Fear and Anxiety 2 Flashcards
What was the first evidence that fear response originates in the amygdala?
Kluver-Bucy Syndrome: occurs when the right and left medial temporal lobes of the brain malfunction. Results in little/no fear response. Recognised that it was areas of the medial-temporal lobes that were missing, such as the amygdala.
What is evidence for the amygdala’s role in fear and anxiety? (case study)
A woman (SM) with bilateral amygdala lesions (Feinstein et al., 2011). Looked at how an not having an amygdala affected her behaviour. Measured SM’s fear responses to fear clips. Elicited little/no fear. Lack of amygdala seems to be stopping her from showing any fear responses. When look at her levels of anxiety, showed fewer anxiety traits.
What do we know about the amygdala?
Sits deep in the temporal lobes, in front of the hippocampus. Lots of specific neuronal sets in the amygdala (complex structure containing 22 separate nuclei).
What is evidence for the amygdala’s role in anxiety? (fMRI study)
Tillfors et al., 2001. Looked at how the brain lights out in people who have social anxiety/social phobias. Increased amygdala activation during public speaking in subjects with social anxiety disorder. Get increased amygdala activation when asked how they would feel in this situation.
How is the amygdala activated in anxiety?
When people see a stimulus of a phobia, you then see an increase of activity in the amygdala (Goossens et al., 2007).
What is involved in a conditioned fear and the amygdala?
Neutral stimulus is being processed in the amygdala (weak stimulus)combined with the conditioned stimulus of foot shock (strong stimulus), this is strengthened in the central amygdala to activate the responses that are associated with a fear response.
What is the interaction of benzodiazepines and the amygdala?
High density of benzodiazepine binding sites in the amygdala. Injection of soluble benzodiazepines into the amygdala induces an anxiolytic effect in rats. Injection of a benzodiazepine antagonist into the amygdala abolishes anxiolytic effect of a benzodiazepine given systematically. However, even after amygdala destruction, benzodiazepine still retain some anxiolytic effect. Also, anxiety is probably also being controlled in other brain areas, not just the amygdala.
How do we categorise fear and anxiety?
Fear = normal response to a threat.
Anxiety = unwarranted/inappropriate fear or stress. Anxiety disorders include PTSD, PD, GAD, phobias, and OCD.
Have emotional symptoms (fear), cognitive symptoms (anxious thoughts), and somatic symptoms (increase heart rate).
Anxiety disorders are where fear responses have gone wrong.
How does fearful stimuli elicit a stress response?
Process by seeing fearful stimulus, would activate fear response in amygdala, other brain areas would assess the situation, top-down processing of how you are going to respond, hippocampus may have a role, the amygdala as well as top-down process will elicit fear response and prepare the brain for the fear response.
What is the response to a threat stimulus?
These responses are fight/flight or freezing response. Will have obvious and hidden affects that your brain is doing to prepare you for that response. If all ok than the system is suppressed. Some activated through sympathetic nervous system (get energy to body parts that allows for an immediate escape, shifts all energy to the muscles - increased heart rate, increased blood pressure, deep fast breathing, inhibited digestion) and some central nervous system (what’s happening in your brain – behavioural arrest = freezing, narrowing of attention, behavioural arousal, augmented startle response, cortical activation, emotional response (fear)).
How is the hippocampus involved in anxiety?
If removed hippocampus get an increase in acquision of active avoidance – without a hippocampus, do not show freezing response.
Hippocampus provides information about contextual stimuli that are important for fear conditioning – if pair shock with tone, the animal learns to associate and respond to tone alone. Amygdala learning about tone and shock, the hippocampus is learning about the environment which can strengthen the learning. Suggests hippocampus is for contextual learning.
How is the Locus Coeruleus involved in anxiety?
Has projections throughout the neo cortex and cortical areas. When activated it makes noradrenaline release all over the brain. This alerts the animal/human to what is happening in the environment, which happens efficiently because in an aroused state. During fight/flight response see an increase in locus coeruleus activity. If put animal into stressful environment, see a significant increase in the amount of noradrenaline released from the locus coeruleus.
Benzodiazepines decrease the release of noradrenaline in the LC (increased GABAergic inhibition of NA neurons)
How is the raphe nuclei involved in anxiety?
Serotonin can be activated by punishment stimuli. Activation of serotonin projections causes behavioral inhibition (freezing). Balance of two systems (noradrenaline) helps you decide how to act. The action of the neurons in the raphe nuclei is controlled by GABAergic system.
Social interaction test (Gonzales and File., 1997) – mice or rats will be showing a certain amount of social interaction: if anxious, will spend less time with the other mouse. Can shift the balance of this by decrease the activity of serotonin release.
How is the fight/flight response affected by noradrenaline and serotonin?
If just had noradrenaline on its own or serotonin on its own, would have very different result. Opposing actions of these are associated with varying arousal states. If one system is dysfunctional, would result in dysfunction in fear response.
What are common treatments for anxiety disorders?
Benzodiazepines - work well in GAD and PD, not so effective in OCD and PTSD.
SSRIs - works in OCD, PTSD, PD, and GAD. However, can be anxiogenic (feel more anxious at the start) in short term first few days of treatment anxiolytic effects may not become apparent for weeks.
Buspirone - works for GAD (4-6 weeks to exert therapeutic potential)
