Questions: Critical Periods: Experience-Dependent Plasticity in Development

Question 1

What is the primary mechanism that closes a critical period, ending the window of heightened experience-dependent plasticity?

• A. Downregulation of NMDA receptors, preventing further calcium-dependent plasticity
• B. Myelination of local interneurons, which slows information processing below the plasticity threshold
• C. Maturation of GABAergic inhibition, which raises the threshold for activity-dependent circuit modification
• D. Loss of trophic factor (BDNF) signaling in the cortex after early development

Answer: (C)

Critical period closure is primarily gated by the maturation of fast-spiking parvalbumin-positive GABAergic interneurons. As these interneurons mature and form perineuronal nets (extracellular matrix structures around them), the excitation/inhibition balance shifts to favor inhibition, making it harder for activity patterns to trigger the synaptic changes that reshape circuits. Reducing GABAergic inhibition experimentally — even in adult animals — can reopen a version of the critical period.

Question 2

After a critical period closes, the affected neural circuit becomes mostly rigid and no synaptic plasticity of any kind is possible in that region.

• T. True
• F. False

Answer: False

Critical period closure reduces plasticity dramatically but does not eliminate it. Adult brains retain forms of synaptic plasticity (LTP, LTD, homeostatic plasticity) throughout life. What closes is the exceptional, experience-driven rapid circuit reorganization characteristic of the critical period. Crucially, experimental interventions (reducing GABAergic inhibition, enriched environments, certain drugs) can partially reopen critical period-like plasticity even in adults, which is why this research has therapeutic implications for amblyopia and other developmental conditions.

Question 3

In the classic ocular dominance critical period experiment, what happens to the visual cortex of a kitten when one eye is sutured shut for several weeks, and what does this demonstrate?

Model answer: Neurons in the visual cortex that normally respond to both eyes shift to respond predominantly to the open eye. The deprived eye loses its cortical representation while the open eye expands its territory. This demonstrates that during the critical period, competitive activity-dependent mechanisms determine which inputs maintain or strengthen their connections — silent or weakly active inputs are pruned, while active inputs are stabilized and expanded.

This monocular deprivation experiment (Hubel and Wiesel) is the foundational evidence for critical periods. It shows that sensory experience literally sculpts cortical circuit organization during a defined developmental window. If deprivation occurs outside the critical period, the same suturing produces little or no cortical reorganization. The asymmetry — easy to disrupt during the critical period, hard to reverse after — has direct implications for treating childhood amblyopia, where early intervention is far more effective than later treatment.