Fear Test: Long Answers Flashcards
Similarities between fear and anxiety
- both involve anticipation of discomfort or danger
- apprehensiveness and unease
- negative affect
- accompanied by bodily sensations
Differences between fear and anxiety
- anxiety is objectless– it is the state of expectation danger and preparing for it. Aka signal anxiety
Fear draws attention precisely to the object that elicits it. It is Primary Anxiety, because it has an immediate object to which a person is afraid.
the anticipation in fear is about if and when a present threat will cause harm, while the anticipation in anxiety is about the UNCERTAINTY of consequences of a threat that is not present and may not occur
fear=threat is present and identifiable, is evoked by specific cues, the connection to threat is reasonable
-anxiety=threat is not present or identifiable, not evoked by specific cues, connection to threat is unreasonable/irrational, involves sustained vigilance
When do lesions of the dorsal hippocampus have their greatest impact on contextual learning?
Electrical lesions work best.
MAREN (1997) Removal of HC AFTER conditioning has a greater effect than making it nonfunctional during conditioning.
pre-training lesions to the dorsal hippocampus barely have an effect—the percentage of conditioned freezing in lesioned rats is nearly the same as the sham rats
-making a lesion before conditioning does not have a significant effect on context or tone extinction
if a particular area is destroyed/blocked before conditioning, like the dorsal hippocampus, then compensatory mechanisms in other areas which normally wouldn’t be involved can take on a greater role in the acquisition of contextual conditioning
if the dorsal hippocampus is lesioned well after conditioning, there is less of an effect on responding because the hippocampus would have had enough time to share the memory of the context with the cortex. So, lesioning ~28 days after contextual conditioning provides enough time for the transfer of contextual memories from short term storage in the hippocampus to longer term storage in the cortex
-destroying the dorsal hippocampus shortly after conditioning means that although the context was processed and the association with the CS-US pair was learned, it can no longer be recalled/retrieved and applied to future encounters, like during extinction trials
Hippocampus is involved with contextual conditioning. What is Immediate Shock Deficit?
Immediate Shock Deficit:
- Immediate shocking results in very poor leaning because animal doesn’t realize the context yer
- Delayed shock: good learning. Gives time for an animal to look at its surroundings before conditioning starts.
Preexposure to context reduced ISD. It allows the rat to learn the context beforehand.
During conditioning, the rat receives a single shock immediately upon placement in the context. Muscimol is infused into the hippocampus during a) context preexposure, b) conditioning, or c) test. What is observed under these three conditions? How are these observations explained? What pattern of effects is observed if AP5 is substituted for muscimol during context preexposure and conditioning?
Recall, preexposure to context reduces ISD because it allows the HC to facilitate contextual conditioning.
adding muscimol (a GABA agonist) to the hippocampus during any stage of contextual conditioning will restore the immediate shock deficit (animal gets shocked immediately after being put in box and then isn’t scared of the box in the future—doesn’t learn to be afraid of the context) -no matter the phase in which musciomol infusion took place, the rats with muscimol would show less freezing during the test trials because either the acquisition or retrieval of the contextual representation was disrupted:
a) context pre-exposure: impairs learning about the context—did not adequately learn about the context in the first place (impaired acquisition of contextual representation), therefore the association between shock and the context will also be disrupted
- the pre-exposure phase allows the rat to bind together bits of contextual features into a single unified Gestalt memory. Having a gap in time between being placed in the box and getting shocked allows for adequate processing of the context
b) conditioning: prevents retrieval of the context representation formed in pre-exposure— hippocampus cannot retrieve the information that was processed about the context, and so it cannot pair it with the shock (impaired retrieval of the contextual representation, and so impaired acquisition of the Pavlovian association)
- during the conditioning phase, the rat is recalling the information it processed about the context during pre-exposure and pairing it with the shock
test: prevents retrieval of the context representation associated with shock in conditioning—the hippocampus is unable to retrieve the association between the context and shock that was developed in the conditioning phase (impaired retrieval of the Pavlovian association), so the rat does not recall that it previously experienced shocks in that context
AP5: blocks NMDA-mediated learning (LTP) *blocks learning, not the functioning of an area (whereas muscimol blocked functioning of the hippocampus)
- during pre-exposure=observe less freezing because prevents learning about the context - during conditioning=no effect on freezing because the hippocampal representation of the context has already been learned
Briefly describe the Grillion’s NPU threat test and describe what comparisons provide measures of fear potentiated versus anxiety potentiated startle. What brain structure does Grillion think might be heavily involved in anxiety but not fear potentiated startle?
NPU threat test: a test used to assess short term (fear) and long term (anxiety) aversive states in humans
- contains three conditions, each with a unique visual stimuli (ex: a different geometric shape) - N condition=no aversive event - P condition=predictable aversive event (paired condition, so the aversive event is signalled by a CS) * evokes fear - U condition=unpredictable aversive event (unpaired condition, so the aversive event can occur at any time) * evokes anxiety - the participants’ fear and anxiety is then assessed using the startle reflex, most commonly through an EMG of the orbicularis oculi to measure the blink reflex - fear-potentiated startle=comparison of startle magnitude between during the cue and the absence of the cue during the P condition (P cue-P no cue) - startle magnitude during the P condition should be higher in the presence of the cue than in the absence of the cue because the cue should come to evoke a fear response via Pavlovian conditioning - anxiety-potentiated startle=comparison of startle magnitude between during the absence of the cue during the U condition and during the absence of the cue during the N condition (U no cue-N no cue) - startle magnitude during the absence of the cue in the U condition should be greater than in the absence of the cue in the N condition because the lack of predictability in the U condition generates persistent unease in anticipation of getting the US at any point in time - anxiety (tonic, long duration) involves the BNST, while fear (phasic, shot duration) does not
Describe an experimental result that shows the hippocampus is not absolutely essential for contextual fear conditioning. What general principle do these examples support?
Wiltgen et al. (2006) trained rats for 10 trials of contextual fear conditioning before removing the hippocampus. After, the rats were re-trained and contextual fear was re-established despite having no hippocampus
- similarly, over-trained rats with amygdala lesions can still acquire conditioned fear - supports the dynamic origins of memory principle—> the idea that particular areas, like the hippocampus, are not absolutely necessary for learning - there must be some other areas of the brain that can do what the hippocampus and amygdala do *demonstrates that contextual fear learning can still be acquired via other areas/secondary pathways
Do the Pearce-Hall and Rescorla-Wagner models agree or disagree about whether new associations are formed in extinction? Support your answer with a description of the approach of these models to extinction
the two models disagree
R-W model: in acquisition, the CS-US association is formed. In extinction, the CS-US association is erased
- during acquisition, V increases towards 1.0—> the excitatory association between the specific CS and US is becoming stronger (CS is a strong predictor of the US) - during extinction, V decreases towards 0—> the inhibitory association between the specific CS and US is becoming stronger (CS no longer is a strong predictor of the US) - P-H model: in acquisition, the CS-US association is formed. In extinction, the excitatory CS-US association still exists, but the inhibitory CS-no US association is also formed ***the correct model - during acquisition, total V increases towards 1.0—> positive V is increasing while negative V stays at 0, so total V is increasing and the excitatory association between the specific CS and US is becoming stronger (CS is a strong predictor of the US) - during extinction, total V decreases towards 0—> positive V stays at the same strength it reached in acquisition while negative V becomes an increasingly negative number towards (-1.0). This represents that the positive association never changes or disappears during extinction, but the negative association is growing stronger so that the negative association can offset and counteract the positive association. The total associative strength of the two associations combined declines, describing that now the CS is a poor predictor of the US
What is spontaneous recovery? How does lengthening the waiting period after extinction affect the magnitude of spontaneous recovery? What is Devenport rule for spontaneous recovery?
spontaneous recovery: the reappearance of an extinguished response caused by the passage of time
- if a rest period is introduced after extinction trials prior to test, performance of the CR returns - the longer the waiting period between extinction training and test trials, the greater the magnitude of spontaneous recovery - Devenport’s rule: all associations in acquisition (excitatory) and extinction (inhibitory) are intact, with recovery determined by extinction to test (units of time) divided by acquisition to test (units of time) - a larger unit of time between extinction to test would result in a larger numerator, and thus a larger spontaneous recovery effect
Describe rapid reacquisition, ABA renewal, ABC renewal, and US reinstatement. How are they explained by Bouton’s theory?
Bouton’s theory—> two different associations are formed: an excitatory CS-US association in acquisition is first learned, and then an inhibitory CS-no US association in extinction is second learned. The old CS-US association does not get erased, but rather it just gets covered up by the new CS-no US association
- the animal learns an exception to the rule, which makes the second learned association context-specific—> the CS can either mean US or no US, and so the animal learns that the no US is enforced during a particular time or place *the inhibitory CS-no US association learned in extinction is context specific - at test, the animal must retrieve the extinction association, or else the CS-US association will be expressed as spontaneous recovery
rapid reacquisition: re-acquisition of an association is quite rapid following extinction training
- suggests that the original learning/CS-US association was preserved somewhere. If it never disappeared, it would explain why it was so easy for re-acquisition to occur - ABA renewal: reappearance of an extinguished response produced by a shift away from the contextual cues present during extinction in context B back to the context of acquisition (context A) - a return to the context of acquisition provides cues that elicit the still existing CS-US association - ABC renewal: reappearance of an extinguished response produced by a shift away from the contextual cues present during extinction in context B to a new, neutral context unrelated to acquisition nor extinction (context C) - suggests that the return to context of acquisition is not necessary for renewal of the extinguished response - even though there are no cues from the context of acquisition to facilitate the retrieval of the excitatory CS-US association, the extinction association/exception to the rule is context-specific according to Bouton. Therefore, because the test context is not the extinction context, the CS-no US association is more difficult to retrieve * conditioned responding reappears with any shift away from the context of extinction because the second learned association is context specific, and without the cues of the extinction context present, it’s difficult to retrieve the inhibitory association - US reinstatement: reappearance of an extinguished response produced by exposure to the US - very strong if presented in the original context - presentation of the US alone reminds the animal of when the US was last present, which was during acquisition, so responding reappears because the US now serves as a cue for the CS-US association acquired in acquisition
Describe two manipulations that reduce ABC renewal. How might these behavioural phenomena be important to a clinician wanting to suppress the return of fear?
massive ABC extinction: results in less fear than moderate levels of ABC extinction
- Pavlov described “extinction beyond zero”—perform a greater number of trials beyond zero responding/no CR - this will cause extinction to stick almost as well as moderate amounts of ABB extinction would - extinction in multiple contexts: using a variety of different contexts for extinction trials results in less fear - ex: A(B,C,D,…)F, where A would be the context of acquisition, B,C, D,… would be the contexts of extinction, and F would be the context of test - often times in therapy, the patient is not in the original context or situation of acquisition. Unfortunately, extinction can become specific to the context of the therapy sessions. To prevent this, the therapist can undergo exposure therapy in a variety of other contexts outside the therapist’s office to promote generalization of the extinguished response. For example, the therapist can use VR so it’s as if the patient is experiencing a variety of real-world contexts - it’s usually the best to combine massive extinction and extinction across multiple contexts
Describe three studies (lesion, infusion, & unit recording) suggesting the infralimbic region of the prefrontal cortex in the rat might be involved in the retention of extinction.
Quirk et al. (2000)—> lesions to the IL region do not prevent extinction, but do interfere with the recall of extinction the following day
- no difference in % freezing between shams and those with IL lesion during day 1 of extinction training - the day after extinction training, the lesioned rats show a greater % freezing than the sham rats—as if they cannot remember being extinguished/cannot retrieve that inhibitory learning that was acquired the day prior - Hadid and Quirk (2002)—> recordings of the IL region revealed neural spiking (activity) when animals are returned to the context of extinction - after extinction training, placing the rats back in the context of this training the next day resulted in heightened activity that was not evident during conditioning or extinction on day 1 - Santini et al. (2014)—> infusion of anisomycin (protein synthesis inhibitor) into the IL region during extinction doesn’t prevent the development of extinction, but it interferes with the retrieval of extinction . if extinction learning has happened, there must be structural changes that occurred (LTP) via gene expression and translation of proteins to remodel the synapse. So, adding anisomycin would block any long term changes from developing in the IL region of the vmPFC - the infused rats and the sham rats show the same % freezing during extinction training, but the next day the infused rats show greater % freezing because they cannot recall the inhibitory learning acquired the day prior
What areas of the brain (visual cortex, frontal/parietal/amygdala) are active when a masked or fully processed visual stimulus (neutral vs. threatening) is presented. Can the amygdala be activated without being consciously aware of the threat?
masked neutral stimulus=visual cortex
- masked threatening stimulus=visual cortex and amygdala
- fully processed neutral stimulus=visual, frontal, and parietal cortices
- fully processed threatening stimulus=visual, frontal and parietal cortices, and amygdala
- yes, the amygdala can be activated without any subjective conscious understanding of the threat
- the amygdala is active whether the threading stimulus is seen consciously (fully processed) or non-consciously (masked)
- so defensive reactions like increased HR, perspiration, and exaggerated startle can occur without conscious awareness of the threat
Identify some of the weaknesses of past drug research on anxiolytics in animals.
only assess state anxiety (the temporary condition elicited by a threat), not trait anxiety, which is chronic and what most people with anxiety disorders suffer from
- animals are not selected because they have high anxiety behaviours but are randomly chosen, so not really matching the real world situation (people suffering from chronic anxiety) - can try to improve by making animals really stressed out before the test, or by genetically modifying their brains - the tests selected are generally chosen because drugs known to be anxiolytic in humans (usually benzos) have weakened the behavioural response on that test - but this will not necessarily be sensitive to other anxiolytics, especially ones with novel mechanisms that might be more effective - drugs are usually only administered to animals once during a given test, but many psychiatric drugs take weeks to reach therapeutic effect (ex: SSRI) - women are far more likely to develop anxiety disorders, but animal models focus mainly on males (true of research in general)
Describe the PID-5 and Research Domain Criteria (RDoC) approaches to anxiety disorders. How do these approaches differ from previous ones?
they both differ from previous approaches by taking a trait route—identifying which particular trait domains are abnormal and using that to guide diagnosis and treatment, rather than assigning patients into a particular category (the DSM is a symptom based categorization procedure—check all the boxes and see what category of disorder the patient falls into)
- this current categorical approach is too unitary, while in reality disorders are on a continuum with varying degrees of abnormality. A trait approach like these options would allow for a continuum approach - personality researchers and researchers from the National Institute of Mental Health were consulted - PID-5 (personality inventory for the DSM-5): uses a trait approach for psychiatric disorders (ex: recklessness, impulsivity) - uses self-report via questionnaires that identify specific personality trait domains and facets within that domain. For example, the domain of disinhibition includes facets of impulsivity, distractibility, and irresponsibility. There are 4 other domains: negative affect, detachment, antagonism, psychoticism - the clinician can measure traits that are relevant to abnormal psychology, where the trait isn’t just at every day levels but at extreme levels - Research Domain Criteria (RDoC) Project: a framework that specifies psychological constructs within key neural domains and describes different units of analysis that pertain to these constructs, independent of traditional diagnostic categories - the psychological constructs fall under 5 broad functional domains/systems, and for each domain, data from a set of objective measurements at a different levels of analysis (ex: cellular, molecular, behavioural) are collected - negative valence=threat processes, fear, anxiety - positive valence=reward processing, learning, habit - cognitive systems=EFs like attention, WM - arousal and regulatory systems=arousal, motivation - social processing=attachment, separation, communication, perception of self - the current and future research compiled for these domains through these various analyses can be used to guide treatment and prevention (can better identify circuits involved) * hopefully can compile enough information to offer new ways to categorize mental and behavioural problems
- RDoC project rests on three concepts:
o Mental and behavioural problems are brain problems
o The tools of neuroscience can identify the brain dysfunctions underlying these problems
o Biological markers of the brain dysfunctions can be discovered and be used to guide diagnosis and treatment of mental and behavioural problems. - RDoC approach allows facts about the brain to suggest how a given problem should be understood, researched, and treated.
o Adds complexity to the therapeutic challenge: drugs that are developed by testing their effects on defensive reactions (freezing and accompanying physiological responses) and actions (avoidanace) are essentially targeting defensive survival circuits and defensive motivational states and thus only indirectly change anxious feelings.
o In order to end up with drugs that specifically make people feel less anxious by directly changing feeling, brain systems that make conscious feelings would have to be targeted.
