Скачать или смотреть Critical Period Regulation: Oscillations, Clocks, And Epigenetics (Reh et al., 2020)

I. Introduction To Critical Periods In Brain Development
Neural circuits are shaped by experience during critical periods.
These are windows of peak plasticity in early life.
They allow individuals to adapt to their specific environment.
Proper timing is essential for functions like language.
Maturation of intrinsic programs must align with input.
Parvalbumin (PV) inhibitory neurons are central to this timing.
PV cells are fast-spiking and control cortical activity.
Their maturation lags behind excitatory pyramidal cells.
Once mature, PV cells trigger the onset of plasticity.
Plasticity is regulated across multiple timescales.
These range from milliseconds to evolutionary time.

II. Milliseconds To Minutes: The Role Of Neuronal Oscillations
Gamma oscillations reflect real-time circuit physiology.
PV cells generate these high-frequency rhythms.
Gamma power reflects the excitatory-inhibitory balance.
These rhythms track the timing of critical periods.
Gamma power increases as animals enter a critical period.
Sensory deprivation can block this increase in gamma power.
In humans, gamma activity increases with age.
This correlates with the maturation of inhibition.
Gamma oscillations are linked to language acquisition.
Infants show gamma spikes when processing native speech.
Attention can enhance gamma power and enable plasticity.
This signals a shift to analyzing external learning cues.

III. Days To Months: The Role Of Circadian Genes
Circadian genes regulate plasticity over longer durations.
Genes like CLOCK and BMAL control temporal expression.
These genes begin oscillating in the visual cortex postnatally.
This rhythmicity coincides with the critical period for vision.
Deleting CLOCK genes delays PV cell maturation.
This delay subsequently postpones the onset of plasticity.
PV cells are highly active and prone to oxidative stress.
Circadian complexes regulate cellular metabolism.
They help manage reactive oxygen species in the brain.
This protects the PV cells during high-activity states.
Circadian disruption may destabilize neural circuitry.

IV. Lifespan And Generations: The Role Of Chromatin Remodeling
Epigenetics regulate the baseline level of plasticity.
Experience alters chromatin structure to change gene expression.
Histone acetylation is high during juvenile critical periods.
Visual stimulation triggers a rise in histone acetylation.
This rise is generally not observed in adult animals.
Pharmacological acetylation can restore plasticity in adults.
DNA methylation patterns also shift with neural activity.
Parental experiences can influence plasticity in offspring.
Stress in parents may alter germline epigenetics.
This can affect the neuroanatomy of future generations.
Enriched environments for parents may benefit offspring.

V. Implications For Mental Health And Disease
Misalignment of critical periods impacts cognitive integration.
Disorders like autism involve disrupted multisensory timing.
Reduced gamma activity is a predictor for autism diagnosis.
Schizophrenia is linked to PV cell disruption.
Patients often show reduced expression of CLOCK genes.
Oxidative stress can perturb plasticity windows.
Early life adversity alters EEG power trajectories.
Stress leads to dramatic reductions in EEG power in infants.
Understanding these timescales aids in treating disorders.
It may help correct aberrant developmental trajectories.

#neuroscience #brainplasticity #criticalperiods #epigenetics #circadianrhythms #brainhealth #mentalhealthresearch #psychology #childdevelopment #neurobiology #psychedelicresearch #psychedelicscience #psychedelictherapy #neuroplasticity #medschool #psychiatry #braindevelopment

Source:
Reh, R. K., Dias, B. G., Nelson, C. A., III, Kaufer, D., Werker, J. F., Kolb, B., Levine, J. D., & Hensch, T. K. (2020). Critical period regulation across multiple timescales. Proceedings of the National Academy of Sciences, 117(41), 23242–23251.

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