Fear and Phobias pt 1

What are the phases of encounter with predators

1. detect/encounter potential predators: freeze, try to avoid detection

2. predator pursues and strikes : try to escape; resist, and fight

3. unable to escape predator: tonic immobility (T)

(freeze, fight, freeze)

Why might tonic immobility be an evolutionarily adaptive response?

It can reduce predator interest, mimic death (“playing dead”), and possibly reduce pain perception.

How is tonic immobility (TI) typically induced in the lab?

By inverting the animal and physically restraining it until it stops struggling.

Why is TI sometimes called “animal hypnosis”?

Because the animal appears frozen and unresponsive, resembling a trance-like state.

What are the physical signs of tonic immobility?

• Muscular rigidity

• physical immobility

• closed or fixed gaze

• Parkinsonian-like tremors.

Does the animal lose awareness during TI?

No — the brain remains active; the animal continues monitoring its environment

What evidence suggests animals are still processing information during TI?

Research shows they respond to environmental cues like predator eyes or movement of other animals.

How does the presence of other mobile animals affect TI?

It makes TI harder to induce because social cues of safety reduce the perceived threat.

What kind of cues facilitate tonic immobility?

Predator-related cues (e.g., visible eyes) can trigger or prolong immobility.

Why might seeing predator eyes intensify or prolong TI?

Because it signals immediate danger and heightens fear response

What physiological response accompanies TI that reduces pain perception?

Analgesia — a loss of responsiveness to pain.

Why could analgesia be adaptive in a life-threatening context?

It minimizes suffering and helps the animal remain still if attacked.

What is the main emotional trigger for tonic immobility?

Fear

What experimental findings support fear as a trigger for TI?

• TI is diminished by tranquilizers

• disrupted by amygdala lesions

• enhanced by adrenaline.

What does the effect of tranquilizers tell us about TI?

Lowering fear reduces the likelihood or intensity of TI.

What does the effect of amygdala lesions tell us about TI?

The amygdala is necessary for fear processing that triggers TI.

How does adrenaline influence tonic immobility?

It potentiates (enhances) the response, showing that heightened arousal promotes TI.

Why is TI considered an involuntary response?

It occurs automatically, after all voluntary escape actions have failed.

How do orcas (killer whales) take advantage of TI to hunt great white sharks?

Orcas hunt great white shark livers
-> Great whites are dangerous prey
-> orcas stun (fear) and then flip the great white on its back (restraint)
-> this induces TI, which allows the orca to get the liver unscathed.

What kind of clinical relevance might tonic immobility have in humans?

It’s linked to extreme fear or trauma responses (e.g., “freeze” or “collapse” in PTSD or assault victims).

How can TI being an involuntary response be relevant to sexual assault survivors?

Many SA survivors feel immense guilt for not defending themselves
- They could not bc they were in TI
- Many SA cases involve restraint and fear
- it would help clients to tell them that their lack of self defense was evolved and is present in all mammals

What was the main goal of Rodd, Rosellini, Stock & Gallup’s (1997) study?

To examine how previous controllable vs. uncontrollable stress influences tonic immobility (TI) responses in chickens.

What were the three experimental conditions used in the study? and What were the two main dependent variables measured?

INESCapable shock (INESC), EScapable shock (ESC), and Control (no shock).

Number of attempts needed to induce TI and duration of TI.

INESCapable shock (INESC), EScapable shock (ESC), and Control (no shock).

Chickens were physically restrained to induce TI under three additional conditions: mobile cohort, predator eyes present, or eyes absent.

What did researchers find regarding the number of attempts needed to induce TI in INESC vs. ESC groups?

INESCapable (INESC) chickens required fewer attempts — they entered TI faster.

What does faster induction of TI suggest about the INESC chickens’ stress system

They were more sensitive to external fear cues, likely due to prior uncontrollable stress.

Why might prior uncontrollable stress increase TI sensitivity?

Because the stress system becomes sensitized, leading to quicker “shutdown” or immobility under threat.

How did the INESC group differ in TI duration compared to the other groups?

INESCapable chickens stayed immobile significantly longer.

What external cue especially lengthened TI duration?

Visible predator eyes — a strong threat cue.

What condition shortened TI duration significantly?

Presence of other chickens (cohort present), which acted as a safety cue

How do predator eyes and social presence differently affect TI?

Predator eyes prolong immobility by enhancing perceived threat, while social cues of safety reduce immobility.

What does the INESC group’s behavior tell us about the long-term effects of uncontrollable stress

It causes heightened sensitivity to threat cues and prolonged freezing or immobility responses.

Why are these results relevant to understanding fear and trauma?

They show how prior uncontrollable stress can “sensitize” the fear system — similar to how trauma increases hypervigilance or freezing in humans.

What is one possible neurobiological mechanism behind the enhanced TI response after INESC?

Overactivation of the amygdala and stress circuits, leading to stronger fear conditioning.

What was the main purpose of Weiskrantz’s 1956 study?

To determine the role of the amygdala in learned avoidance behavior (fear conditioning).

Weiskrantz (1956) — Study Design

• 18 monkeys divided into three surgical groups

  • Bilateral removal of the amygdala

  • bilateral removal of the inferior temporal (IT) region

  • bilateral sham surgery.

Describe the conditioned avoidance task used in the study.

Monkeys were placed in a shuttlebox with an electrified floor. Lighting alternated between compartments; darkness was paired with shock.

What behavior did the monkeys need to learn to avoid shock?

Move into the lighted compartment when the lights switched

What happened during the extinction phase?

No shock was delivered, but the lighting continued to switch — testing whether avoidance behavior persisted.

How did control monkeys (IT and sham) behave during extinction?

They rapidly jumped to the lighted side, showing strong retention of avoidance learning.

How did monkeys with amygdala lesions behave differently?

They still learned the association (no amnesia) but jumped much less rapidly and their avoidance behavior extinguished faster.

What does “rapid extinction” of avoidance behavior suggest?

They remembered the task but lost the emotional motivation (fear) to continue avoiding.

What conclusion did Weiskrantz draw about the amygdala?

It is not necessary for learning or memory itself but is crucial for attaching emotional significance (fear) to a stimulus.

Why did monkeys with amygdala lesions seem “less emotionally invested”?

Because the amygdala mediates the emotional reinforcement (fear) that sustains avoidance behavior.

How does this study connect to fear conditioning in general?

It shows that the amygdala links sensory cues to emotional responses — essential for fear-based learning.

How might these findings translate to human fear and anxiety disorders?

Dysregulation in the amygdala could lead to either excessive or blunted fear responses, affecting avoidance and emotional learning.

Why do results differ across avoidance learning studies involving the amygdala?

Because the amygdala has multiple subnuclei with different roles in processing fear and motivation.

What are the four types of avoidance learning tasks mentioned?

Passive, active, signaled, and unsignaled

What distinguishes passive from active avoidance

Passive avoidance = withholding a behavior to avoid punishment (e.g., don’t enter a dark area).
Active avoidance = performing a specific behavior to prevent punishment (e.g., move to the lighted side).

What is the difference between signaled and unsignaled avoidance?

Signaled = there’s a clear warning cue (like a tone or light) before the shock.
Unsignaled = no warning cue; animal must learn the pattern.

Why is avoidance behavior usually preceded by fear conditioning?

Because animals first need to learn that a specific cue predicts threat before they can learn to avoid it.

What are the two main steps in avoidance learning according to the slide notes?

(1) Recognizing a cue as threatening (fear recognition), and (2) Performing an action to prevent the threat (learning the avoidance behavior).

What happens if the amygdala is impaired during avoidance learning?

The animal may still perform the learned behavior (memory intact) but the emotional “fear” motivation fades quickly, making avoidance inconsistent.

Why can avoidance behavior become inconsistent when the amygdala is damaged?

Because the emotional significance of the threat cue is lost; the animal no longer “cares” about avoiding it even if it remembers how.

What key function does the amygdala play in avoidance learning?

It links threat recognition (fear) to appropriate avoidance action through emotional reinforcement.

What is the acoustic startle reflex?

A fast, automatic defensive response (like an ear twitch or whole-body freeze) to a sudden, loud sound

Where in the nervous system is the ASR mediated?

In the spinal cord — it does not involve the cortex.

Why is the ASR considered a useful model for studying fear?

Because it is an automatic physiological reflex that can be enhanced through conditioning.

What happens when a rat hears a loud sound before any conditioning?

It shows a brief startle — a short spike in blood pressure and momentary freezing — then returns to normal.

What physiological changes accompany the startle response?

A temporary increase in blood pressure and cessation of movement.

What happens when the sound is paired with an electric shock?

The rat learns that the sound predicts the shock, developing a conditioned fear response.

How does the rat’s physiological response change after pairing sound with shock?

The combination produces stronger blood pressure spikes and longer freezing, showing fear learning.

What role does the amygdala play in this conditioning process?

It links the neutral sound to fear, creating a conditioned emotional memory.

What happens when the sound is played alone after conditioning?

The rat shows the same heightened fear response (increased blood pressure, freezing), even without a shock.

What does it mean to “potentiate” the acoustic startle reflex?

To increase its magnitude by associating it with a learned threat cue.

How can the ASR be potentiated experimentally?

By pairing a neutral cue (like a light or odor) with shock.

What happens after the neutral cue (light) is paired with shock?

The light alone elicits fear, and when combined with sound, the startle reflex becomes much stronger.

. What does the potentiation of ASR tell us about emotional learning?

Fear conditioning enhances reflexive defensive behaviors, even when the threat isn’t immediately present.

How might fear-potentiated startle relate to human anxiety disorders?

Individuals with overactive amygdala responses may show exaggerated startle reactions to perceived threats.

What is the main function of the amygdala in this diagram?

It integrates sensory information (visual, auditory, pain) with emotional significance and sends output to motor and autonomic systems that generate fear responses.

Which sensory systems feed into the amygdala in this model?

Visual, auditory, and somatosensory (pain) systems.

Where does visual information travel before reaching the amygdala?

From the retina → lateral geniculate nucleus (LGN) → lateral posterior nucleus → perirhinal cortex → lateral & basolateral nuclei of the amygdala.

Where does pain information travel before reaching the amygdala?

From the spinal cord → posterior thalamic, parabrachial, and insular regions → amygdala.

Which nuclei within the amygdala receive sensory input?

The lateral and basolateral nuclei.

Which amygdala nuclei project to motor and autonomic control areas?

The central and medial nuclei.

What is the role of the central nucleus in fear responses?

It acts as the main output hub, triggering physiological fear reactions via brainstem and hypothalamic pathways.

What structures does the central nucleus send output to?

Deep mesencephalic (SC/Me) layers, ventromedial hypothalamus (VM), and periaqueductal gray (PA).

What functions do these target regions control?

VM and PA regulate autonomic and defensive behaviors (e.g., freezing, changes in blood pressure, vocalization).

What is the startle pathway?

A reflex circuit from the ear → cochlear root neurons (CRN) → brainstem (pontis caudalis, PnC) → spinal cord → muscles.

How does the amygdala influence the startle pathway?

By modulating its activity through projections from the central nucleus to the PnC, increasing startle magnitude during fear states (fear-potentiated startle).

Which brainstem region integrates sensory input for the startle reflex?

The pontis caudalis (PnC).

Why is the amygdala crucial for fear-potentiated startle but not for the basic startle reflex?

Because the startle reflex itself is spinal (automatic), but its enhancement (fear potentiation) requires emotional context provided by the amygdala.

How does this circuit explain fear learning?

Sensory inputs (e.g., visual, auditory, pain) converge in the lateral amygdala, which learns associations between neutral and aversive cues, then activates fear responses via the central nucleus.

What does the diagram demonstrate about the brain’s organization of emotion and reflexes?

There are parallel sensory and motor pathways that meet in the amygdala — linking perception of threat with immediate physical reaction.

How could lesions to the amygdala affect these processes?

They would prevent emotional modulation of reflexes (like fear-potentiated startle) while leaving the basic reflex itself intact.

What is the goal of auditory fear conditioning?

To teach an animal to associate a neutral sound (tone) with an aversive event (shock)

Trace the normal auditory pathway in the rat brain from sound to cortex.

Ear → auditory nerve → auditory midbrain → auditory thalamus → auditory cortex.

What happens when a sound is paired with a shock during fear conditioning?

The auditory information (sound) and somatosensory information (shock) converge in the amygdala, creating a learned fear association.

What happens when the auditory midbrain is lesioned?

Fear conditioning is disrupted.

What happens when the auditory thalamus is lesioned?

Fear conditioning is also disrupted.

What happens when the auditory cortex is lesioned?

There is no effect — animals can still form the sound–shock association.

What does this pattern of results imply about the location of fear conditioning?

That fear conditioning occurs in subcortical pathways (midbrain and thalamus), not in the auditory cortex.

Why is the amygdala considered the convergence point for sensory and aversive information?

Because it receives input from both auditory (tone) and somatosensory (shock) systems.

Where does auditory information first go in the brain during fear conditioning?

To the thalamus, which acts as a relay for sensory information.

Which amygdala nucleus receives the auditory input from the thalamus?

The lateral nucleus (LN), also known as the sensory interface of the amygdala.

What happens after information reaches the lateral nucleus?

It is transmitted to the basolateral (or basal) nucleus and then to the central nucleus.

What is the role of the central nucleus in this pathway?

It sends output to the hypothalamus and brainstem to produce physiological fear responses (e.g., freezing, heart rate increase).

process of learning to associaate a sound with shock

auditory stimulus → thalamus → lateral nucleus → basal (basolateral) Nucleus → central nucleus

Where can long-term potentiation be created in the route that auditory learning uses to associate sound with a shock?

Auditory stimulus can cause long-term potentiation (LTP) of the connection between the thalamus and the Lateral nucleus ( LN)

What does long-term potentiation (LTP) do to the postsynaptic neuron?

makes the neuron fire more easily by increasing depolarization (greater excitability).