This is an important and relevant question because it emphasizes how difficult it is to deal with words while approaching brain functions and mental states ("ceci n'est pas une pipe" de Magritte).

A correlation is a statistical process assessing the relation between two variables, ideally continuous ones. In the present case, neither stress nor memory can be quantified simply outside a well defined measurement device. And then, what is measured is neither stress not memory, but what the test itself measured, as Binet may have commented about his IQ test.

Thus words such as stress or memory must first be defined.

Stress can be measured from the strength of the applied constraint AND the subject (rat?) state (age, sex, strain, hormonal level, memory of the issue of similar situations etc). It combines both objective and subjective dimensions (evaluation) as for any emotion. Hence the "kind of stress", that supposes a comparison between different stress inducing tools, must be related to the subject.

Memory is not unitary, simply starting from the slow episodic-spatial vs rapid associative dichotomy. In the case of stress, episodic-spatial memory might be reduced, whereas associational memory attributing an emotional tag to an item, is enhanced. PTSD are a good indication that some sort of memory is coded and consolidated.

My position is perhaps scholar, but I am convinced that a good question must induce developments and arguments helping overcoming our natural tendency to direct causality and reification, hence Magritte. However, I wonder how to what extent such a forum might allow to such elaboration.

thank you very much for your explanation. There are many types of test to stress the rat, such as restrain stress, environment stress, foot-shock-electric-stress, auditory stress, etc; among them, which one is the most powerful test than can make the rat become stress? and which one is really related with spatial memory performance of the rat?

From an animal modeling perspective one of the more common approaches is to use chronic stress to disrupt working memory performance. This effect has been shown most clearly using a task known as the delayed alternating T maze (DAT) task. Briefly, this requires the animal to remember which arm of a T apparatus that a reward was located in and on the next trial retrieve the food reward from the opposite arm. Working memory burden is created by increasing the time delay in between completion of one trial and starting the next. The first good evidence that chronic stress could disrupt DAT performance was by Mitzoguchi and colleagues (J Neuroscience) in either 2000 or 2001. This effect has been replicated several times including a particularly interesting study that was undertaken by Liston and McEwen and colleagues, published for memory in PNAS. Our research group has also recently found evidence that microglia may mediate the effects of chronic stress on working memory using the DAT task (see Hinwood, Cerebral Cortex 2012)

thank you very much for your explanation. What kind of parameter to assess the level of stress in rat?

Common parameters to assess the level of chronic stress include:

Weight loss, decrease in thymus wet weight, increase in adrenal wet weight and a variety of behavioural disturbances including increased levels of anxiety (as assessed using tests such as the elevated plus maze and open field), decreased motivation to consume or obtain previously rewarding stimuli (usually sucrose or an equivalent analogue).

Direct assessments of autonomic and endocrine function can also be made. For instance, a variety of assays can be used to confirm the presence of elevated levels of corticosterone in rats (cortisol in humans). Less frequently researchers will also measure changes in level of corticosterone binding globulin - which normally binds and inactivates up to 95% of circulating corticosterone. Also people do assess changes in the levels of adrenocorticotropin releasing hormone (ACTH). The issue with many of these is the time that they are assessed relative to the stressful events. Each changes with a different temporal profile. Complicating matters further release of hormones is pulsatile. Finally, you can also measure and asses changes in the level of central glucocorticoid and mineralocorticoid receptors directly or at the mRNA level using PCR (more common) in stress regulatory nuclei such as the hippocampus and paraventricular hypothalamus.

In terms of autonomic assessment you can measure medullary released nor/epinephrine - the challenge here in small animals is obtaining a sufficiently large sample size. Most commercial ELISA's require substantial amounts of plasma - which are often difficult to obtain. You could also go down the HPLC route - but this usually takes a large amount of time and energy to get setup. A more feasible but also more indirect approach is to go after changes in the expression and phosphorylation of enzymes, involved in catecholamine production such as tyrosine hydroxylase. See some beautiful work by Peter Dunkley and Phil Dickson of the Uni of Newcastle.

thank you very much for your explanation. Would you like to explain to me, why decreased motivation to consume or obtain previously rewarding stimuli (usually sucrose), become a parameter to assess the chronic stress?

A reduced interest in engaging in social activity/interaction, sex, and in other activities that mammals typically find enjoyable (i.e. consumption of sweet things) are all hallmark behavioural changes associated with exposure to persistently stressful situations. They are, however, not directly associated with the classical endocrine/autonomic measures of stress such as adrenal corticosterone or epinephrine release. Available evidence for why these changes occurs tends to favor significant modifications in cortical and limbic dopaminergic pathways. There is also a very large body of experimental examining these specific mechanisms.

Thank you very much for your explanation. Does certain type of stress influence certain region of the rat brain?