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measured blood sugar level after and before electrical stress. I have statically no incidence of stress on the blood glucose values. Do you have more information on the stress response and catecholamines, corticosterol and blood glucose level for broilers?
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I following the best answer.
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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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I'm trying to do research into Behavioural Endocrinology, as I am considering it for my final project for my masters. But I can't seem to find information anywhere, regarding equipment etc. Any help would be appreciated!
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I am trying to find a way and equipment to measure non-invasively, stress and wellbeing. Any suggestions. I have already identified HRV as one modality.
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I am trying to administer a hormone daily to a rat for up to 6 months without causing the rats any unneeded stress.
My current options:
- Daily subcutaneous injections.
- Implanted osmotic pumps.
- Daily force feed using gavage.
- Daily syringe feeding .
- Some type of treat containing hormone??? (please let me know if you know of something like this)
Essentially aside from some form of a treat containing the hormone I am not a fan of the 4 other options.
Daily injections would be time consuming for a large sample, and would be inherently stressful to the rats.
Osmotic pumps would require routine changing over the course of the experiment, meaning that the rats would be going into minor surgery every 2-3 weeks.
Daily force feed would be inherently stressful on the rats, and according to the literature on using gavage, can cause throat ruptures, and becoming increasingly difficult over time.
Syringe feeding is the most viable option of all those aside from feeding them some form of capsule or pellet containing the hormone, but would still be quite time consuming to do daily.
Any recommendations or advice on how to proceed here is very welcome. Please help.
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Hi Jesse,
I am from the manufacturer of iPRECIO pumps. I am very late but I thought I would still share. Our pumps will infuse up to 6 months at 1ul/hour. See www.iprecio.com . You can even program the pump to infuse intermittently or to try to simulate the hormonal cycle.
Some references for the choices you mentioned.
Good luck and feel free to contact if you have more questions.
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I have flash frozen brains in the past using isopentane with dry ice in it but I found that some of them cracked. What is the optimal time to leave the brain in the isopentane such that it is frozen solid but the cells are still viable?
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Er....what?
If all you're using these brains for is western blotting, cell viability is irrelevant: all you care about is protein.
You'll be crushing the tissue under liquid nitrogen and then dissolving some tissue powder in some sort of lysis buffer (RIPA or SDS or similar).
You don't even need to use isopentane: you could just drop the brains straight into liquid N2, or place them on dry ice. The time taken to freeze solid is far shorter than the half-life of virtually every protein you might be interested in.
The only time isopentane is really necessary is for rapid freezing: to preserve cellular architecture for histology (liquid n2 alone freezes too slowly, due to leidenfrost effect).
If you want cell viability (!?) then you shouldn't be freezing them like this at all, you should be isolating and amplifying the cells of interest in culture, then freezing them as for normal cultured cells.
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Can anyone let me know if GH has been used in MS? Is it a viable treatment in relation to other treatments used for MS. I do not have any expertise in the area of MS, and it is a case that has been brought to me recently.
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We have, and the effects of GH are, among others, produced by the stimulation of the proliferation of neural stem cells and generating increased oligodendrocytes. 
But of course, GH can not block the autoimmune-inflammatory response causing the disease. 
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I want to examine insulin like peptides in crickets, however no primers exist for ILP's in crickets nor any methods of detection. They exist in the drosophila literature- I just am at a standstill on trying to figure out how I could do this without spending a fortune. 
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Hi Rik!
Happy New Year to you as well =). We've now put that aside to answer more immediate questions with my time left (1 year) at my institution. 
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Dear Researchers,
I am working on a behavioral and molecular study in a transgenic mice model. I want to evaluate the improvement in cognitive ability among mice after using certain agents. I want to know if it is necessary to test Morris maze among both male and female? 
Please, if possible provide me with an article to read more about this. 
Regards, 
Mohammed 
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I agree that it is important for any of the studies to test both males and females.  Long history of differences in neuronal plasticity alone makes such studies important.
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My experiment plan is to make mice depressive model by CUMS on mice and then mice would subjected to behavior tests (such as a forced swimming test, tail suspension test etc.). Is it needed to do a forced swimming test before the mice modeling, in order to eliminate the mice who have big difference of the test results? Have you done such test and how much is the Elimination Ratio?
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I would suggest that model validity is better if extremes are not removed a priori.  They are expressing normal variation which will also exist in the target population.
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Does anyone either know how long it takes for glucocorticoids type 1 to become saturated in baboons? or how long after an acute stressor the hormone takes to reduce to baseline or non-behavioural change levels? or maybe just how long it takes for them to start decreasing? I understand this may depend on whether the animal is dominant or subordinate depending on deficits in negative feedback loops...
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Speaking from personal experience (and that of other researchers at the Yerkes National Primate Research Center), it seems that cortisol peaks 30-60min after acute social stressors as well.  I work with rhesus monkeys and typically use the human intruder paradigm (invited by Ned Kalin & Steve Shelton at the Uni. of Wisc) as my acute stressors (30min stressor). I've taken blood samples immediately before and after the stressor (Raper et al, 2013 Psychoneuroendo, Raper et al 2013 Horm Beh, Raper et al, 2016 Brain Beh Immun), as well as examined cortisol at 45 min post-stressor (unpublished data) and 24 hours post-stressor (Raper et al, 2016 Brain Beh Immun). I typically do these test at sunrise and/or lights-on, so the baseline/pre-stress cortisol levels are fairly high because of the awakening cortisol response. However, other colleagues and I choose to test at this time of day to avoid any other potential confound, such as the animal having a social conflict earlier in the day prior to testing that I might not be aware of (testing them first thing in the morning avoids that potential confound).   Even with the high basal cortisol I still see a significant increase in cortisol to the acute 30 min stressor, and in a manuscript I'm working on now I see a significant decline in cortisol at 45 min after the stressor has ended.
I'm not sure if the human intruder paradigm will work well for baboons, I know it doesn't work well in African Green Monkeys, they largely just ignore the "intruder" and don't react with cooing, freezing, or hostility that rhesus monkeys exhibit on the task. If the human intruder paradigm won't work for baboons, you might consider a social separation stressor, which is just separating them from their social group and/or cagemate and putting them alone in a novel environment for 30 min. Dettmer et al, 2012 (Psychoneuroendocrinology, 37, 191-199), published on using relocation as a stressor and examined cortisol levels in hair.   Lastly, you could also use pharmacological challenges of the HPA axis (Raper et al, 2014 J Neurosci).
If you have any additional questions please feel free to contact me.  I'm faster at responding if you send me a direct email jraper@emory.edu.
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Hi:
We run behavioral experiments with goldfish (as prey) and Egret (as predator). The goldfish groups (10 to 20 individuals) are in a pond (1000 Liters) and Egret preys (or attacks) on them regularly. When attacked, the goldfish seeks refuge under a central cover (circular disks in the middle of pool, that prevent egret from hunting). Is it possible to measure stress hormones in water without capturing or killing the goldfish (non invasive method)? Is it possible to measure the stress hormones through time (we run the behavioral expt. for 6 hours)? If yes, what kind of stress hormones can be measured? I would be very happy to get your feedback's. Please let me know if you need further details. Thank you.
Vijay 
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Hi Gordon and Diogo:
Thank you very much for your comments. I really appreciate your help.
Vijay
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I am planning to do 4 or 5 behavior test on my respected groups after drug administration, I have to do test after every two weeks for about 8 weeks. I have eight groups and each group comprised of 30 animals. After behavior experiment i have to kill the animal for other studies. Can we select six or seven animal per group for each week experiment and kill them at the end. I have to do training in all the behavior experiments before trial. So, i need suggestion that is it fine to select 6-7 animals for each 2 weeks or not. Kindly explain if possible if we cant do it. 
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How about the control animals and baseline values for the biochemical markers?
I assume you also have a control group that does not receive the treatment but only vehicle administration. You should include this control group in the 3-6-9 weeks tests. The number of animals should be similar to the treatment groups.
Additionally, you should consider baseline values for the biochemical markers in naive rats without any behavioral testing and drug treatment, because behavioral testing or possible stress from the drug/vehicle administration may also impact your biochemical markers.
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I have 2 group of mice, one of them should have seizure like behaviors, however, I didn't notice that phenotype, so I want to induce seizure in mice, and check if there are some difference between the 2 groups, anyone can give me some suggestions? thanks a lot!  Hailong Hou
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I agree with the answers already given, but I would like to add: ECS can be used to measure seizure threshold.  If you are for example, testing antiepileptic drugs, it might be useful to find out if the threshold rises when the mouse has been given the drug.  Good luck!
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I am looking for an answer to a rather systemic biology question - is there a 1:1 relationship between HPA axis activation and stress response (in terms of the whole body, I mean not the cellular or tissue stress). I mean could an experimental model without functional HPA axis experience stress in its proper sense of word? I know that it depends on what how we actually define stress, but still, is there any possibility of generalized stress response without HPA axis activation? Will be very grateful for any suggestions, Julie
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dear Julie, 
My opinion is that stress in its proper sense involves the activation of the HPA axis. 
Stress is defined as a state of real or perceived threat to homeostasis, which maintenance in the presence of stressors requires activation of  responses involving the endocrine, nervous, and immune systems. 
Dialogues Clin Neurosci. 2006 Dec; 8(4): 383–395.The role of the hypothalamic-pituitary-adrenal axis in neuroendocrine responses to stress
Sean M. Smith, Wylie W. Vale,
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Dear All,
   How do perform Maternal Odor Preference/Homing Behavior in pups? and how many day old pups should be used for this behavior study??
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An alternative to avoiding litter effects is to test multiple subjects in the litter, but run statistics on litter means, not individual scores.
Yes, pups are sensitive to temperature and should be handled with gloves. The ideal temperature you wish to test them at depends on the behavior of interest and their age. We ran most of our experiments on P1 pups (24-hours after birth); to ensure behavioral activity, we ran in a regulated environment at 34-35°C. Cooler than that and they cannot maintain body temperature and will thermally crash over 20-30 min.
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Hello to everyone!!!
I am working in the field of stress physiology, my work is about i will stress to mother during pregnancy and will check cognitive functions of its offspring.. I will using 40 days old pups for further experimental studies,, will it differ maternal stress effect and cognitive functions of the offspring before and after puberty period of the animal...
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Hi Sakthivel, I previously worked on the effect of early life stress on anxiety, visceral sensitivity and pain in adulthood using rat models.  Early life stress is a major contributory factor to psychopathology later life. Effective maternal care is essential for proper development of the HPA axis (stress axis) – first week is crucial. There are chances that stressing their mother during pregnancy will consequently affect the ability to nurture the pups and this may potentially increase stress (through corticosterone) and cognitive function in adulthood. I believe you may see some significant changes in stress and cognitive function after purberty in pups from stressed mothers compared to controls provided you make use of good experimental paradigm. Good luck!
For further reading, see Lippmann et al. (2007); Wilkinson et al. (2011, 1999) and Sant et al. (1994);Smith et al. ( 2011).
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In relation to finding mechanisms of pain catastrophizing in healthy humans and what it will likely be when HPA axis is disrupted by disease.
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first of all, their are many studies regarding PCS in relation to experimental pain sensetivity.
second, HPA axis disruption will be likely be only in a disease state, but it can only influence pain sensitivity and not PCS because catastrophization is a trait and it cant be changed by hormonal changes.
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There are many publications using fluoxetine as a standard treatment in corticosterone induced depression and in these publications it is shown that fluoxetine lowers serum corticosterone levels. Through which mechanism fluoxetine lowers serum corticosterone concentration.
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thank you sir.............
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I ask this because I postulated in our most recent paper that one reason girls are more susceptible to the traumatic effects of child abuse may be because they perceive and remember social cues differently, perhaps appraising them as being more threatening than do boys. Is there evidence for this idea?
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Could I point you to a completely different perspective on scientific exploration of sex differences between men and women, boys and girls. Delusions of Gender: The real science behind sex differences is a highly praised book by Cordelia Fine who is a Future Fellow of Psychological Sciences and Associate Professor at the University of Melbourne in Australia. Fine rigorously challenges scientific accounts of sex differences. Not only is it very well researched, it is also just a plain fascinating read. I commend it to you.
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I am working on a connection with colic and brain development in infants.
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Thank you! I am investigating the connection with early dysregulation symptoms in infants (colic) and later development of Sensory Processing Disorder in children. I am looking at the microbiome's possible influence in this neurodevelopmental disorder. As you may know, rodent studies are finding a disturbed HPA axis in GF mice with a critical window of development for a healthy stress response. I wonder if this is also happening in a sub-set of infants ( those who do not regulate at 3 months per Wessel's criteria).
Thank you so much for your response and support!! My daughter has SPD and I need to find answers to help our family and others like us.
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I'm curious whether there's a consensus as to whether chronic stress can damage the hypothalamic-pituitary-adrenal axis, diminishing the efficacy of negative feedback and leading to further damage, including hippocampal atrophy. This position was argued by Robert Sapolsky: Is there convincing evidence that it is correct? Thanks!
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Hi,
Interesting question!
To follow up on Petra's answer, I think that neuron dendritic atrophy is reversible. For example in rodents, hippocampal neurons can grow back within a few days only after chronic exposure to stress has stopped (would need to look a bit deeper into my files for the actual references, let me know if you need them).
As a field evolutionary ecologist, I have seen some studies in animals (excluding mice) that may relate to the concept of chronic stress. However, the particular component of the HPA axis affected by the 'chronic stress' differs from one system to the next.
- work on the so called 'Dasyrurid syndrome' by various authors
- Rudy Boonstra's work on the adaptive stress reactivity in sciurids.
- Norbert Sachser's work in guinea pigs
- Micheal Sheriff's work on how intense and sustained predation stress can lead to population decline through an increase in cortisol profile.
Laboratory studies can indeed induce pathology, but I am not aware of any study in free ranging animals where Sapolski's hypothesis (chronic stress leads to pathological symptoms and 'castrates' subordinate individuals) has been verified. A related issue is perhaps that chronic stress as a concept, is not so useful when one is primarily interested in free ranging/wild animals. My opinion is that stress reactivity should be analysed from a life history perspective even in humans and mice. For example a lot of the stress reactivity profile of an individual is programmed through maternal effects and there is evidence that such a programmation is increasing the 'fit' between an organism's stress reactivity and the predictability of the environment. This could lead us to see pathologies as a mismatch between such a programming and the environment experienced.
I hope it helps, if it is too far from your interests I apologize!
Best.
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New evidence exists that replicates the results of Weaver et al. (2004) about the increase in demethylation of DNA in exon 1 (7) of GR? What new evidence supports the non-genetic transmission of stress responsivity of the mother through maternal care to her offspring? Which mechanisms are implicated? Specific neurotransmitter actions are related to the process?
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There has been some studies regarding the effect of maternal separation and miRNA expression of the offspring (this counts as non-genetic transmission). Work by Uchida et al. focused on the effects of maternal separation and early life adversity on the behavioural response to RRS as well as vulnerability to chronic stress in adult rats [87]. Maternally separated rats showed increased expression of repressor element-1 silencing transcription factor 4 (REST4), a neuron-specific splicing variant
of the transcriptional repressor REST. REST regulates certain brain-enriched miRNAs postulated to be associated with neuronal functions such as brain development and plasticity. The maternally separated rats also showed a marked increase in a variety of REST target gene mRNAs and miRNAs in the medial prefrontal cortex (mPFC). The expression of pre-mir132, -124-1, -9-1, -9-3, -
212 and -29a as well as the mature miR132, -124, -9 and - 29a were found to be significantly up-regulated in maternally separated rats compared to control rats. Altogether the study provides additional insights into factors that could influence susceptibility to developing mood and anxiety disorders in adulthood following exposure to early life stress. For more info see the miRNA review I have published - it is on my profile to download :)
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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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Are the individual differences of the mother's anxiety behaviors and their maternal care predictors of the anxiety response of offspring? Could that be enhance by impoverished social and physical environment?
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Alan refers to the work of the group of Michael Meaney and Moshe Szyf in McGill (Canada). The quick reply to your question is that yes there is a lot of literature on early life adversity and anxiety and stress response in later life, and yes maternal care is important, as is the social environment, and offspring can adopt the maternal phenotype.
However, I think that the underlying mechanisms are not as clear-cut as in the suggested web page.
Back in 2004 the McGill group published a paper (first author: IGC Weaver) that suggested that the stress behaviour of rats was transmitted epigenetically through the glucocorticoid receptor promoter. This study has not yet been reproduced despite several attempts that I know of. Several other studies have been published looking at this promoter in slightly different paradigms (Herbeck et al, and Daniels et al), and neither saw similar methylation levels in the corresponding sites, nor any effect of the paradigm on methylation.
We published in 2005 the structure of the human GR promoter and its close homology to the rat. After this, again the Meaney group published an important study on the human 1F promoter, and found a link between suicide, prior childhood abuse, and methylation of the GR promoter, although not in a corresponding region (McGowan et al 2009).
There are quite a few differences that are now becoming clear between the rat and the human, and I would even suggest that even the rat is not as clear cut as proposed. The regulation of the promoter 1F / 1-7 hinges on a transcription factor called Ngfi-a, and it was in the binding site for this factor that Weaver at al first saw the methylation back in 2004. We have just published a study where we upregulated endogenous Ngfi-a expression, and there was no effect on the associated GR transcript levels, suggesting the regulation is more complicated than previously thought. Similarly, Weaver et al observed methylation levels of 0 or 100% in the Ngfi-a binding site, levels that have never been re-observed.
Similarly, it is doubtful that methylation at one single CpG dinucleotide is as important as reported by Weaver et al, we have reported a clear correlation in expression between the sum of methylation throughout promoter 1-7 rather than any single CpG (Witzmann et al 2012). We have similar preliminary data from the human, although IIRC Tyrka et al and de Rooji et al have observations that correlate with single CpG methylation levels.
So, as a word of warning, read all the papers from the subject, and make your own mind up!
Jon