Critical period

If, for some reason, the organism does not receive the appropriate stimulus during this "critical period" to learn a given skill or trait, it may be difficult, ultimately less successful, or even impossible, to develop certain associated functions later in life.

[3] For example, the critical period for the development of a human child's binocular vision is thought to be between three and eight months, with sensitivity to damage extending up to at least three years of age.

[1] Examples of strong critical periods include monocular deprivation, filial imprinting, monaural occlusion,[5] and Prefrontal Synthesis acquisition.

Two major factors influence the opening of critical periods: cellular events (i.e. changes in molecular landscape) and sensory experience (i.e. hearing sound, visual input, etc.).

[19][20] Neurons who received less frequent input from retinal ganglion cells during early postnatal periods were more prone to be engulfed and pruned by microglia, as per monocular deprivation experiments.

Blocking these receptors or performing a knockout experiment significantly lowered microglial interactions and synaptic pruning during the early visual cortex critical period.

[20] More recently, the expression of the complement component 4 gene has been found to significantly contribute to abnormally high levels of microglial synaptic pruning during early stages of development in the neurons and microglia of schizophrenics, suggesting a genomic connection between the immune system and critical periods.

[31] For example, PNN digestion by ABC chondroitinase in rats leads to a shift in ocular dominance upon monocular deprivation, which is normally restricted to its critical period much earlier in development.

[34] In all, these data suggest a role for PNNs in the maturation of CNS inhibition, the prevention of plastic axonal growth, and subsequently, critical period closure.

[36][39] Research has shown that social isolation of mice leads to reduced myelin thickness and poor working memory, but only during a juvenile critical period.

[11][43][44][45][47][48][49] For example, in kittens, a shift in ocular dominance resulting from monocular deprivation during the critical period is reduced by combined destruction of noradrenergic and cholinergic neurons.

[48] In addition, prenatal exposure to selective serotonin reuptake inhibitors (SSRI) causes a shift in perceptual narrowing on language to earlier in development.

[52] The hypothesis that language is acquired during a critical period was first proposed by neurologists Wilder Penfield and Lamar Roberts in 1959 and popularized by linguist Eric Lenneberg in 1967.

Studies conducted by these researchers demonstrated that profoundly deaf individuals who are not exposed to a sign language as children never achieve full proficiency, even after 30 years of daily use.

[55] Other evidence comes from neuropsychology where it is known that adults well beyond the critical period are more likely to suffer permanent language impairment from brain damage than are children, believed to be due to youthful resiliency of neural reorganization.

Research shows that infants who were unable to develop this attachment had major difficulty in keeping close relationships, and had maladaptive behaviors with adopted parents.

Some aspects of language, such as phoneme tuning, grammar processing, articulation control, and vocabulary acquisition can be significantly improved by training at any age and therefore have weak critical periods.

The theory[58] has often been extended to a critical period for second language acquisition (SLA), which has influenced researchers in the field on both sides of the spectrum, supportive and unsupportive of CPH, to explore.

In general electrophysiological analyses of axons and neurons in the lateral geniculate nucleus showed that the visual receptive field properties was comparable to adult cats.

They found that in the long term, monocular deprivation causes reduced branching at the end of neurons, while the amount of afferents allocated to the nondeprived eye increased.

[68] Studies of people whose sight has been restored after a long blindness (whether from birth or a later point in life) reveal that they cannot necessarily recognize objects and faces (as opposed to color, motion, and simple geometric shapes).

[69] The general belief that a critical period lasts until age 5 or 6 was challenged by a 2007 study that found that older patients could improve these abilities with years of exposure.

Pheromones play a key role in the imprinting process, they trigger a biochemical response in the recipient, leading to a confirmed identification in the other individual.

Approximately at the same time, both an electroencephalographic study by Sharma, Dorman and Spahr[76] and an in-vivo investigation of the cortical plasticity in deaf cats by Kral and colleagues[77] demonstrated that the adaptation to the cochlear implant is subject to an early, developmental sensitive period.

Rats that were exposed to pulsed noise during the critical period had cortical neurons that were less able to respond to repeated stimuli; the early auditory environment interrupted normal structural organization during development.

In a related study, Barkat, Polley and Hensch (2011) looked at how exposure to different sound frequencies influences the development of the tonotopic map in the primary auditory cortex and the ventral medical geniculate body.

[80] These studies support the notion that exposure to certain sounds within the critical period can influence the development of tonotopic maps and the response properties of neurons.

Also, the results' conjunction with the aforementioned chronological observations suggests that early to mid-childhood exposure to environments whose interpretation depends on pitch is a developmental "trigger" for whatever aptitude an individual possesses.

The results of the studies done on ferrets and rats reinforced the idea that the vestibular system is very important to motor development during the initial neonatal period.

If the vestibular receptors are present during the initial six months to a year when the infant is learning to sit and stand, then the child may develop motor control and balance normally.