Topic 10 Flashcards
How would you define habituation in general? Habituation of the gill and syphon reflex has been studied extensively in which marine animal? Is this habituation thought to involve direct changes to the sensory or motor systems of the animal? Is this habituation thought to be associative or non-associative learning?
Habituation: adaptation to repeated presentation of the SAME stressor
Habituation of the gill and syphon reflex: Aplysia (sea slug)
This habituation is thought NOT to involve sensory or motor systems.
This habituation is thought to be from non-associative learning.
In people, poor response habituation to stimuli that elicit a startle response seems to be associated with what kind of mental health symptom?
Anxiety
How would you define stress habituation? Does habituation of stress responses generalize across different stressors?
In higher animals and people, many responses to aversive stimuli (i.e. stress responses) also habituate.
For example, multiple presentations of the SAME stressor (particularly a psychological stressor) results in smaller responses for heart rate, ACTH and cortisol/corticosterone etc.
Poor response habituation to repeated experience of the same stressor may be associated with negative health outcomes
The mechanisms behind stress response habituation in mammals and people are not well-understood.
If animals become habituated to a stressor, and then are not exposed to the stressor for a period of time, for approximately how long would animals show habituated responses to that particular stressor? What is the implication of this? Are responses to stress more long lasting if the stressor exposure are close together or spaced apart? Is this surprising?
3 weeks (28 days)
Stress habituations can be long lasting
More spaced apart
Yes, perhaps would have thought they would have been better close together.
Which experiment we covered in class suggested that response habituation to restraint stress is context-specific? What was a limitation of this experiment? How was that limitation overcome as a subsequent student performed at CU Boulder using noise stress? Did data from this second study support that of the first?
Rats exposed to repeated restraint stress with the same odor throughout (match) had a lower ACTH response than rats exposed to repeated restraint and a novel odor on the test day.
However, the novelty of the odor was not controlled for.
rats were exposed to 30 min. loud noise in context A OR context C for 7 days, AND familiarized with the alternate context without noise on the same days. On test day, the ACTH (and corticosterone) responses showed the same habituation, regardless of context.
=> this study showed that stress response habituation is NOT context-specific, and these data did not support the data from the first experiment.
Which type of receptor does muscimol primarily bind to? Is muscimol an agonist or antagonist at these receptors? Will its binding to the receptor hyperpolarize or depolarize the neuron? Is this effect permanent or temporary? Why does this make it useful for behavioral studies?
GABAa It is an agonist Hyperpolarization Temporary You can measure effects after the neurons come back online
What would you expect to see in terms of heart rate response to acute stressor exposure if you injected muscimol into the raphe pallidus, compared with vehicle injection/stressor exposure? If you repeated these injections and stressor exposures on 3 successive days, and then tested the animals’ response to the same stressor without an injection, 48 hours later, what would you expect to see in terms of the heart rate response? What does this imply?
Injecting muscimol into the raphe pallidus would decrease heart rate
It would not have an effect, implying that it only affects acute heart rate responses and is NOT necessary for stress response habituation
If you thought that one brain area projected to 2 other areas, how could you show that initially? How could you confirm that? If you wanted to show that this area was also active during stress, what kind of technique could you use?
You could use different retrograde tracers in each region, and use Fos expression to show neural activity in response to noise stress (shows that these are active during stress). You could confirm with anterograde tracing.
You could stress the animal and see if there is Fos expression in these regions, indicating neural activity.
Which brain area was shown to project to both the PVN and raphe pallidus? What would you expect to see in terms of HPA axis response to acute stressor exposure if you injected muscimol into this brain region, compared with vehicle injection/stressor exposure? If you repeated these injections and stressor exposures on 3 successive days, and then tested the animals’ response to the same stressor without an injection, 48 hours later, what would you expect to see in terms of the HPA axis response? What does this imply?
Posterior hypothalamus.
You see decreases HPA axis response to acute stress, showing the posterior hypothalamus is necessary for HPA axis response to acute stress
You see increased HPA axis response, indicating that the posterior hypothalamus is necessary for stress habituation.
