2 Neuroscience2.10 Neurodevelopment and neuroplasticity
2.10.4.2 Neurobiological effects of learning and psychological therapies
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Written by Resident Doctor Committee · Published
Synaptic plasticity
Hebbian learning strengthens connections between neurones that are active together, mainly through N-methyl-D-aspartate (NMDA) receptor plasticity.
Process | Trigger | Mechanism |
|---|---|---|
Long-term potentiation (LTP) | Presynaptic activity coincides with postsynaptic depolarisation | Depolarisation removes the NMDA receptor's magnesium block, calcium enters, and kinases add α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors |
Long-term depression (LTD) | Weaker activity | Phosphatases remove AMPA receptors, which refines memories and supports forgetting |
Early and late plasticity
Early plasticity moves existing AMPA receptors and lasts minutes to hours unless it is stabilised.
Late plasticity needs protein synthesis: cyclic adenosine monophosphate (cAMP) and protein kinase A signalling activate cAMP response element-binding protein (CREB), and lasting dendritic spines form.
Brain-derived neurotrophic factor (BDNF) supports late LTP and spine growth, and is implicated in the effects of exercise, antidepressants and electroconvulsive therapy.
Consolidation and sleep
Systems consolidation shifts memories that first depend on the hippocampus into cortex through reactivation and sleep.
Slow-wave sleep supports hippocampal replay, and rapid eye movement sleep contributes to emotional and procedural processing.
Extinction
Extinction creates a competing safety memory rather than erasing fear, and prefrontal control of the amygdala and hippocampal context decide which memory is retrieved.
Phenomenon | Fear returns | Implication |
|---|---|---|
Spontaneous recovery | After a delay | Booster sessions protect gains |
Renewal | Outside the extinction context | Practise in many settings |
Reinstatement | After an unsignalled aversive event | Warn of relapse after unrelated stress |
Rapid reacquisition | Faster than first learning | The original association is intact |
Anxiety disorders and post-traumatic stress disorder can involve impaired extinction learning or recall.
Reconsolidation
Reconsolidation restabilises a reactivated, temporarily labile memory; it needs protein synthesis and offers a window for updating.
Blocking protein synthesis alters memory in animals, but human propranolol studies are mixed, so reconsolidation is not an established standalone treatment.
Therapy mechanisms
Therapy | Mechanism | Detail |
|---|---|---|
Exposure | Expectancy violation: feared predictions are tested against experience | Anxiety need not fall within a session; drop safety behaviours and vary cues and contexts |
Cognitive reappraisal | Practising alternative interpretations | Dorsolateral and ventrolateral prefrontal and dorsal anterior cingulate activity alter amygdala response |
Mindfulness | Decentring: seeing thoughts as mental events, not facts | Default mode, insular and prefrontal changes |
Behavioural activation | Scheduling meaningful activity before motivation returns | Counters reduced anticipated reward and raised perceived effort in depression |
Imaging after therapy
Before-and-after scans show amygdala, prefrontal, cingulate and striatal changes but cannot establish a causal mechanism.
An undetected change does not exclude learning, and scans do not reliably guide the choice of therapy for an individual.
Conditions for therapeutic learning
Factor | Effect |
|---|---|
Spacing and retrieval | Distributed practice, homework and recalling the formulation aid retention |
Alliance and expectancy | Alliance predicts outcome; a credible rationale supports response |
Emotional arousal | Moderate arousal helps, but excess impairs contextual encoding |
Sleep | Supports consolidation, so treat insomnia |
Alcohol and benzodiazepines | May interfere with extinction |