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Depression & Anxiety Pathways

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Lesson Plan

Neurobiology Lesson Plan

Participants will review the neurobiological pathways of depression and anxiety—identifying key brain structures and neurotransmitters—and describe how SSRIs modulate serotonin reuptake to alleviate symptoms.

Understanding the anatomy and chemistry behind mood disorders empowers adults to interpret treatment mechanisms, reduce stigma, and support mental health–focused conversations.

Audience

Adult learners

Time

45 minutes

Approach

Interactive lecture with visuals, handouts, and guided discussion.

Materials

Prep

Setup and Review Materials

10 minutes

Step 1

Introduction

5 minutes

  • Welcome participants and state session objectives
  • Briefly define depression and anxiety in clinical terms
  • Outline the lesson structure: anatomy, neurotransmitters, SSRI action, Q&A

Step 2

Brain Structures Overview

10 minutes

  • Display the Brain Anatomy Diagram
  • Highlight and describe the roles of the amygdala, hippocampus, and prefrontal cortex in mood regulation
  • Invite participants to share observations from the diagram

Step 3

Neurotransmitter Pathways

10 minutes

  • Distribute the Neurotransmitter Pathways Chart
  • Explain serotonin, norepinephrine, and GABA pathways involved in depression and anxiety
  • Facilitate a brief discussion: How might imbalances manifest symptomatically?

Step 4

SSRIs Mechanism

10 minutes

  • Present the SSRI Mechanism Slide Deck
  • Describe how SSRIs block serotonin reuptake transporters, increasing synaptic serotonin levels
  • Connect pharmacology to symptom improvement in depression and anxiety

Step 5

Assessment & Q&A

10 minutes

  • Have participants complete the short quiz on pages 3–4 of the Depression & Anxiety Handout
  • Review answers as a group, clarifying misconceptions
  • Open the floor for questions and further discussion
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Slide Deck

Brain Anatomy: Key Regions

[Image: Lateral view of brain with highlighted regions]

• Amygdala (red): processes fear and threat detection – hyperactivity linked to anxiety symptoms
• Hippocampus (green): memory consolidation and context regulation of emotion – volume loss associated with depression
• Prefrontal Cortex (blue): executive function and top-down emotion regulation – reduced activity seen in mood disorders

Use this slide to introduce the major brain regions involved in mood regulation. Point to each highlighted area, describe its function, and relate it to depression and anxiety symptoms. Invite participants to note any questions about structure–function links.

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Slide Deck

Neurotransmitter Pathways in Depression & Anxiety

[Chart: Major mood-related neurotransmitter pathways]

• Serotonin (5-HT)
– Origin: Raphe nuclei
– Projections: Prefrontal cortex, hippocampus, amygdala
– Role: Mood stabilization, anxiety modulation

• Norepinephrine (NE)
– Origin: Locus coeruleus
– Projections: Prefrontal cortex, limbic system
– Role: Arousal, stress response, attention

• GABA
– Origin: Local interneurons throughout cortex and limbic regions
– Role: Inhibitory tone, anxiety restraint

Arrows indicate directions of projections to key regions (PFC, hippocampus, amygdala).

Use this slide to introduce the key neurotransmitter systems involved in mood regulation. Walk participants through each pathway, noting origin nuclei, projection targets, and functional roles. Ask learners how alterations in these systems might contribute to symptoms of depression and anxiety.

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Slide Deck

SSRIs: Mechanism of Action

[Diagram: Serotonergic synapse before and after SSRI]

• SSRIs block the serotonin transporter (SERT) on presynaptic neurons
• Inhibition of reuptake increases extracellular serotonin levels
• Enhanced serotonergic signaling in key regions: PFC, hippocampus, amygdala

Explain the role of SERT in terminating serotonergic signals and how SSRIs competitively inhibit this transporter. Show how increased synaptic serotonin modulates mood circuits.

Pharmacodynamics & Onset of Action

• Acute effect: elevated synaptic serotonin within hours
• Autoreceptor desensitization (1–2 weeks) leads to sustained 5-HT release
• Clinical improvement typically emerges at 4–6 weeks
• Longer-term neuroplastic changes: ↑ BDNF, hippocampal neurogenesis

Discuss why patients may not feel immediate relief even though serotonin levels rise quickly. Emphasize the importance of autoreceptor adaptation and neuroplasticity.

Clinical Considerations

• Common side effects: GI upset, headache, sexual dysfunction
• Withdrawal/discontinuation syndrome: taper slowly
• Drug interactions: avoid MAOIs, caution with tramadol
• Importance of adherence: consistent dosing enhances efficacy
• Monitor and educate: set realistic expectations

Highlight the need for patient counseling on side effects and adherence. Encourage discussion on how to manage common adverse effects and the importance of communication.

Summary & Key Takeaways

• SSRIs increase synaptic serotonin by blocking SERT
• Therapeutic effects require receptor adaptation and neuroplasticity over weeks
• Patient education on side effects and timelines is essential
• Pharmacological insight fosters compassionate, informed care

Wrap up the SSRI section, reiterating how understanding SSRI mechanisms can reduce stigma and empower informed discussions about mental health treatments.

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Worksheet

Depression & Anxiety Handout

Part 1: Neurobiology Summary

1. Brain Structures Involved in Mood Regulation

  • Amygdala: Processes fear and threat detection; hyperactivity linked to anxiety symptoms.
  • Hippocampus: Involved in memory consolidation and contextual regulation of emotion; volume loss associated with depression.
  • Prefrontal Cortex: Governs executive function and top-down emotion regulation; reduced activity seen in mood disorders.

2. Neurotransmitter Systems

  • Serotonin (5-HT)
    Origin: Raphe nuclei → Projections: Prefrontal cortex, hippocampus, amygdala
    Role: Mood stabilization, anxiety modulation
  • Norepinephrine (NE)
    Origin: Locus coeruleus → Projections: Prefrontal cortex, limbic system
    Role: Arousal, stress response, attention
  • GABA
    Origin: Local interneurons throughout cortex and limbic regions
    Role: Inhibitory tone, anxiety restraint

3. SSRIs: Mechanism of Action

  • Block SERT (serotonin transporter) on presynaptic neurons → increases extracellular serotonin levels
  • Therapeutic timeline:
    • Acute rise in synaptic serotonin within hours
    • Autoreceptor desensitization (1–2 weeks)
    • Clinical improvement typically at 4–6 weeks
    • Longer-term neuroplastic changes (↑ BDNF, hippocampal neurogenesis)
  • Clinical considerations:
    • Common side effects: GI upset, headache, sexual dysfunction
    • Taper slowly to avoid discontinuation syndrome
    • Monitor drug interactions and counsel on adherence

Part 2: Assessment Quiz

  1. Label each region on the lateral view of the brain: Amygdala, Hippocampus, Prefrontal Cortex. Refer to Brain Anatomy Diagram.





  2. Explain how decreased hippocampal volume is associated with symptoms of depression.










  3. Describe the role of GABA in anxiety modulation, using insights from the Neurotransmitter Pathways Chart.





  4. Briefly outline the mechanism by which SSRIs increase synaptic serotonin levels. Refer to the SSRI Mechanism Slide Deck.





  5. Why might patients only experience symptom relief after several weeks of SSRI treatment?





  6. List two common side effects of SSRIs and suggest one strategy to manage each.





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