protocols that achieve the exposure we see in humans following continuous oral dosing with extended release methylphenidate formulations. I am aware of the acute studies that attempted to establish such a protocol (e.g. Bhide's group: 10.1016/j.neuropharm.2009.07.025) or the attempts in rats (e.g. Thanos group: 10.1016/j.pbb.2015.01.005), but I can't find what would be a relevant chronic oral dosing regimen with methylphenidate in mice. Do you have any ideas who might be using such a protocol? What would be important to take into account when trying to establish it if it still does not exist (e.g. the metabolic rate seems to be quite different between humans and rodents? Also can we expect the same brain exposure given stable plasma concentrations?).
Thanks!
Jan
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I'm interested in analytical protocols for measuring exposure to methylphenidate in mice, especially HPLC-based methods. What are the possibilities regarding detectors and sample preparation procedures? Also, considering limited volume of blood can be obtained from mice (and sampling in more time-points probably affects the obtained results) - what would be the best option in the context of the minimal volume of sample needed for the analysis? What about enantiomers (e.g. 10.1002/bmc.3312). I'd like to find/establish a protocol for clinically relevant chronic oral dosing of methylphenidate in mice that reflects what we see in humans (https://www.researchgate.net/post/Protocols_for_clinically_relevant_chronic_oral_dosing_of_methylphenidate_in_mice)
Any info is greatly appreciated.
Jan
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Please advise on naltrexone stability.
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Yes, this will work. But why -4 degree and not a normal -20 degree freezer? In general, stability of compounds which are used in humans is really good
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A young patient attempted suicide by taking 63 tabs of carbamazepine 200 mg. she was managed with CRRT - CVVH and discharged 10 days later well and couscous.
data supporting the use of hemodialysis in managing carbamazepine poisoning is increasing, so I am not sure if it is worth publishing or not ( if it has a chance to get accepted for publishing)
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you must publish your findings
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I'm currently testing ketamine as an anti-depressant in female ovariectomized rats. Am curious what size field would be ideal to test the effects of ketamine 24h or 1 week after administration.
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Hi Colin,
We used a 60x60x30 cm white wooden box, with four 4 cm holes. As Caroline mentioned, you might want to use an elevated plus maze for measuring anxiety (recording time spent in closed areas). Measurements for the plus maze are 50x10 cm on each side, and the two opposite side closed areas have a 40 cm height. Maze is elevated by 50 cm.
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Dear researchers,
What are the detection methods for Estrogen hormone in the aqueous solution?
Can we use the UV-visible spectroscopy for Estrogen hormone (E1, E2 or EE2) detection? What is the suitable wavelength?
Best regards
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Please look at the following below attached files which may help you in your analysis.
Thanks
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The animal model should depict that the mechanism is through serotonin re-uptake transporter.
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A couple of behavioural pharmacology preclinical screens could be used in which SSRIs are active. Forced swim (Porsolt) test and tail suspension test (in mice) are the classic two. Would be better to quantify that you really only see a serotonin increase and not a noradrenaline / dopamine decrease to show selectivity of the serotonin transporter blockade over that of other amine transporters. Microdialysis with HPLC-ECD would be an option here. SSRIs also are used in OCD like behaviours so reversal of sub-chronic quinpirole induced compulsive checking of objects in the open field is also a possibility. Feel free to contact me if I can further advise.
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We're trying to inject the cascade blue dextran into mouse visual cortex by the protocol described in Wang & Burkhalter, 2007, but seem to have issues with the pipette clogging. We'd like to do it by iontophoretic injections so that we can closely control the injection amount, in order to only inject a small area. Any advice helps, thanks!
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What concentration of dextranamine are you using? I am using dextran, Alexa Fluor 488, 10000MW, anionic, fixable.
What volumes do you (try to) inject? 0.5
What injection system are you using? Simple syringe, with tubing and a glass pipette
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I have collected rats blood plasma, and serum & stored it at -4°C but the problem is that the serum and plasma have preserved more than 1 month.
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You can study mRNA expressions, they are quite stable.
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I am working on neuropharmacological activity & want to estimate total cholesterol, glucose, and saturated and unsaturated fatty acids in rat tissue. The available kit in the market is costly. I want to know Can I did this test with the help of reagent.
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Hello, cholesterol, saturated and non saturated fatty acids is cheapest possible way to analyse with good accuracy is by GC-FID. For glucose you can use different methods such as titrimetry, spectrophotometry or by HPLC wit refractive index detector.
Hope this info will help you.
Good luck!
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Background:
Professional-school student with extensive ACE (child adverse events) history along with severe depression and anxiety diagnosed over previous year, presented with recent severe ADHD (I-Type) diagnosis at age 26.
Documentation confirmed maximum dose step therapy for various Amphetamine-based stimulants was completed but still not found to be fully affective.
Unexpectedly, they are currently prescribed daily 50mg Mydayis (Mixed salts of single-entity amphetamine product) along with 80mg Prozac, and consumming 300-400mg of caffeine.
Due to initial medication-only use producing very minimal stabilizing effects, but found to increase at re-introduction of SSRI and further increase with Caffeine reintroduction.
No adverse effects (cardiac, neuromuscular, neurocognitive) have been reported/measured in 4 months of aforementioned therapeutic combination.
NOTE: Adverse reaction to methylphenidate-based medications were identified early on.
Assessment of (remaining) presenting symptoms seems to overlap with tentatively defined SCT Criteria.
NOTE: Student has never been prescribed Strattera (only presently confirmed SCT-symptom relief medication)
Specific question:
Recent research has shown SCT + ADHD to correlate with much greater impairment in adults, do you think a combination of severe ADHD + SCT may result in required use of excess pharmacotherapy dosages that surpass established safe therapeutic/combination parameters?
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Remember both PTSD and major depression can produce significant cognitive impairment including issues with attention equal to ADHD.
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I am doing research on learning and memory activity in rats. I have bought piracetam injection which is used for IM and IV route in human but I want to give through IP route in rats. can I do this?
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I think the injection which is available commercially would not be a decent experimental drug to test in animals because of the presence of other compounds in it.
Best thing to do would be buy the pure drug from a good company like sigma and reconstitute it with normal saline or whatever vehicle instructed to inject it intraperitoneally to the rats. This would be a proper way to study the effect of a particular drug.
Some of the nootropics have also used per oral in animal studies.
You should go through studies in the PubMed and then decide.
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I will do first-time electrophysiology of rats hippocampus. How can I interpret the learning and memory activity in rats by electrophysiology graph?
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In the hippocampus a well-known correlate of learning and memory is long-term-potentiation.
An electrophysiological correlate of working memory is e.g. persistent activity.
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In the elevated plus maze , Barnes maze test and many more behavioral models it is mentioned that 70 percent of ethanol is used for cleaning of maze. Is there any rationality behind it.
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Hi MSc Sharma, most studies use ethanol 70% because this is enough to eliminate any olfactory cues present in the apparatus used. If any cues remain, the next animal tested may repeat the behavior of the predecessor or at least have its behavior altered. But if you use ethanol 70%, you have to dry out the ethanol (paper towel) before placing the next animal because, otherwise, the smell of the alcohol could be very strong and also alter behavior. Some studies use more diluted concentrations of ethanol, like 10 or 20%, to avoid that the apparatus smells a lot like alcohol. Some studies even don't use the ethanol because they want to leave the olfactory cues between animals. I think it depends on what you're trying to answer.
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Project management in research project
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Yes, it is one of the foundations of research
Best Regards Javan Doloei
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I am working out a double-labeling immunofluorescence protocol.  I want to double label for ERa and cannabinoid receptor-1 in the brain tissue of rats. My ERa antibody is made in a rabbit and I have a protocol that is working for single labeling.  I would like to find an anti-CR1 antibody that is not made in a rabbit (or goat, as my 2º antibody is goat anti-rabbit).    
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We routinely use CB1 antibodies from Frontiers Institute (http://www.frontier-institute.com/wp/antibodies/?lang=en) for IHC/IF and have found them to be among the best commercially available CB1 antibodies.  Their goat version is the best but they also have a guinea pig version.
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I want to use DREADD inhibitory system to manipulate the activity of mPFC and use it in social behavior in mice. I bought the virus and I used it -for testing- in Fear conditioning and OFL (Observational Fear Learning) in mPFC and ACC respectively, but the is no effect and no change in mice behavior. After that, I test the expression of the fluorescent protein and It was ok. What is the probability of the problem?
Note: the ligand is CNO. (1mg/gm) .. injected 10 min before exp.
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Dear Abdelrahman Mohsen Alkahwaji,
As others have already indicated, the timing between your CNO injection and  behavior experiment (10min post-injection) is likely too soon to have a behavioral effect. We've shown that 10mg/kg dose of CNO doesn't peak in cerebrospinal fluid until 90min after a subcutaneous injection in monkeys (http://pubs.acs.org.proxy.library.emory.edu/doi/abs/10.1021/acschemneuro.7b00079 ). Our study also demonstrated that CNO is metabolized into clozapine at levels that would activate the DREADD receptor. Last, but not least. Dr. Michael Michaelides recently published an article in Science demonstrating CNO is only activating the DREADD receptor through this conversion to clozapine (http://science.sciencemag.org.proxy.library.emory.edu/content/357/6350/503.long). Therefore, it's possible that not only is the timing between injection and behavioral test too early, but also that you may not have enough CNO being converted into clozapine to active your DREADD receptor.  I suggest first increasing your CNO dose and testing at 90 min post-injection.  I also suggest that you try low dose (0.1mg/kg) clozapine to activate the DREADD instead of CNO, as Dr. Michaelides demonstrates in his paper. However, the timing between clozapine injection and behavior will be much shorter (5-10min post-injection) because clozapine enters the brain more freely as compared to CNO.
If you have any further questions or need clarification on anything I said please let me know.   
Sincerely,
Jessica
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What is the mechanism of action of Clomipramine "Anafranil" used for the treatment of nocturnal enuresis?
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Hi, The mechanism of action can be related to the anticholinergic side effect of the drug, which include urinary retention. Also, all three lower urinary tract controls, i.,e, parasympathetic, sympathetic, and somatic are associated with serotonin and norepinephrine-containing receptors, so increased extracellular levels of serotonin (5GT) and norepinephrine (NE) with clomipramine, which is a 5HT and NE reuptake inhibitor, expect to produce the observed effect. Finally, enuresis is classified as a disorder of arousal, and can occur in both REM and NREM sleep. The drug supresses REM duration, and increases N2, and is also known to lower seisure threshold, suggesting it has an impact on the arousal threshold. Kind regards. 
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We are studying the neurobiological basis of ethnic variations in responses to similar life events.
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Dear Adejoke,
We humans are all genetically very, very similar. The variations found within an ethnic group are large compared with the differences between the means of various ethnic groups. Most humans have genetic components from many, many ethnic groups - we are a mixture. (See National Geographic's Genome Project.)
The differences in values and behaviors are principally due to differences in culture.
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Please respond to this and I will "message" or contact you via RG messaging system. I would like to do a survey/questionnaire for a paper of those who teach such programs and those who supervise such interns and those who are/were such interns for a masters or PhD of Clinical Research.
So those studying or supervising those who were or are clinical research interns [including CRC, CRA, PI etc], please respond to this question or send me a private RG message.
Thank you in advance,
Respectfully,
Jeanetta Mastron
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Profa. Jeanetta, mi personal e-mail is cmariamar@hotmail.com
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I have existing code for a self administration study that I have been trying to alter so it can record the time interval of both active and inactive responses.  I seem to be able to have it record the total number of active/inactive responses in addition to the time of infusions but not the time array of each lever response. Any thoughts? 
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Here's an example below - in this case a single array (x) codes 3 different events, denoted by 0.1 as active response, 0.2 as inactive, 0.4 as end of infusion.  so 130.1 means active response at 13.0 seconds.  
Alternatively, you could use Z pulses (as Zachary mentioned and as we have done for end of infusion) for active and inactive responses instead of #R^active:, etc. 
- here's the link for the programmers guide (previous link was user guide) : http://www.mednr.com/pdf/doc003_MedPCProgramr.pdf  
s.s.3 \state set for event array
s1,
#start: set e=1 --->s2
s2,
#R^active: add a; show 1,active,a; set x(e)=t+0.1; set e=e+1; set x(e)=-987.987--->sx \0.1 is subscript for active press
#R^inactive: add b; show 2,inact,b; set x(e)=t+0.2; set e=e+1; set x(e)=-987.987 --->sx \0.2 is subscript for inactive press
#z1: set x(e)=t+0.4; set e=e+1; set x(e)=-987.987 --->sx \0.4 is subscript for end of infusion
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As far as I know only the L enantiomer of adrenaline has been found in the blood. But   collisions of this enantiomer in the blood could lead to a racemization producing a certain amount of the D enantiomer.
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the D(+) - adrenaline has not been tested on human beings. Moreover, no
endogenous D (+) - adrenaline has been found in the human body yet.
However, it is known that the L (-) - adrenaline in solution is inactivated by
racemization, that is, half of it is transformed into D (+) - adrenaline
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What are the minimum number of doses required to calculate ED50 of a sample in animal models? Is there any strict rules for minimum number of doses for ED50 calculation? For example, if there are only two doses one is showing less than 50% activity and another exhibiting more than 80% of activity, is it possible to calculate ED50 with these two doses? Sharing ideas and supporting documents are welcome.
Thanks in advance.
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Hi ,  Md. Moniruzzaman 
I think you must make a  pilot experiment to determine the maximum effect and the dose which given no effect according to the studied substance.  Dosing was set by the Dixon sequential up-down method; that is, a greater or less than certain %  of reduction in effect  decreased or increased the dose, respectively, by a fixed interval for the next subject. The median effective dose (ED50) was derived once 7 changes in dose direction occurred. A dose - response relation ship could be helpful in vitro.
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Doing a PK study on rosuvastatin in parrots
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Dear Hugues Beaufrere,
I am really sorry that i have not your expected data ...i do not get a sound scope for working on this field .
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I have treated ICR mice with an anxiolytic drug. I observed that almost 60% mice are responding to treatment (means giving anxiolytic effect) and 40% aren't (same as that of control group). Can I divide that treatment group in to Responders and non-responders? I have not see people do this before. Any suggestions? 
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It depends on your hypothesis. But: I've done this twice in my publications. Once for animal behavioral data, and once for analyzing the proportion of different types of responsive neurons to a drug stimulus (i.e., non-responsive neurons, neurons that showed increased activity in response to stimulus, and neurons that showed decreased activity to a stimulus). In this latter case, in my analyses, I eliminated the non-responders and I did a binomial exact test to see if the proportion of neurons showing an increased response were significantly greater/fewer in proportion to neurons showing a decreased response. 
Behavioral example:
Physiology example: (Attached). 
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It has been known for a long time now that cotinine, a metabolite of nicotine, is a nootropic and more importantly, is somewhat neuroprotective for PD and AD.  It is also known that cotinine is well tolerated by human subjects and has none of the negative side effects of nicotine itself.  Given today's great concern regarding both PD and AD, how can it be that research on this compound, very closely approximating a "silver bullet" if you will, is not being conducted with great intensity by NIH and/or the pharma industry?  Why does this seemingly magical solution to so many problems sit on the side while less practicable molecules get to dance?  
I don't get it. There is tons of research supporting this but not much is happening.  Why?
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Yes, Paul, I agree.  I was being a bit hyperbolic and put "silver bullet" in quotes for that very reason.  Thanks for the links; I read one of them previously.  I have read much on this and chatted with someone very active in research in this area.  The question still stands:  Why is this going nowhere?
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I have been thinking about using Clarity to compare the expression of specific protein before and after addictive drug treatment, to kind of visualizing aberrant plasticity at molecular level. But wondering if the resolution of Clarity would be good enough for this purpose, since the abnormal circuits are the primary reports from the Clarity methodology.
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In the case of major depressive disorder treatment (MDD) a full remission is main goal of the treatment, however about 2/3 of patients fail to achieve remission in first year of the treatment with antidepressant. In this point of view achieving remission is often connected with use of 2 different antidepressants (e.g. bupropion and SSRI, trazodone and SSRI, mirtazapine and venlafaxine ... ) or switching. In real clinical practice antipsychotics are also often added (e.g. aripiprazole, quetiapine and olanzapine). 
When you make decision which way (combine or switch) is more appropriate for the patients with MDD?
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This is a huge question and virtually with no simple answer. Partially responsive patients often represent a mixture of biological, psychosocial, personality, addictions and even economic or legal problems. Drugs provide no real benefit then. However, generally speaking, I try to keep treatment simple and prefer multiacting drugs over combinations. What I always try to add are BDNF-related therapies (such as fitness training or yoga:-) and CBT elements.
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The particular research study am conducting research about the efficacy of the “strengths” component in treatment plans for substance abuse, particularly with adolescents. My research  focuses on 2 areas:
When and why did the inclusion of “strengths” in the treatment plan begin?
What research is out there to show if it is helping with outcomes or not?
I was wondering if anyone could point me in the direction of resources?
Many thanks
Christine Rhodes
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Hi Christine,
In addition to the AA (Alcoholic Anonymous) model and the CBT (Cognitive-behavioral therapy) approaches to the treatment of substance-related disorders, there are strengths-based approaches such as motivational interviewing (MI) and solution-focused brief therapy (SFBT), etc. They attempt to elicit the client's motivation, cooperation, and strengths from the very beginning in the treatment process. Please see the following links.
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I feel that most researchers treat craving/cue-reactivity as an associative mechanism, but it could be described through operant mechanisms. I seem to remember Ken Perkins discussing this at SRNT a couple of years ago, but can't find a good write up by him or others in the field.
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We have several papers in which we explicitly use cues as discriminative stimuli presented in the start box of an alley, and predictive of the available (S+) or non-availability (S-) of a reward in the goal box. See papers by McFarland & Ettenberg for a start.
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Dear all,
I have to administer bromocriptine (BC) to mice to inhibit prolactin release to analyse the role of this hormone in behaviour. BC has a very low solubility in water. People usually do a stock (saturated) solution of BC in pure ethanol and then disolve it in PBS or water and inject it s.c. Since the final concentration of alcohol might be nearly 10%, BC injections are probably very painful, and this may invalidate the results of the ensuing behavioural analysis.
I've thought of using DMSO, in which it is much more soluble. Has anybody experience of drug administration in solutions containing relatively high concentrations of DMSO (about 1%)? Could I use i.p. injections, in that case?
Many thanks
Fernando
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I agree with most of the above answers, i also like to add that  the researcher can dissolve the proper dose of BK 0.2 ml of DMSO and then inject.
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My 5XFAD transgenic mice ( Alzheimer's disease) model raised in a 14h/10h light/dark cycle room.In both left-right discrimination T test and radial arm test, both are appetite motivated, the results showed no difference after training. I wonder whether is the longer light cycle affect the behaviour of the mice?
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I think that you are focusing to strong a variable which alone might not explain the effect you are observing. Every single animal facility is particular: light, food, air humidity, exposure to noise, exact genetic background of the mice you backcross...
Not reproducing already published and accepted results unfortunately happen, therefore running pilots might avoid to spend time and money on paradigm not adaptable to your facility.
To my mind, the most important parameters to control if you are doing cognition and anxiety tests are (please ignore the order): light and noise intensity in the testing room, age and gender of the mice, light/dark phase, training of your personal and handling of the animals (I mean the number of other tests that these mice experienced before going to these tasks).
Good luck to figure out the best conditions to run your project!
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Has anyone used time delay to induce amnesia instead of scopolamine or MK-801 for Y-maze or modified Y-maze before? I can find this method only in ORT, so I'm not sure it's possible to do in Y-maze or not.
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If you're talking about using longer inter-trial delays in reinforced matching or non-matching maze tasks to impair performance, then that is very commonly done.  If you're talking about spontaneous alternation in a y-maze, you can also use delays to induce amnesia.  Below is a link to a good full text review on spontaneous alternation Y-maze memory tasks and also a link to a paper that used delay, instead of drugs or stress, to worsen memory (in mutant's, WT's retained performance). 
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We are trying to inactivate the posterior parietal cortex in a behavioral task using archaerhodopsin under a general (CAG) promoter. At a high laser power (15mW), continuously stimulating over the course of 1s, I am not seeing any effect in the LFPs. We haven't observed any consistent behavioral effect either. On a different animal injected with arch, we were able to see an effect in the LFPs but we didn't get a consistent behavioral effect. This could be from the arch - we're not sure. Any advice for getting arch work reliably? 
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Consider
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If i have left over solution of CNO + DMSO that has been diluted in saline... Can i store this in -20 and reuse it in the future?
Or is making it fresh every time my only option?
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I make a big batch and freeze it in aliquots. I thaw one aliquot and dilute it to working concentration and use that for about 2 weeks (storing at 4C in between uses). It has worked fine for me. I can't remember if I ever refroze it and used it again. I probably did, but my experiments worked, so I didn't think twice about it.
Also I make up CNO in saline, not DMSO.
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Hello,
I am using 'metyrapone' to inhibit an stress-induced increase in the level of corticosterone in animal experiments.
What is the comparable agents of metyrapone for the catecholamine levels?
the agent should
1) should lower the level of catecholamine both in the brain and the peripheral tissue
2) should not change the baseline level of the catecholamines (because complete depletion of catecholamine would bring some undesired results in our study)
Now, I am considering 1) reserpine, 2) metyrosine (AMPT)
However, there are some issues on both two agents,
for 1) reserpine, I found that reserpine would depletes the baseline level of catecholamines, which would bring dopamine-mediated oxidative damage in the brain
for 2) metyrosine,  I could find only few researchers who have used this in their study
If you have any suggestion or idea, please let me know that
Thank you very much
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Hi Hwijin,
I'm not sure what you mean by wanting to #1) lower "levels" and #2) not lower "baseline levels". I think if you clarified this, the question might be easier to answer. Do you want a temporary depletion of catecholamines that will recover over time? If you do, then I think either resperine or AMPT would work.
I believe reserpine is a VMAT2 inhibitor so it will reduce the release but not synthesis of serotonin, dopamine and norepinephrine. By contrast, alpha methyl para tyrosine (AMPT) inhibits tyrosine hydroxylase so it will block the synthesis but not release of dopamine and norepinephrine.
I think there are plenty of studies that use AMPT that should help you decide if it's appropriate for your study. This is one study I like alot that used the combination of AMPT and L-DOPA to rapidly switch on and off dopamine synthesis. http://www.ncbi.nlm.nih.gov/pubmed/17046697
Hope that helps! ~ David
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Working on Open Field Test (OFT) animal tracking, i recently noticed that there is actually -no-  some )* "ground truth" published about the "normal" behavior of laboratory mice and rats in OFT. Being aware of the big influence of the specific environment in which OFT is done, nonetheless it should be possible to detect some kind of common characteristics in the animals behavior. And this may help researchers in future to evaluate their testing environment and improve their experimental settings to get more reliable results.
If you like to share video recordings of naive mice/rats for this purpose, please contact me via researchgate 
)* UPDATE: there is some data at Rat Genome Database - rgd.mcw.edu . see below for the actual access information. 
)* UPDATE: there is data on mice too: see Marin Jukic's answer below for the Mouse Phenome Database phoneme.jax.org 
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Dear Amdreas,
Ik have two suggestions for you.
- Contact Ruud Tegelenbosch (ruud@noldus.nl), the product manager of EthoVision, our video tracking system. He may have OFT video files that he can share with you.
- Post your question on the LinkedIn group "Measuring Behavior". Then you reach > 2.500 scientists, many of whom are users of video tracking systems and must possess video files of the type you are looking for.
Kind regards,
Lucas Noldus
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I am a research scholar currently focusing on ASDs. Impaired social interactions are a hallmark of ASDs. I need to know whether the terms social interaction and social behavior can be used synchronously or there is a difference?
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Hi,
In animal behaviour research social interaction is a valid and reliable measure of social behaviou. 
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Understanding the link between behavioral pharmacology in mice/rats/cats and clinical efficacy in uniquely human disorders like schizophrenia might provide insights re:neurobiological underpinnings of complex disorders.
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Thank you Béatrice Marianne Ewalds-Kvist for this very interesting paper !
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Hello,
For a behavioral paradigm, if the main measure does not show significant difference, but other measure related to the paradigm shows significant difference, can the other measure be correlated with deficiency?
To be specific, in Light/Dark Box assay, mice did not show significant changes in amount of time spent in light zone, but did show significant differences in number of transitions between the two zones. Can I use this measure to prove my hypothesis?
Thanks,
Goutham Kodakandla
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Number of transitions could be confounded by increased locomotor activity so you should also determine that your drug/treatment is not having this effect. Typically amount of time spent in the light versus dark side is the primary measure examined for indications that a drug treatment may increase/reduce anxiety-like behavior. You should be deciding on the measure you are interested in a priori and then running your experiment in order to either accept or reject the null hypothesis.
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Hi
I work with self-administration, and, as you know, performing a patency test by injecting methohexital (Brevital) into the catheter is essential. The problem is that this ultrashort- barbiturate is very difficult to find if you don't have a DEA license. Is there a similar compound that can do the same thing? or maybe another technique to verify that the catheter is working? I hope someone can give me suggestions! Thank you!
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I've used xylazine (Anased) to test catheter patency in the past and it has worked well. It's not scheduled so it should be easier to get. For rats, we would give IV administration of 0.05 ml of xylazine (20 mg/ml) and if we saw motor ataxia within 5 seconds, the catheter would be considered patent. I'm not sure if you're using mice or rats but it should work for both.
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The patient has responded to several APs regarding positive features but the negative features are quite treatment resistant to risperidone, olanzapine, amisulpride, ziprasidone, and aripiprazole.  Thanks.
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Consider to add mirtazapine as a coadjuvant therapy for antipsychotic treatment (e.g., aripiprazole). There is several clinical trials supporting the usefulness of mirtazapine for treating negative symptomatology when a given antipsychotic alone is unable to do it. See for instance: 
- Caforio et al. Mirtazapine add-on improves olanzapine effect on negative symptoms of schizophrenia. J Clin Psychopharmacol. 2013 Dec;33(6):810-2.
- Terevnikov et al. Add-on mirtazapine improves depressive symptoms in schizophrenia: a double-blind randomized placebo-controlled study with an open-label extension phase. Hum Psychopharmacol. 2011 Apr;26(3):188-93.
- Stenberg et al. More evidence on proneurocognitive effects of add-on mirtazapine in schizophrenia. Prog Neuropsychopharmacol Biol Psychiatry. 2011 Jun 1;35(4):1080-6.
- Cho et al. Mirtazapine augmentation enhances cognitive and reduces negative symptoms in schizophrenia patients treated with risperidone: a randomized controlled trial. Prog Neuropsychopharmacol Biol Psychiatry. 2011 Jan 15;35(1):208-11.
- Terevnikov et al. More evidence on additive antipsychotic effect of adjunctive mirtazapine in schizophrenia: an extension phase of a randomized controlled trial. Hum Psychopharmacol. 2010 Aug;25(6):431-8.
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The "dopamine argument" is one of the most enduring claims in texts about the effects of games and gamification.
The popular idea simplifies the functions of dopamine in the organism, by presenting it as a  "reward molecule". As scientists we are aware that this is a gross simplification. Yet it is a highly persistent claim, which we'd like to test in order to address the central claims in the popular discourse head on.
I am aware that the dopaminergic system can be monitored using e.g. PET, and I have found several references on the web about measuring it in blood samples, but are these viable ways of testing responses to e.g. game experiences?
The setup would be a factorial design or a RCT with game-elements as the 'treatment', and measures of game behavior plus subjectives experience as supportive DVs in addition to dopamine levels.
How could something like this be achieved? And is the idea realistic?
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Short answer: With current technology, measuring real-time dopamine release in vivo in humans is not really possible.
Longer answer:
(1) To measure dopamine responses to particular stimuli, you need a tool that allows good temporal resolution, so PET is not viable. In rare cases, you can get data on dopamine release in people using fast-scan cyclic voltammetry during surgery on patients, but that is not generally available. See:
Kishida, K. T., Sandberg, S. G., Lohrenz, T., Comair, Y. G., Sáez, I., Phillips, P. E., & Montague, P. R. (2011). Sub-second dopamine detection in human striatum. PloS one, 6(8), e23291.
(2) Dopamine is not simply a “reward molecule”. A better, but still simplified, characterization is that dopamine encodes a reward prediction error—the difference between expected reward and received reward. See:
Glimcher, P. W. (2011). Understanding dopamine and reinforcement learning: the dopamine reward prediction error hypothesis. Proceedings of the National Academy of Sciences, 108, 15647-15654.
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Does anybody know about the different kinds of video tracking softwares, besides ethovision, for monitoring animal's movement in open field test? 
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I have a paper coming out with Lyons in Behavioral Research Methods describing how to use the Microsoft Kinect gaming device. You should observe the animal, then you need to writ the scoring program, so it is not off the shelf. The Kinect costs several hundred dollars. 
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Thanks in advance!
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Hi Felipe,
Impairment of PPI is thought to be a measure of sensorimotor gating deficits, which appears to be also impaired in several neurological and psychiatric diseases (e.g. schizophrenia, Alzheimer, etc.). However, there is no robust evidence suggesting consistent relationships between lower levels of PPI and higher levels of specific symptoms of schizophrenia such as positive or negative symptoms scores. Similarly, no relationships between acoustic PPI and working memory as well as other formal indices of neurocognitive function, have been detected among schizophrenia patients (e.p., Swerdlow wt al. Psychopharmacology 2009, 199(3):331). It is my suspect that, by now, PPI models would rather be useful to evaluate mechanism involved (or thought involved) in antipsychotic effects (p.e., D2 antagonism, serotonergic, cholinergic, NMDA, etc.) than to evaluate specific effects of schizophrenia simptomatology of antipsychotic drugs.
Regards,
Jordi S
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These days I read in some article about behavior asymmetry coefficient that is calculated from parameters of open field test. However I didn't downloaded that paper. Now I can't find anything about that subject.
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Well ok thanks for advice. It is a constant room lightning we do not turn lights on during the experiment. In Light/Dark test we have constant light source 
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This is in rats. We also don't currently have operant chambers. Would there be any way to get to the answer without a lot of investment in materials?
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 I would just like to add a cautionary note about using the Forced Swim Test (FST) to assess depressive-like behavior, per se. This test has been used for a number of years by the pharmaceutical industry, primarily because it robustly predicts the therapeutic efficacy of monoamine uptake inhibitors for antidepressant activity in humans. In other words, the behavioral assay is exquisitely sensitive to this particular pharmacological mechanism of action, but this should not be taken to mean that the assay is necessarily measuring depressive-like behavior in rodents.
In terms of assay validity, as described above, the predictive validity of FST for the therapeutic efficacy of monoamine uptake inhibitors is quite high, while face and construct validity are modest at best (we don't know that the amount of time struggling corresponds to "despair"). Moreover, this screen is sensitive to acute drug administration, while therapeutic effects of the same compounds in humans are observed following several days or weeks of chronic dosing.
All of that said, right or wrong, FST is used fairly commonly in the literature for the purpose of measuring depressive-like behavior, although I think its explanatory power is fairly limited. Nevertheless, since you're interested in a low-cost, rapid screen, it may be worthwhile, keeping the above-mentioned caveats in mind.
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Is it possible to check the Acute toxicity of CCL4 in Olive oil (1:1) directly after 24 hrs of CCl4 administration (1ml/kg, i.p; CCL4 in Olive oil; 1:1) in Toxic Group of Mice instead of giving Olive oil (1 ml/kg, i. p.) for 6 days and on 7th days CCl4 (1ml/kg, i.p; CCL4 in Olive oil; 1:1)?
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Dear Ashu
I completely agree with suggestions made by Nikola and Pavle. Olive oil you are using is a vehicle for drug delivering, And the toxicity will be determined after 24 h of CCl4 administration. You can keep a separate group of vehicle control who will receive olive oil only in order to compare the results of the toxicity study.
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Based in your experience in research, what tests are more applied to evaluation of nociception behavior in orofacial region (skin, muscles or sinovial joint)? Thank you for your answer.
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I think rubbing time of upper lip (site of fomalin injection) will be used for sceening of pharmacological agent in formalin induced orofacial pain in rodents
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Let's say drug X produces a maximum response of 50, so its ED50 is the dose that elicits a response of 25. Drug Y produces a maximum response of 30, so its ED50 is the dose that elicits a response of 15. Isn't comparing these two with statistics like comparing apples and oranges? Yes, you could normalize the maximum response of each to 100, but that seems to be misleading when comparing two drugs. What I really need is a good published reference about the do's and don't of ED50 values, maximum responses, etc. and their analyses, especially in behavioral pharmacology.
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I may not be a good source for the book you want but I will tell you it's the ED50 that is reliable and repeatable. At best, maximal doses will be estimated as something like an ED99 and have much larger confidence intervals than ED50s. At worst, the maximal dose will be some imaginary number like twice the ED50.
I'm sure it's the maximal dose that is wanted by physicians and biologists. Unfortunately, it's easier (smaller confidence intervals) for statistics to estimate central tendencies than it is to estimate extreme values. You generally need a very expensive sample and a strong ethical rationale to obtain a maximal dose estimate with a confidence interval small enough to actually inspire confidence in the estimate.
It's not an easy read but my most current favorite on estimating ED50s (with a couple of short references to ED99s) is Statistical Techniques in Bioassay by Z. Govindarajulu (2001). The classic reference is Probit Analysis by Finney (1952).
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Is there any work already reported on S-nitrosothiol used against AD in animal models?
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Hi Sharma,
There are other things you can do about it. For example, go to Comparative Toxicogenomics Database (free)
Under search - select Chemical
Enter "S-nitrosothiol" and click on Search
The results page will show a number of tabs on top
Click on the "Diseases tab" - arrange it alfabeticaly by clicking on the arrows next to the disease heading in the tab
Look for Alzheimers disease - it will show two rows for Alzheimer- it contains genes regulated, etc, and also references from where the data is coming from (papers)
This is a starting point but you could explore other resources
I hope this helps
Good luck!
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As we know, mercury is poisonous and it can damage the human nervous system and brain. I want to clean the surface of the floor where mercury has spilled, without using sulphur and wet towel.
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Regarding the toxicity of metal Hg, I agree with the position of Zbigniew Zawada and with the suggestions for removing it. Those by B. Zhuikov and Alan Dyer , are also very effective
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Would chronic treatment through i.p. injections be considered a prolonged stressor affecting behavioral responses? What kind of conclusions could one draw if multiple-time vehicle-injected mice show significant differences in certain behavioral responses (for example, startle reactivity) compared to non-injected ones?
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Acclimatization is important to reduce pain to reduce the effect of it being a stressor. In the case of mice, I play with them for a week, each mice couple of minutes a day. 3 days prior to ip, I acclimatize the mice to sham injections daily with the exact size of needle I would use for IP (in my case 31G insulin syringe). Just like what Ian said, I use a needle per injection. Using these acclimatization techniques, I do not see a difference in the functional properties via electrophysiological recordings in control (non ip) and acclimatized ip animals.
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I would like to develop an amnesic model in mice or rats possibly for PhD research studies. I am interested in discussing possible protocols for this work with interested researchers. Histological, immunohistochemical, biochemical, pharmacological and other ideas are welcomed.
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There are several models you can look at.
Beside the scopolamine you can administer MK-801 (NMDA antagonist).
You can also make lesions of the basal forebrain cholinergic system. which is frequently used.
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What is the role of kynurenine aminotransferase in humans?
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kynurenic acid is a ligand of NMDA receptors. It has been related to neurological diseases, but I do not know the role of inhbitors of those enzymes
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I´m having troubles with my protocols. With ketamine/ xylazine either they don´t anesthetize or they die.
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Do you mix up your ket/xylazine or do you buy it premixed? You should try mixing your own and lowering the dose of xylazine. You can up the dose of ketamine if you need to (100 mg/kg, most likely) and keep the dose of xylazine around 5 mg/kg, which is this drug's lowest active dose. If that doesn't produce a deep enough level of anesthesia, you could try adding acepromazine (ket: 100 mg/kg; Xyl: 20 mg/kg; Ace: 3 mg/kg, IP). With the addition of acepromazine, you should be able to increase the dose of xylazine. However, we've found a lower dose of xylazine and a higher dose of ketamine increases survivability; we didn't want to add a third drug when altering the ket/xyl mixture seemed to work. Do you leave the mice on a heating pad after surgery? If so, only let them stay on it for 5-10 minutes, then put them back in their home cage to finish recovering. Good luck!
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We are looking for ways to improve the analysis of avoidance behavior of laboratory rodents in an arena. Currently we are using as a measure the time an animal spent in a defined area around a stimulus which is avoided. However, this measure is highly variable and I heard that there are better but more complex measures ("algorithms") which can be used to characterize avoidance. The animals are tracked by a video-tracking software which also recognizes the nose of the animals. Any advice is appreciated.
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I would not remove extreme individuals, unless they are really rare, as they are part of the population as well. Outliers should be rare, otherwise they are not outliers.
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I know that most antidepressants involve the monoaminergic system and have been shown to enhance brain (FC and HP) levels of 5-HT and NE. Do such antidepressants also enhance 5-HT and NE in the blood? Is it rational to investigate serum levels of monoamines as proof of antidepressant-like effect of a novel therapy?
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While most antidepressants block monoamines uptake, it is not clear at all which is the role of this blockade on antidepressants pharmacological activity. In fact, AD exert such effect after the first dose but antidepressant effect requires two or three weeks of continuous treatment. Several other theories have been proposed to explain antidepressant action: downregulation of adrenergic or serotonergic receptors, increments in the synthesis of BDNF and neurotrophic response, promotion of adult neurogenesis in hippocampus, epigenetic mechanisms as well.
On the other hand, you are right: antidepressants act not only on the brain but also in nerve terminals in the body. However, measuring monoamine leves after administrating a potentially antidepressant drug is not a validated method to assess antidepressant-like effect. Activity in experimental models of depression (forced swimming test, learned helplessness, etc.) are much better.
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I'm aware that MPH can improve skill writing in children with ADHD but I have not seen any systematic research describing the therapeutic effect of MPH in children with motor disturbances. Any suggestions?
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Hi, Stephane, They`ve tried small doses of amphetamines to treat for PD. Even the old MAO- B inhibitor selegiline metabolises to amphetamines. Concerning animals, I`ve found 2 more interesting (for me) abstracts: http://www.ncbi.nlm.nih.gov/pubmed/6420823
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For hypertensive model.
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Please contact Dr. Harikrishnan, DLAS, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum (www.sctimst.ac.in) They has SHR rats.
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To what the science refers when speaks about a "model" of something, and in this case, about an animal model? Exist a general perspective about the concept, beyond the specific definitions of specific interest topics?
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A model, in science, is a simplified and more accessible version of a complex entity, though sharing several similarities with it. In the particular case of animals, since we share phylogenetic ancestries with many degrees, a model is an organism that is phylogenetically the closest possible to our ideal. Usually, because we are humans and research in humans is commonly banned by ethics, our ideal organism is the 'Homo sapiens', but a very common model organism is the mouse ('Mus musculus') or the rat ('Rattus norvegicus'). These models can be "better" than, say, a chick, if we are studying complex mental processes such as spatial navigation, because the rat brain resembles much more that of the human than it does the chick's. However, chick embryos are extremely useful as development models and can be followed much more easily than a rat. So, all in all, what a model is, is also intimately connected to our particular question. Extremely simple invertebrate organisms, for example, such as the sea snail, have given us much knowledge about the biochemistry of simple behaviours.
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These terms are used very often. But what is the exact difference between them? Are they all interrelated because they point towards the same activity i.e. brain, fear and mental illness. How much is the antioxidant activity related in each case?
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Hi Alok,
Drugs are classified in two ways and the names that are given to the different classes of drugs depends on their target audience.
1. When they are targeted at practitioners, such as doctors and pharmacists, they are classified by the kind of symptoms that they purport to alleviate. The classes that you have mentioned fall into this category. So, for example, anxiolytics are marketed as suitable for treating anxiety, whilst hypnotics are marketed as being suitable for treating sleep disorders. Of course, someone may be having sleep problems because they have something on their mind that is making them worry (anxious) so much that they can't sleep. If the doctor perceives the relationship to be this way around, they would prescribe an anxiolytic, expecting the sleep disorder to be helped also. On the other hand, if the doctor thinks that the excessive anxiety is a result of the patient not being able think their problems through properly because of their sleep problem, he or she may prescribe hypnotics instead. In some cases, practitioner may consider these as two separate problems ad prescribe both types of medication at the same time, although this is not the procedure of choice.
2. Pharmacologists and those involved with medical research (and others interested in how medicines do what they do) classify drugs on the basis of their mode of action. For example, there is a class of drugs called SSRIs (Selective Serotonin Reuptake inhibitors) which are marketed as antidepressants. However, they are also used to treat anxiety disorders, stress disorders, even eating disorders.
In your question you refer to pointing "towards the same activity". The term activity can have different meanings. On the one hand, mental disorders are currently diagnosed on the basis of what the person says they feel or think (mental activity) and on how they behave (physical activity). On the other hand, medical practitioners refer to mental activity to mean what the brain is doing (for example, by using various imaging techniques). To complicate matters, there is a third kind of activity which refers to the effect that a drug has on its target cells (pharmacological activity).
When you later talk about 'antioxidant' activity, you are moving towards the realm of pharmacological activity, but indirectly since antioxidants do not have any particular 'target' cells. As such, they are not used to treat any problems. Their function, I think is going to need to have to be the subject of a different thread!