LEARNING Flashcards

Question

**Q: Why is the hippocampus important for therapy and relapse risk? 🧠🗺️🔁✨**

Answer 1

The **hippocampus** encodes **contextual memory** (where and when). 🗺️⏱️ • Safety learning can be context-specific • Changing context can unmask old fear (renewal) 🔁😨 Stem cue: improved in clinic but worse elsewhere → hippocampal context gating. 📝🏥➡️🏙️

Answer 2

The **vmPFC** supports safety valuation and inhibits amygdala output. 🛡️🛑😨 With successful learning: • vmPFC control strengthens • Threat cues produce less amygdala response This acts as a learned “safety brake.” 💪🛡️⬇️😨

Answer 3

The **dlPFC** mediates cognitive control: 🎛️🧠 • Working memory • Attention shifting • Deliberate reappraisal Stem cue: challenging thoughts or holding alternative interpretations → dlPFC engagement. 📝💭🔄✅

Answer 4

The **ACC** detects conflict and error between expectation and outcome. ⚖️🎯 It supports: • Strategy shifting • Implementation of control Stem cue: mismatch detection or conflict monitoring → ACC involvement. 📝✅

Answer 5

The **striatum** mediates reinforcement learning and habit formation. 🏆🔁 • Avoidance: relief reinforces avoidance habits 😌➡️🔁 • Compulsions: distress reduction reinforces behaviour 😖⬇️🔁 Therapy weakens old loops and builds new ones via repeated corrective outcomes. 🔁✨

Answer 6

**Extinction** = repeated cue exposure without the aversive outcome, reducing fear. 🔔🚫😨➡️📉 **Inhibitory learning model**: • New safety memory (cue → safe) inhibits old fear memory • Original fear trace may persist Fear can therefore return under certain conditions. ⏳🔁

Answer 7

• Amygdala → threat encoding and expression 😨 • vmPFC → safety valuation and top-down inhibition 🛡️🛑 • Hippocampus → context coding 🗺️ Repeated safe exposure strengthens vmPFC control and context-tagged safety learning, reducing threat output. 🔁✅📉😨

Answer 8

Because extinction is inhibitory and context-dependent. ⏳🛡️🗺️ Classic effects: • **Spontaneous recovery** → return with time ⏱️🔁 • **Renewal** → return in a new context 🗺️🔁 • **Reinstatement** → return after stress or aversive event ⚡🔁 Key concept: new learning competes with, not deletes, old fear. ⚖️🧠

Answer 9

**Reconsolidation** occurs when a memory is reactivated and becomes temporarily **labile** before being restabilised. 🔔🫧➡️🧱 During this window: • New information or meaning can be incorporated 🛠️ • The memory may be updated rather than erased 🔄 Exam-safe link: therapy may exploit reconsolidation by reactivating memories and introducing corrective meaning in a safe context (without overclaiming). 📝⚖️

Answer 10

**Prediction error** arises when an expected outcome does not occur (or coping is better than expected). 🎯😨❌➡️✅ This mismatch: • Triggers dopamine-linked teaching signals ⚡🧠 • Enhances plasticity at relevant synapses and circuits 🔄🔗 Therefore, learning is strongest when there is a clear expected–actual discrepancy. 🎯✅✨

Answer 11

Reported findings commonly include: 📌🧠 • Reduced **amygdala reactivity** to threat cues 😨📉 • Increased **prefrontal recruitment** during regulation tasks (dlPFC/ACC/vmPFC) 🧠⬆️ • Stronger **PFC–amygdala functional connectivity** (better top-down control) 🔗🧠 • Changes consistent with altered reward and habit circuitry (striatal patterns) 🔁🏆

Answer 12

Symptom: cue-triggered fear and avoidance 😨🚪 Circuit: amygdala and insula (threat) regulated by vmPFC, with context via hippocampus 🧠🛡️🗺️ Transmitters: glutamate (NMDA/AMPA plasticity), dopamine (prediction error), GABA (inhibition) ⚡🧲🛑 Learning outcome: new safety memory (cue → safe), stronger vmPFC inhibition, reduced avoidance habits 🔁✅📉

Answer 13

Symptom: distress from maladaptive appraisal 💭😨 Circuit: dlPFC (working memory and control) + ACC (conflict detection) regulate limbic activity and safety valuation via vmPFC 🎛️⚖️🛡️ Mechanism: repeated reappraisal strengthens control circuits Outcome: reduced emotional reactivity and improved regulation 📉😨✨

Answer 14

Symptom: low activity and low reinforcement 💤📉 System: impaired reinforcement learning Circuit: striatum (action–outcome learning) with PFC planning 🧠🏆 Mechanism: scheduled activities increase contact with reward, generating prediction errors ⚡🎁 Outcome: rebuilt reward contingencies and new adaptive habits 🔁✅✨

Answer 15

• Therapy isn’t biological ❌ → therapy is experience-driven learning causing neuroplasticity 🔄 • NMDA mediates fast excitation ❌ → AMPA is fast; NMDA gates plasticity via Ca²⁺ 🧲 • Extinction erases fear ❌ → extinction is inhibitory learning; fear can return 🛡️🔁 • Dopamine equals pleasure ❌ → dopamine encodes prediction error 🎯⚡ • More arousal is always better ❌ → noradrenaline follows an inverted-U 🎢 • GABA only sedates ❌ → GABA provides inhibition, gating, and stability 🛑🛡️

Answer 16

• Expected catastrophe does not occur → prediction error (dopamine) 🎯❌➡️⚡ • Exposure works but relapse in new context → inhibitory learning + hippocampal context (renewal) 🗺️🔁 • Reappraisal or thought challenging → dlPFC + ACC control; vmPFC safety valuation 🎛️⚖️🛡️ • Panic with bodily focus → insula + amygdala threat circuitry 🫀😱➡️😨 • Avoidance maintained by relief → striatal negative reinforcement loop 😌➡️🔁 • Overwhelmed during learning → noradrenaline too high (inverted-U failure) 😱🎢📉

Answer 17

Psychological therapies work by creating structured learning experiences that engage glutamate-dependent synaptic plasticity, neuromodulatory teaching signals, and circuit-level reweighting across prefrontal, limbic, and striatal systems. 🔄🧠⚡✨

LEARNING Flashcards

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