Overview
This lecture explains how fear, anxiety, and stress are processed in the brain, their physiological effects, and how they impact health, including the role of different brain regions and immune responses.
Fear Conditioning and the Amygdala
- The amygdala has three main regions involved in fear: lateral, basal, and central nuclei.
- The lateral nucleus acquires conditioned emotional responses via synaptic strengthening (long-term potentiation).
- Inputs to the lateral amygdala come from the prefrontal cortex, thalamus, and hippocampus; outputs go to the ventral striatum and dorsal thalamus.
- The basal nucleus receives information from the lateral nucleus and sends it to the central nucleus.
- The central nucleus drives emotional responses by sending signals to the hypothalamus, midbrain, pons, and medulla.
- Damage to the amygdala impairs the ability to learn and express new fear responses.
Emotional Responses and Extinction
- The ventromedial prefrontal cortex (vmPFC) inhibits emotional responses and aids extinction of conditioned fears.
- The central amygdala outputs trigger physiological fear and stress responses: sympathetic/parasympathetic activation, hormonal secretion, facial expressions, and freezing.
Anxiety Disorders
- Anxiety is an irrational, prolonged fear response often occurring without real danger.
- Panic disorder features repeated panic attacks, increased sympathetic activity, and anticipatory anxiety.
- Panic disorder is associated with lower GABA activity and high levels of orexin.
- PTSD involves heightened emotional responses, nightmares, and flashbacks after traumatic events; associated with low hippocampal volume.
Treatments for Anxiety
- Benzodiazepines (e.g., Valium, Xanax) activate GABA-A receptors to enhance inhibitory signals and reduce anxiety.
- Chronic use of benzodiazepines can lead to addiction.
- Alcohol also acts on GABA-A receptors but is not prescribed for anxiety.
Stress Mechanisms and Responses
- Stress occurs when perceived resources are inadequate to meet demands.
- Selye’s General Adaptation Syndrome describes three stages: alarm (adrenaline, cortisol released), resistance (continued hormone release), and exhaustion (immune suppression, illness).
- The HPA axis (hypothalamus-pituitary-adrenal) coordinates the hormonal response to stress, releasing cortisol.
Effects of Cortisol and Immune Function
- Short-term cortisol boosts energy and alertness; chronic cortisol impairs memory, raises blood pressure, and suppresses immunity.
- Stress increases immune activity by producing leukocytes (B cells, T cells, natural killer cells).
- B cells release antibodies; T cells attack infected cells; natural killer cells target viruses or tumors.
- Cytokines released by leukocytes cause fever, sleepiness, and appetite loss, aiding recovery.
Key Terms & Definitions
- Amygdala — brain region critical for emotional processing and fear learning.
- Long-term potentiation (LTP) — strengthening of synaptic connections for memory formation.
- Ventromedial prefrontal cortex (vmPFC) — brain area that inhibits emotional responses.
- Panic Disorder — anxiety disorder with repeated panic attacks and fear of recurrence.
- PTSD (Post-Traumatic Stress Disorder) — disorder with heightened stress after trauma.
- GABA — inhibitory neurotransmitter reducing neural activity.
- HPA Axis — system coordinating stress hormone release (hypothalamus, pituitary, adrenal).
- Cortisol — stress hormone increasing blood sugar and metabolism.
- Leukocytes — white blood cells defending against infection.
- Cytokines — immune system proteins inducing sickness behaviors.
Action Items / Next Steps
- Review diagrams of the amygdala, HPA axis, and immune cell interactions.
- Read about mechanisms of action for anti-anxiety medications and effects on neurotransmission.