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Critical period

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(Redirected from Sensitive period)
For the critical period in language development, see Critical period hypothesis.
For other uses, see window of opportunity.

In developmental psychology and developmental biology, a critical period is a maturational stage in the lifespan of an organism during which the nervous system is especially sensitive to certain environmental stimuli. 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. Functions that are indispensable to an organism's survival, such as vision, are particularly likely to develop during critical periods. "Critical period" also relates to the ability to acquire one's first language. Researchers found that people who passed the "critical period" would not acquire their first language fluently.[1]

Some researchers differentiate between 'strong critical periods' and 'weak critical periods' (also known as 'sensitive' periods)—defining 'weak critical periods' / 'sensitive periods' as more extended periods, after which learning is still possible.[2] Other researchers consider these the same phenomenon.[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. Further critical periods have been identified for the development of hearing[4] and the vestibular system.[1]

Strong versus weak critical periods

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Examples of strong critical periods include monocular deprivation, filial imprinting, monaural occlusion,[5] and Prefrontal Synthesis acquisition.[6] These traits cannot be acquired after the end of the critical period.

Examples of weak critical periods include phoneme tuning, grammar processing, articulation control, vocabulary acquisition, music training, auditory processing, sport training, and many other traits that can be significantly improved by training at any age.[7][8]

Critical period mechanisms

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Critical period opening

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Critical periods of plasticity occur in the prenatal brain and continue throughout childhood until adolescence and are very limited during adulthood. 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.). Both need to coincide for the critical period to open properly. At the cellular level, critical periods are characterized by maturation of the inhibitory circuits.[9] More precisely, factors such as brain-derived neurotrophic factor (BDNF) and orthodenticle homeobox 2 (Otx2) contribute to the maturation of a major class of inhibitory neurons: parvalbumin-positive interneurons (PV cells).[9] Prior to the onset of the critical period, modulation of this circuit is hampered by early factors such as polysialic acid (PSA).[9] PSA acts, in part, by preventing Otx2 interaction with PV cells.[10] Soon after the opening of the critical period, PSA levels decrease, allowing PV cell maturation by activating inhibitory GABAa receptors that facilitate inhibitory circuit remodeling. Artificially removing PSA, or experimentally manipulating inhibitory transmission can result in early opening of the critical period.[10][11] While the timing of these molecular events seems to be partially explained by clock genes,[12] experience is crucial as sensory deprivation experiments have been shown to interfere with the proper timing of critical periods.[13][14][15]

Activity-dependent competition

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Hebbian theory guides the idea of activity-dependent competition: if two neurons both have the potential to make a connection with a cell, the neuron that fires more will make the connection.

Ocular dominance

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This phenomenon of activity-dependent competition is especially seen in the formation of ocular dominance columns within the visual system. Early in development, most of the visual cortex is binocular, meaning it receives roughly equal input from both eyes.[16] Normally, as development progresses, the visual cortex will segregate into monocular columns that receive input from only one eye.[16] However, if one eye is patched, or otherwise prevented from receiving sensory input, the visual cortex will shift to favor representation of the uncovered eye. This demonstrates activity-dependent competition and Hebbian theory because inputs from the uncovered eye make and retain more connections than the patched eye.[17]

Axon growth

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Further information: Axon guidance

Axon formation and growth is another key part of plasticity and activity-dependent competition. Axon growth and branching has been shown to be inhibited when the neuron's electrical activity is suppressed below the level of an active neighbor.[18] This shows that axonal growth dynamics are not independent but rather depend on the local circuits within which they are active (i.e. the activity of the other neurons competing for connections).

Microglia

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Microglia inherently play a role in synaptic pruning during adolescence. As resident immune cells of the central nervous system, microglia's main role is phagocytosis and engulfment. Studies have found that during critical periods in the visual cortex, neural synapses become the target of microglial phagocytosis.[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.[19] Similar results were found when manipulating G-coupled purinergic receptors on microglial processes. 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.[21]

Spine motility

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Dendritic spine motility is the altering of the dendritic morphology of a neuron, specifically the appearing and disappearing of the small protrusions known as spines. In early postnatal development, spine motility has been found to be at very high levels. Due to its most pronounced occurrence during postnatal days 11 through 15, spine motility is thought to have a role in neurogenesis.[22] Motility levels significantly decrease before the start of the visual cortex critical period and monocular deprivation experiments show that motility levels steadily decrease until the critical period is over, hinting that motility might not be explicitly involved in this process.[23] However, binocular deprivation before eye-opening resulted in a significant up-regulation of spine motility until the peak of the critical period,[24] resulting in controversial findings regarding the role of dendritic spine motility.

Excitatory-inhibitory balance

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Another critical component of neuronal plasticity is the balance of excitatory and inhibitory inputs. Early in development, GABA, the major inhibitory neurotransmitter in the adult brain, exhibits an excitatory effect on its target neurons.[25] However, due to changes in internal chloride levels due to the up-regulation of potassium chloride pumps, GABA then switches to inhibitory synaptic transmission.[25] The maturation of the GABAergic inhibitory system helps to trigger the onset of critical periods.[11] Strengthened GABAergic systems can induce an early critical period, while weaker GABAergic inputs can delay or even prevent plasticity.[26][27] Inhibition also guides plasticity once the critical period has begun. For example, lateral inhibition is especially important in guiding columnar formation in the visual cortex.[28] Hebbian theory provides insight on the importance of inhibition within neural networks: without inhibition, there would be more synchronous firing and therefore more connections, but with inhibition, fewer excitatory signals get through, allowing only the more salient connections to mature.[29]

Critical period closure

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Perineuronal nets

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Critical period closure has been shown to be modulated by the maturation of inhibitory circuits, mediated by the formation of perineuronal nets around inhibitory neurons.[11] Perineuronal nets (PNNs) are structures in the extracellular matrix formed by chondroitin sulfate proteoglycans, hyaluronan, and link proteins.[30] These structures envelop the soma of inhibitory neurons in the central nervous system, appearing with age to stabilize mature circuits.[30][31] PNN development coincides with the closure of critical periods, and both PNN formation and critical period timing is delayed in dark-rearing.[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.[32]

Additionally, PNNs are negatively charged, which is theorized to create a cation-rich environment around cells, potentially leading to an increased firing rate of inhibitory neurons, thereby allowing for increased inhibition after the formation of PNNs and helping to close the critical period.[33] The role of PNNs in critical period closure is further supported by the finding that fast-spiking parvalbulmin-positive interneurons are often surrounded by PNNs.[33]

Perineuronal nets have also been found to contain chemorepulsive factors, such as semaphorin3A, which restrict axon growth necessary for plasticity during critical periods.[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.

Myelin

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Another mechanism that closes the critical period is myelination. Myelin sheaths are formed by oligodendrocytes in the CNS that wrap around segments of axons to increase their firing speed.[35] Myelin is formed in the early stages of development and progresses in waves, with brain areas of later phylogenetic development (i.e. those associated with "higher" brain functions like the frontal lobes) having later myelination.[36] The maturation of myelination in intracortical layers coincides with critical period closure in mice, which has led to further research on the role of myelination on critical period duration.[37]

Myelin is known to bind many different axonal growth inhibitors that prevent plasticity seen in critical periods.[38] The Nogo receptor is expressed in myelin and binds to the axonal growth inhibitors Nogo and MAG (among others), preventing axon growth in mature, myelinated neurons.[38] Instead of affecting the timing of the critical period, mutations of the Nogo receptor prolong the critical period temporarily.[37] A mutation of the Nogo receptor in mice was found to extend the critical period for monocular dominance from around 20–32 days to 45 or 120 days, suggesting a likely role of the myelin Nogo receptor in critical period closure.[37]

Additionally, the effects of myelination are temporally limited, since myelination itself may have its own critical period and timing.[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.[39] In primates, isolation is correlated with abnormal changes in white matter potentially due to decreased myelination.[40]

In all, myelin and its associated receptors bind several important axonal growth inhibitors which help close the critical period.[37][38] The timing of this myelination, however, is dependent on the brain region and external factors such as the social environment.[36][39]

Neuromodulation

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While the presence or absence of sensory experiences most robustly shapes brain development during the critical period, the behavioral context (i.e. the amount of attention, arousal, fear and reward experienced) concurrent with the sensory inputs have been suggested to be important in regulating the brain remodeling mechanisms.[41][42][43][44][45] In terms of brain connectivity, these behavioral and contextual inputs activate the neuromodulatory system, which have substantial connectivity to the cortex.[43][44][46][47] The molecular effectors released by the neuromodulatory system are called neuromodulators, which include acetylcholine, dopamine, and noradrenaline among others.[46] Investigating the effect of these molecules, as well as the neurons that release and bind them, has been one approach to elucidate the biology of neuromodulation. Research using this approach has highlighted the role of neuromodulation in sensory processing during the 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.[50] On the other hand, neuromodulatory stimulation has been shown to induce brain plasticity in adult mice.[43][44] While being subjected to cholinergic or dopaminergic stimulation, adult mice listening to a tone of specific frequency exhibited expansion of the tonotopic area in the auditory cortex that responds specifically to sounds of that frequency.[43][44]

Mechanistically, neuromodulation is increasingly being recognized for its fine-tuning of the PV cell-mediated inhibition of excitatory pyramidal neurons' soma.[45][49][51] Central to the neuromodulatory regulation of PV cell activity is the existence of distinct subsets of inhibitory neurons, which are responsive to activation by neuromodulators and which inhibit PV cells.[9][45][49][51] Within these cells, some also inhibit specific pyramidal cell dendrites.[45][49] By inhibiting PV cells activity, the neuromodulator-sensitive inhibitory cells such as those expressing vasoactive intestinal peptide (VIP) or somatostatin (SST) lift the inhibition of the pyramidal neurons; in other words, the activity of VIP and SST-expressing cells result in the disinhibition of pyramidal neurons.[9][45][49][51] Then, by inhibiting only certain dendritic branches of these now dis-inhibited pyramidal neurons, the neuromodulation-activated cells allow select sensory inputs to excite the pyramidal neurons and be represented in the brain circuitry.[45][49] Thus, in a landscape of global inhibition by maturing inhibitory signaling, neuromodulation allows windows of dis-inhibition, temporally and spatially, that allow behaviorally important sensory inputs the opportunity to influence the brain.[45][49]

Linguistics

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Main article: Critical period hypothesis

First language acquisition

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The critical period hypothesis (CPH) states that the first few years of life constitute the time during which language develops readily and after which (sometime between age 5 and puberty) language acquisition is much more difficult and ultimately less successful.[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. Lenneberg argued for the hypothesis based on evidence that children who experience brain injury early in life develop far better language skills than adults with similar injuries.

Maria Montessori was one of the earlier educators who brought attention to this phenomenon and called it "sensitive periods", which is one of the pillars of her philosophy of education.

The two most famous cases of children who failed to acquire language after the critical period are the feral children Victor of Aveyron and Genie.[53] However, the tragic circumstances of these cases and the moral and ethical impermissibility of replicating them make it difficult to draw conclusions about them. The children may have been cognitively disabled from infancy, or their inability to develop language may have resulted from the profound neglect and abuse they suffered.[52]

Many subsequent researchers have further developed the CPH, most notably Elissa Newport and Rachel Mayberry. 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.[54] While the effect is most profound for individuals who receive no sign language input until after the age of 12, even those deaf people who began learning a sign language at age 5 were significantly less fluent than native deaf signers (whose exposure to a sign language began at birth). Early language exposure also affects the ability to learn a second language later in life: profoundly deaf individuals with early language exposure achieve comparable levels of proficiency in a second language to hearing individuals with early language exposure. In contrast, deaf individuals without early language exposure perform far worse.[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.[52]

Steven Pinker discusses the CPH in his book, The Language Instinct. According to Pinker, language must be viewed as a concept rather than a specific language because the sounds, grammar, meaning, vocabulary, and social norms play an important role in the acquisition of language.[56] Physiological changes in the brain are also conceivable causes for the terminus of the critical period for language acquisition.[57] As language acquisition is crucial during this phase, similarly infant–parent attachment is crucial for social development of the infant. An infant learns to trust and feel safe with the parent, but there are cases in which the infant might be staying at an orphanage where it does not receive the same attachment with their caregiver. 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.[1]

The discussion of language critical period suffers from the lack of a commonly accepted definition of language. 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.[7][8] Other aspects of language, such as prefrontal synthesis, have strong critical periods and cannot be acquired after the end of the critical period.[6] Consequently, when language is discussed in general, without dissection into components, arguments can be constructed both in favor and against the strong critical period of L1 acquisition.

Second language acquisition

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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.[59] However, the nature of this phenomenon has been one of the most fiercely debated issues in psycholinguistics and cognitive science in general for decades.

Certainly, older learners of a second language rarely achieve the native-like fluency that younger learners display, despite often progressing faster than children in the initial stages. This is generally accepted as evidence supporting the CPH. Incorporating the idea, "younger equals better" by Penfield, David Singleton (1995) states that in learning a second language there are many exceptions, noting that five percent of adult bilinguals master a second language even though they begin learning it when they are well into adulthood—long after any critical period has presumably come to a close. The critical period hypothesis holds that first language acquisition must occur before cerebral lateralization completes, at about the age of puberty. One prediction of this hypothesis is that second language acquisition is relatively fast, successful, and qualitatively similar to first language only if it occurs before the age of puberty.[60] To grasp a better understanding of SLA, it is essential to consider linguistic, cognitive, and social factors rather than age alone, as they are all essential to the learner's language acquisition.[59]

Over the years, many experimenters have tried to find evidence in support of or against the critical periods for second language acquisition. Many have found evidence that young children acquire language more easily than adults, but there are also special cases of adults acquiring a second language with native-like proficiency. Thus it has been difficult for researchers to separate correlation from causation.[61]

In 1989, Jacqueline S. Johnson and Elissa L. Newport found support for the claim that second languages are more easily acquired before puberty, or more specifically before the age of seven.[62] They tested second language learners of English who arrived in the United States at various ages ranging from three to thirty-nine, and found that there was a decline in grammatical correctness after the age of seven. Johnson and Newport attributed this claim to a decline in language learning ability with age. Opponents of the critical period argue that the difference in language ability found by Johnson and Newport could be due to the different types of input that children and adults receive; children received reduced input while adults receive more complicated structures.

Additional evidence against a strict critical period is also found in the work of Pallier et al. (2003) who found that children adopted to France from Korea were able to become native-like in their performance of French even after the critical period for phonology.[63] Their experiment may represent a special case where subjects must lose their first language in order to more perfectly acquire their second.

There is also some debate as to how one can judge the native-like quality of the speech participants produce and what exactly it means to be a near-native speaker of a second language.[64] White et al. found that it is possible for non-native speakers of a language to become native-like in some aspects, but those aspects are influenced by their first language.

Recently, a connectionist model has been developed to explain the changes that take place in second language learning assuming that sensitive period affects lexical learning and syntactic learning parts of the system differently, which sheds further light on how first and second language acquisition changes over the course of learners development.[65]

Vision

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In mammals, neurons in the brain that process vision actually develop after birth based on signals from the eyes. A landmark experiment by David H. Hubel and Torsten Wiesel (1963) showed that cats that had one eye sewn shut from birth to three months of age (monocular deprivation) only fully developed vision in the open eye. They showed that columns in the primary visual cortex receiving inputs from the other eye took over the areas that would normally receive input from the deprived eye. 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. However, the layers of cortex that were deprived had less activity and fewer responses were isolated. The kittens had abnormally small ocular dominance columns (part of the brain that processes sight) connected to the closed eye, and abnormally large, wide columns connected to the open eye. Because the critical period time had elapsed, it would be impossible for the kittens to alter and develop vision in the closed eye. This did not happen to adult cats even when one eye was sewn shut for a year because they had fully developed their vision during their critical period. Later experiments in monkeys found similar results consistent with the strong critical period.[66]

In a follow-up experiment, Hubel and Wiesel (1963) explored the cortical responses present in kittens after binocular deprivation; they found it difficult to find any active cells in the cortex, and the responses they did get were either slow-moving or fast-fatiguing. Furthermore, the cells that did respond selected for edges and bars with distinct orientation preferences. Nevertheless, these kittens developed normal binocularity. Hubel and Wiesel first explained the mechanism, known as orientation selectivity, in the mammalian visual cortex. Orientation tuning, a model that originated with their model, is a concept in which receptive fields of neurons in the LGN excite a cortical simple cell and are arranged in rows. This model was important because it was able to describe a strong critical period for the proper development of normal ocular dominance columns in the lateral geniculate nucleus, and thus able to explain the effects of monocular deprivation during this critical period. The critical period for cats is about three months and for monkeys, about six months.[67]

In a similar experiment, Antonini and Stryker (1993) examined the anatomical changes that can be observed after monocular deprivation. They compared geniculocortical axonal arbors in monocularly deprived animals in the long term (4 weeks) to short term (6–7 days) during the critical period established by Hubel and Wiesel (1993). 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. Even in the short term, Antonini and Stryker (1993) found that geniculocortical neurons were similarly affected. This supports the aforementioned concept of a critical period for proper neural development for vision in the cortex.[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). Some hypothesize that being blind during childhood prevents some part of the visual system necessary for these higher-level tasks from developing properly.[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.[70]

Expression of the protein Lynx1 has been associated with the normal end of the critical period for synaptic plasticity in the visual system.[71]

Imprinting

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Konrad Lorenz

In psychology, imprinting is any type of rapid learning that occurs in a particular life stage. While this rapid learning is independent of the behavioral outcome, it also establishes it and can affect behavioral responses to different stimuli. Konrad Lorenz is well known for his classic studies of filial imprinting in graylag geese. From 1935 to 1938, he presented himself to a group of newly hatched gosling and took note of how he was instantly accepted, followed, and called to as if he were the one who laid them himself. As the first moving object they encountered, Lorenz studied the phenomenon in how quickly the geese were able to form such an irreversible bond. Through his work he demonstrated that this only developed during a brief "critical period", which was about a few hours after hatching, suggesting a strong critical period.[72]

Lorenz also discovered a long-lasting effect of his studies, and that was a shift in the species' sexual imprinting as a result from imprinting upon a foster mother of a second species. For certain species, when raised by a second one, they develop and retain imprinted preferences and approach the second species they were raised by rather than choose their own, if given a choice.[73]

Imprinting serves as the distinguishing factor between one's own mother and other mother figures. The mother and the infant both identify with each other, this is a strong bonding moment for humans. It provides a sort of model or guide to adult behaviors in addition to other factors such as nurture, protection in infancy, guidance, and nourishment. The imprinting process, Lorenz also found, brought about a sense of familiarity for the young animals. When such a strong bond is formed at such an early stage, it creates a sense of security and comfort for the subject and actually encourages the imprinting behavior.

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. If direct contact between mother and infant is not maintained during the critical imprinting period, then the mother goose may reject the infant because she is unfamiliar with her newborn's scent. If that does happen, then the infant's life would be in jeopardy unless it were claimed by a substitute mother, possibly leading to awkward social behavior in later life.[74] In relation to humans, a newborn during the critical period identifies with its mother's and other peoples' scents since its scent is one of the most developed senses at that stage in life. The newborn uses this pheromone identification to seek the people it identifies with, when in times of distress, hunger, and discomfort as a survival skill.[75] Inferences could be made for newborns based upon Lorenz's studies. When imprinting on their mothers, newborns look to them for nourishment, a sense of security, and comfort. Human newborns are among the most helpless known with orangutang newborns ranking second. Newborns of these species have a very limited array of innate survival abilities. Their most important and functional ability is to form bonds with close individuals who are able to keep them alive. Imprinting is a crucial factor of the critical period because it facilitates the newborn's abilities to form bonds with other individuals, from infancy to adulthood.

Auditory processing

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Many studies have supported a correlation between the type of auditory stimuli present in the early postnatal environment and the development on the topographical and structural development of the auditory system.[4]

First reports on critical periods came from deaf children and animals that received a cochlear implant to restore hearing. 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. The closure of sensitive periods likely involves a multitude of processes that in their combination make it difficult to reopen these behaviorally.[4] The understanding of the mechanisms behind critical periods has consequences for medical therapy of hearing loss.[78] M. Merzenich and colleagues showed that during an early critical period, noise exposure can affect the frequency organization of the auditory cortex.[79]

Recent studies have examined the possibility of a critical period for thalamocortical connectivity in the auditory system. For example, Zhou and Merzenich (2008) studied the effects of noise on development in the primary auditory cortex in rats. In their study, rats were exposed to pulsed noise during the critical period and the effect on cortical processing was measured. 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. In this experiment, mice were reared either in normal environments or in the presence of 7 kHz tones during early postnatal days. They found that mice that were exposed to an abnormal auditory environment during a critical period P11-P15 had an atypical tonotopic map in the primary auditory cortex.[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. Critical periods are important for the development of the brain for the function from a pattern of connectivity. In general, the early auditory environment influences the structural development and response specificity of the primary auditory cortex.[81]

Absolute pitch

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Main article: Absolute pitch

Absolute pitch manifests itself almost always before adolescence and rarely if ever among individuals who are first exposed to music after mid-childhood, suggesting that exposure to music or similar phenomena (e.g., tonal languages) in early to mid-childhood is a necessary condition for its development or refinement. Studies that ask musicians and non-musicians to sing or hum well-known popular songs that have definitive recordings (and hence are sung in standardized keys) show that—on average—participants sing within a semitone of the standardized key but that outside the small subset of participants with absolute pitch there is broad variation (the "bell curve" that reflects the degree of approximation to the standard key is broad and flat).[citation needed] These results suggest that almost all humans have some innate aptitude for absolute pitch recognition—though other factors may enhance or limit the level of that aptitude. 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.

Vestibular system

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In our vestibular system, neurons are undeveloped at neuronal birth and mature during the critical period of the first 2–3 postnatal weeks. Hence, disruption of maturation during this period can cause changes in normal balance and movement through space. Animals with abnormal vestibular development tend to have irregular motor skills.[82] Studies have consistently shown that animals with genetic vestibular deficiencies during this critical period have altered vestibular phenotypes, most likely as a result of insufficient input from the semicircular canals and dopaminergic abnormalities. Moreover, exposure to abnormal vestibular stimuli during the critical period is associated with irregular motor development. Children with hypofunctioning vestibular receptors frequently have delayed motor development. 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.[83]

The vestibulo-ocular reflex (VOR) is a reflex eye movement that stabilizes images on the retina during head movement. It produces an eye movement in the direction opposite to head movement, thus preserving the image on the center of the visual field. Studies in fish and amphibians revealed a sensitivity in their VOR. They launched into space flight for 9–10, some with developing VORs and others with already developed reflexes. The fish with developing reflexes developed an upward bend in their tails. The altered gravity resulted in a shift of orientation. Those who were already matured with the reflex were insensitive to the microgravity exposure.[84]

Memory

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Recent studies also support the possibility of a critical period for the development of neurons that mediate memory processing. Experimental evidence supports the notion that young neurons in the adult dentate gyrus have a critical period (about 1–3 weeks after neuronal birth) during which they are integral to memory formation.[85] Although the exact reasoning behind this observation is uncertain, studies suggest that the functional properties of neurons at this age make them most appropriate for this purpose; these neurons: (1) Remain hyperactive during the formation of memories; (2) are more excitable; and (3) More easily depolarizable due to GABAergic effects. It is also possible that hyperplasticity makes the neurons more useful in memory formation. If these young neurons had more plasticity than adult neurons in the same context, they could be more influential in smaller numbers.[85] The role of these neurons in the adult dentate gyrus in memory processing is further supported by the fact that behavioral experiments have shown that an intact dentate gyrus is integral to hippocampal memory formation.[85] It is speculated that the dentate gyrus acts as a relay station for information relating to memory storage. The likelihood of a critical period could change the way we view memory processing because it would ultimately mean that the collection of neurons present is constantly being replenished as new neurons replace old ones. If a critical period does indeed exist, this could possibly mean that: (1) Diverse populations of neurons that represent events occurring soon after one another may connect those events temporally in the memory formation and processing; or (2) these different populations of neurons may distinguish between similar events, independent of temporal position; or (3) separate populations may mediate the formation of new memories when the same events occur frequently.[85]

See also

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References

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  1. ^ a b Robson AL (2002). "Critical/Sensitive Periods". In Salkind NJ (ed.). Child Development. Gale Virtual Reference Library. New York: Macmillan Reference USA. pp. 101–3.
  2. ^ Brainard MS, Knudsen EI (May 1998). "Sensitive periods for visual calibration of the auditory space map in the barn owl optic tectum". The Journal of Neuroscience. 18 (10): 3929–42. doi:10.1523/JNEUROSCI.18-10-03929.1998. PMC 6793138. PMID 9570820.
  3. ^ Hensch TK (2004). "Critical period regulation". Annual Review of Neuroscience. 27: 549–79. doi:10.1146/annurev.neuro.27.070203.144327. PMID 15217343.
  4. ^ a b c Kral A (September 2013). "Auditory critical periods: a review from system's perspective". Neuroscience. 247: 117–33. doi:10.1016/j.neuroscience.2013.05.021. PMID 23707979.
  5. ^ Knudsen EI, Esterly SD, Knudsen PF (April 1984). "Monaural occlusion alters sound localization during a sensitive period in the barn owl". The Journal of Neuroscience. 4 (4): 1001–11. doi:10.1523/JNEUROSCI.04-04-01001.1984. PMC 6564776. PMID 6716127.
  6. ^ a b Vyshedskiy A, Mahapatra S, Dunn R (31 August 2017). "Linguistically deprived children: meta-analysis of published research underlines the importance of early syntactic language use for normal brain development". Research Ideas and Outcomes. 3: e20696. doi:10.3897/rio.3.e20696.
  7. ^ a b Tallal P, Miller SL, Bedi G, Byma G, Wang X, Nagarajan SS, Schreiner C, Jenkins WM, Merzenich MM (January 1996). "Language comprehension in language-learning impaired children improved with acoustically modified speech". Science. 271 (5245): 81–4. Bibcode:1996Sci...271...81T. doi:10.1126/science.271.5245.81. PMID 8539604. S2CID 2045591.
  8. ^ a b Kilgard MP, Merzenich MM (December 1998). "Plasticity of temporal information processing in the primary auditory cortex". Nature Neuroscience. 1 (8): 727–31. doi:10.1038/3729. PMC 2948964. PMID 10196590.
  9. ^ a b c d e Takesian AE, Hensch TK (2013). "Balancing plasticity/stability across brain development". Changing Brains – Applying Brain Plasticity to Advance and Recover Human Ability. Progress in Brain Research. Vol. 207. Elsevier. pp. 3–34. doi:10.1016/b978-0-444-63327-9.00001-1. ISBN 9780444633279. PMID 24309249.
  10. ^ a b Joliot A, Pernelle C, Deagostini-Bazin H, Prochiantz A (March 1991). "Antennapedia homeobox peptide regulates neural morphogenesis". Proceedings of the National Academy of Sciences of the United States of America. 88 (5): 1864–8. Bibcode:1991PNAS...88.1864J. doi:10.1073/pnas.88.5.1864. PMC 51126. PMID 1672046.
  11. ^ a b c d Hensch TK (November 2005). "Critical period plasticity in local cortical circuits". Nature Reviews. Neuroscience. 6 (11): 877–88. doi:10.1038/nrn1787. hdl:10533/174307. PMID 16261181. S2CID 5264124.
  12. ^ Kobayashi Y, Ye Z, Hensch TK (April 2015). "Clock genes control cortical critical period timing". Neuron. 86 (1): 264–75. doi:10.1016/j.neuron.2015.02.036. PMC 4392344. PMID 25801703.
  13. ^ Balmer TS, Carels VM, Frisch JL, Nick TA (October 2009). "Modulation of perineuronal nets and parvalbumin with developmental song learning". The Journal of Neuroscience. 29 (41): 12878–85. doi:10.1523/JNEUROSCI.2974-09.2009. PMC 2769505. PMID 19828802.
  14. ^ McRae PA, Rocco MM, Kelly G, Brumberg JC, Matthews RT (May 2007). "Sensory deprivation alters aggrecan and perineuronal net expression in the mouse barrel cortex". The Journal of Neuroscience. 27 (20): 5405–13. doi:10.1523/jneurosci.5425-06.2007. PMC 6672348. PMID 17507562.
  15. ^ Ye Q, Miao QL (August 2013). "Experience-dependent development of perineuronal nets and chondroitin sulfate proteoglycan receptors in mouse visual cortex". Matrix Biology. 32 (6): 352–63. doi:10.1016/j.matbio.2013.04.001. PMID 23597636.
  16. ^ a b Miller KD, Keller JB, Stryker MP (August 1989). "Ocular dominance column development: analysis and simulation". Science. 245 (4918): 605–15. Bibcode:1989Sci...245..605M. doi:10.1126/science.2762813. PMID 2762813.
  17. ^ Erwin E, Miller KD (December 1998). "Correlation-based development of ocularly matched orientation and ocular dominance maps: determination of required input activities". The Journal of Neuroscience. 18 (23): 9870–95. doi:10.1523/JNEUROSCI.18-23-09870.1998. PMC 6793311. PMID 9822745.
  18. ^ Hua JY, Smear MC, Baier H, Smith SJ (April 2005). "Regulation of axon growth in vivo by activity-based competition". Nature. 434 (7036): 1022–6. Bibcode:2005Natur.434.1022H. doi:10.1038/nature03409. PMID 15846347. S2CID 4429878.
  19. ^ a b Schafer, Dorothy P. (24 May 2012). "Microglia Sculpt Postnatal Neural Circuits in an Activity and Complement-Dependent Manner". Neuron. 74 (4): 691–705. doi:10.1016/j.neuron.2012.03.026. PMC 3528177. PMID 22632727.
  20. ^ a b Sipe, G.O.; et al. (28 October 2015). "Microglial P2Y12 Is Necessary for Synaptic Plasticity in Mouse Visual Cortex". Nature Communications. 7: 10905. Bibcode:2016NatCo...710905S. doi:10.1038/ncomms10905. PMC 4786684. PMID 26948129.
  21. ^ Sellgren, Carl M.; et al. (4 March 2019). "Increased Synapse Elimination by Microglia in Schizophrenia Patient-Derived Models of Synaptic Pruning". Nature Neuroscience. 22 (3): 374–385. doi:10.1038/s41593-018-0334-7. PMC 6410571. PMID 30718903.
  22. ^ Dunaevsky, Anna; et al. (7 September 1999). "Developmental Regulation of Spine Motility in the Mammalian Central Nervous System". Proceedings of the National Academy of Sciences. 96 (23): 13438–13443. Bibcode:1999PNAS...9613438D. doi:10.1073/pnas.96.23.13438. PMC 23966. PMID 10557339.
  23. ^ Konur, Sila; Yuste, Rafael (1 August 2003). "Developmental Regulation of Spine and Filopodial Motility in Primary Visual Cortex: Reduced Effects of Activity and Sensory Deprivation". Journal of Neurobiology. 59 (2): 236–246. doi:10.1002/neu.10306. PMID 15085540.
  24. ^ Majewska, Ania; Mriganka, Sur (27 May 2003). "Motility of Dendritic Spines in Visual Cortex in Vivo: Changes during the Critical Period and Effects of Visual Deprivation". Proceedings of the National Academy of Sciences. 100 (26): 16024–16029. Bibcode:2003PNAS..10016024M. doi:10.1073/pnas.2636949100. PMC 307686. PMID 14663137.
  25. ^ a b Ganguly K, Schinder AF, Wong ST, Poo M (May 2001). "GABA itself promotes the developmental switch of neuronal GABAergic responses from excitation to inhibition". Cell. 105 (4): 521–32. doi:10.1016/S0092-8674(01)00341-5. PMID 11371348. S2CID 8615968.
  26. ^ Fagiolini M, Hensch TK (March 2000). "Inhibitory threshold for critical-period activation in primary visual cortex". Nature. 404 (6774): 183–6. Bibcode:2000Natur.404..183F. doi:10.1038/35004582. PMID 10724170. S2CID 4331566.
  27. ^ Hensch TK, Fagiolini M, Mataga N, Stryker MP, Baekkeskov S, Kash SF (November 1998). "Local GABA circuit control of experience-dependent plasticity in developing visual cortex". Science. 282 (5393): 1504–8. doi:10.1126/science.282.5393.1504. PMC 2851625. PMID 9822384.
  28. ^ Hensch TK, Stryker MP (March 2004). "Columnar architecture sculpted by GABA circuits in developing cat visual cortex". Science. 303 (5664): 1678–81. Bibcode:2004Sci...303.1678H. doi:10.1126/science.1091031. PMC 2562723. PMID 15017001.
  29. ^ Sillito AM, Kemp JA, Patel H (1980-12-01). "Inhibitory interactions contributing to the ocular dominance of monocularly dominated cells in the normal cat striate cortex". Experimental Brain Research. 41 (1): 1–10. doi:10.1007/BF00236673. PMID 7461064. S2CID 24537788.
  30. ^ a b Kwok JC, Carulli D, Fawcett JW (September 2010). "In vitro modeling of perineuronal nets: hyaluronan synthase and link protein are necessary for their formation and integrity". Journal of Neurochemistry. 114 (5): 1447–59. doi:10.1111/j.1471-4159.2010.06878.x. PMID 20584105.
  31. ^ a b Pizzorusso T, Medini P, Berardi N, Chierzi S, Fawcett JW, Maffei L (November 2002). "Reactivation of ocular dominance plasticity in the adult visual cortex". Science. 298 (5596): 1248–51. Bibcode:2002Sci...298.1248P. doi:10.1126/science.1072699. PMID 12424383. S2CID 14254863.
  32. ^ Pizzorusso T, Medini P, Landi S, Baldini S, Berardi N, Maffei L (May 2006). "Structural and functional recovery from early monocular deprivation in adult rats". Proceedings of the National Academy of Sciences of the United States of America. 103 (22): 8517–22. Bibcode:2006PNAS..103.8517P. doi:10.1073/pnas.0602657103. PMC 1482523. PMID 16709670.
  33. ^ a b Härtig W, Derouiche A, Welt K, Brauer K, Grosche J, Mäder M, Reichenbach A, Brückner G (September 1999). "Cortical neurons immunoreactive for the potassium channel Kv3.1b subunit are predominantly surrounded by perineuronal nets presumed as a buffering system for cations". Brain Research. 842 (1): 15–29. doi:10.1016/S0006-8993(99)01784-9. PMID 10526091. S2CID 19980614.
  34. ^ Vo T, Carulli D, Ehlert EM, Kwok JC, Dick G, Mecollari V, Moloney EB, Neufeld G, de Winter F, Fawcett JW, Verhaagen J (September 2013). "The chemorepulsive axon guidance protein semaphorin3A is a constituent of perineuronal nets in the adult rodent brain". Molecular and Cellular Neurosciences. 56: 186–200. doi:10.1016/j.mcn.2013.04.009. PMID 23665579. S2CID 21526309.
  35. ^ Hartline DK, Colman DR (January 2007). "Rapid conduction and the evolution of giant axons and myelinated fibers". Current Biology. 17 (1): R29-35. Bibcode:2007CBio...17R..29H. doi:10.1016/j.cub.2006.11.042. PMID 17208176. S2CID 10033356.
  36. ^ a b c Holmes GL, Milh MD, Dulac O (2012). "Maturation of the human brain and epilepsy". Epilepsy. Handbook of Clinical Neurology. Vol. 107. Elsevier. pp. 135–43. doi:10.1016/b978-0-444-52898-8.00007-0. ISBN 9780444528988. PMID 22938967.
  37. ^ a b c d McGee AW, Yang Y, Fischer QS, Daw NW, Strittmatter SM (September 2005). "Experience-driven plasticity of visual cortex limited by myelin and Nogo receptor". Science. 309 (5744): 2222–6. Bibcode:2005Sci...309.2222M. doi:10.1126/science.1114362. PMC 2856689. PMID 16195464.
  38. ^ a b c Yiu G, He Z (August 2006). "Glial inhibition of CNS axon regeneration". Nature Reviews. Neuroscience. 7 (8): 617–27. doi:10.1038/nrn1956. PMC 2693386. PMID 16858390.
  39. ^ a b c Makinodan M, Rosen KM, Ito S, Corfas G (September 2012). "A critical period for social experience-dependent oligodendrocyte maturation and myelination". Science. 337 (6100): 1357–60. Bibcode:2012Sci...337.1357M. doi:10.1126/science.1220845. PMC 4165613. PMID 22984073.
  40. ^ Sánchez MM, Hearn EF, Do D, Rilling JK, Herndon JG (November 1998). "Differential rearing affects corpus callosum size and cognitive function of rhesus monkeys". Brain Research. 812 (1–2): 38–49. doi:10.1016/s0006-8993(98)00857-9. PMID 9813233. S2CID 23976772.
  41. ^ Hensch TK (January 2014). "Bistable parvalbumin circuits pivotal for brain plasticity". Cell. 156 (1–2): 17–9. doi:10.1016/j.cell.2013.12.034. PMC 4183967. PMID 24439367.
  42. ^ Frémaux N, Gerstner W (2015). "Neuromodulated Spike-Timing-Dependent Plasticity, and Theory of Three-Factor Learning Rules". Frontiers in Neural Circuits. 9: 85. doi:10.3389/fncir.2015.00085. PMC 4717313. PMID 26834568.
  43. ^ a b c d e Kilgard MP, Merzenich MM (March 1998). "Cortical map reorganization enabled by nucleus basalis activity". Science. 279 (5357): 1714–8. Bibcode:1998Sci...279.1714K. doi:10.1126/science.279.5357.1714. PMID 9497289.
  44. ^ a b c d e Bao S, Chan VT, Merzenich MM (July 2001). "Cortical remodelling induced by activity of ventral tegmental dopamine neurons". Nature. 412 (6842): 79–83. Bibcode:2001Natur.412...79B. doi:10.1038/35083586. PMID 11452310. S2CID 4353142.
  45. ^ a b c d e f g h Yaeger CE, Ringach DL, Trachtenberg JT (March 2019). "Neuromodulatory control of localized dendritic spiking in critical period cortex". Nature. 567 (7746): 100–104. Bibcode:2019Natur.567..100Y. doi:10.1038/s41586-019-0963-3. PMC 6405296. PMID 30787434.
  46. ^ a b Avery MC, Krichmar JL (2017-12-22). "Neuromodulatory Systems and Their Interactions: A Review of Models, Theories, and Experiments". Frontiers in Neural Circuits. 11: 108. doi:10.3389/fncir.2017.00108. PMC 5744617. PMID 29311844.
  47. ^ a b Levelt CN, Hübener M (2012-07-21). "Critical-period plasticity in the visual cortex". Annual Review of Neuroscience. 35 (1): 309–30. doi:10.1146/annurev-neuro-061010-113813. PMID 22462544.[permanent dead link‍]
  48. ^ a b Bear MF, Singer W (March 1986). "Modulation of visual cortical plasticity by acetylcholine and noradrenaline". Nature. 320 (6058): 172–6. Bibcode:1986Natur.320..172B. doi:10.1038/320172a0. PMID 3005879. S2CID 29697125.
  49. ^ a b c d e f g Takesian AE, Bogart LJ, Lichtman JW, Hensch TK (February 2018). "Inhibitory circuit gating of auditory critical-period plasticity". Nature Neuroscience. 21 (2): 218–227. doi:10.1038/s41593-017-0064-2. PMC 5978727. PMID 29358666.
  50. ^ Weikum WM, Oberlander TF, Hensch TK, Werker JF (October 2012). "Prenatal exposure to antidepressants and depressed maternal mood alter trajectory of infant speech perception". Proceedings of the National Academy of Sciences of the United States of America. 109 Suppl 2 (Supplement_2): 17221–7. Bibcode:2012PNAS..10917221W. doi:10.1073/pnas.1121263109. PMC 3477387. PMID 23045665.
  51. ^ a b c Pi HJ, Hangya B, Kvitsiani D, Sanders JI, Huang ZJ, Kepecs A (November 2013). "Cortical interneurons that specialize in disinhibitory control". Nature. 503 (7477): 521–4. Bibcode:2013Natur.503..521P. doi:10.1038/nature12676. PMC 4017628. PMID 24097352.
  52. ^ a b c Siegler, Robert (2006). How Children Develop, Exploring Child Develop Student Media Tool Kit & Scientific American Reader to Accompany How Children Develop. New York: Worth Publishers. ISBN 0-7167-6113-0.
  53. ^ Curtiss S (1977). Genie: a psycholinguistic study of a modern-day wild child. New York: Academic Press.
  54. ^ Newport EL (1990). "Maturational constraints on language learning". Cognitive Science. 14 (1): 11–28. doi:10.1207/s15516709cog1401_2. S2CID 207056257.
  55. ^ Mayberry RI, Lock E, Kazmi H (May 2002). "Linguistic ability and early language exposure". Nature. 417 (6884): 38. Bibcode:2002Natur.417...38M. doi:10.1038/417038a. PMID 11986658. S2CID 4313378.
  56. ^ Johnson, Eric. "First-Language Acquisition." Encyclopedia of Bilingual Education. Ed. Josué M. González. Vol. 1. Thousand Oaks, CA: SAGE Publications, 2008. 299–304. Gale Virtual Reference Library. Web. 22 Oct. 2014.
  57. ^ Pinker S (1994). The Language Instinct. New York: Morrow.
  58. ^ DeKeyser RM (2000-12-01). "The Robustness of Critical Period Effects in Second Language Acquisition". Studies in Second Language Acquisition. 22 (4): 499–533. doi:10.1017/S0272263100004022. ISSN 1470-1545.
  59. ^ a b Jia, Li. "Learning a Language, Best Age." Encyclopedia of Bilingual Education. Ed. Josué M. González. Vol. 1. Thousand Oaks, CA: SAGE Publications, 2008. 520–523. Gale Virtual Reference Library. Web. 20 Oct. 2014.
  60. ^ Snow CE, Hoefnagel-Höhle M (December 1978). "The Critical Period for Language Acquisition: Evidence from Second-Language Learning". Child Development. 49 (4): 1114–1128. doi:10.1111/j.1467-8624.1978.tb04080.x. JSTOR 1128751.
  61. ^ Birdsong D (1999). Second Language Acquisition and the Critical Period Hypothesis. Routledge. ISBN 9781135674892.
  62. ^ Johnson JS, Newport EL (January 1989). "Critical period effects in second language learning: the influence of maturational state on the acquisition of English as a second language". Cognitive Psychology. 21 (1): 60–99. doi:10.1016/0010-0285(89)90003-0. PMID 2920538. S2CID 15842890.
  63. ^ Pallier C, Dehaene S, Poline JB, LeBihan D, Argenti AM, Dupoux E, Mehler J (February 2003). "Brain imaging of language plasticity in adopted adults: can a second language replace the first?" (PDF). Cerebral Cortex. 13 (2): 155–61. doi:10.1093/cercor/13.2.155. PMID 12507946.
  64. ^ White L, Genesee F (1996-01-01). "How native is near-native? The issue of ultimate attainment in adult second language acquisition". Second Language Research. 12 (3): 233–265. doi:10.1177/026765839601200301. JSTOR 43104516. S2CID 146433640.
  65. ^ Janciauskas M, Chang F (May 2018). "Input and Age-Dependent Variation in Second Language Learning: A Connectionist Account". Cognitive Science. 42 Suppl 2 (Suppl Suppl 2): 519–554. doi:10.1111/cogs.12519. PMC 6001481. PMID 28744901.
  66. ^ Wiesel TN, Hubel DH (November 1963). "Effects of visual deprivation on morphology and physiology of cell in the cat's lateral geniculate body". Journal of Neurophysiology. 26 (6): 978–93. doi:10.1152/jn.1963.26.6.978. PMID 14084170. S2CID 16117515.
  67. ^ Experiment Module: Effects of Visual Deprivation During the Critical Period for Development of Vision. McGill University, The Brain from Top to Bottom
  68. ^ Antonini A, Stryker MP (June 1993). "Rapid remodeling of axonal arbors in the visual cortex". Science. 260 (5115): 1819–21. Bibcode:1993Sci...260.1819A. doi:10.1126/science.8511592. JSTOR 2881379. PMID 8511592.
  69. ^ Man with restored sight provides new insight into how vision develops
  70. ^ Out Of Darkness, Sight: Rare Cases Of Restored Vision Reveal How The Brain Learns To See
  71. ^ Higley MJ, Strittmatter SM (November 2010). "Neuroscience. Lynx for braking plasticity". Science. 330 (6008): 1189–90. Bibcode:2010Sci...330.1189H. doi:10.1126/science.1198983. PMC 3244692. PMID 21109660.
  72. ^ Kisilevsky BS, Hains SM, Lee K, Xie X, Huang H, Ye HH, Zhang K, Wang Z (May 2003). "Effects of experience on fetal voice recognition". Psychological Science. 14 (3): 220–4. doi:10.1111/1467-9280.02435. PMID 12741744. S2CID 11219888.
  73. ^ Mertz LA. "Imprinting and Establishment of Ethology". Gale Virtual Reference Library. Neil Schlager and Josh Lauer. Retrieved 20 October 2014.
  74. ^ Hollar DW. "Imprinting". Salem Health: Psychology & Mental Health. 3: 980–984.
  75. ^ Stone SM. "Imprinting". Gale Virtual Reference Library. SAGE Reference. Retrieved 20 October 2014.
  76. ^ Sharma A, Dorman MF, Spahr AJ (2002). "A sensitive period for the development of the central auditory system in children with cochlear implants: implications for age of implantation". Ear Hear. 23 (6): 532–29. doi:10.1097/00003446-200212000-00004. PMID 12476090. S2CID 14004538.
  77. ^ Kral A, Hartmann R, Tillein J, Heid S, Klinke R (August 2002). "Hearing after congenital deafness: central auditory plasticity and sensory deprivation". Cerebral Cortex. 12 (8): 797–807. doi:10.1093/cercor/12.8.797. PMID 12122028.
  78. ^ Kral A, Sharma A (February 2012). "Developmental neuroplasticity after cochlear implantation". Trends in Neurosciences. 35 (2): 111–22. doi:10.1016/j.tins.2011.09.004. PMC 3561718. PMID 22104561.
  79. ^ Nakahara H, Zhang LI, Merzenich MM (May 2004). "Specialization of primary auditory cortex processing by sound exposure in the "critical period"". Proceedings of the National Academy of Sciences of the United States of America. 101 (18): 7170–4. Bibcode:2004PNAS..101.7170N. doi:10.1073/pnas.0401196101. PMC 406484. PMID 15118079.
  80. ^ Barkat TR, Polley DB, Hensch TK (July 2011). "A critical period for auditory thalamocortical connectivity". Nature Neuroscience. 14 (9): 1189–94. doi:10.1038/nn.2882. PMC 3419581. PMID 21804538.
  81. ^ Zhou X, Merzenich MM (March 2008). "Enduring effects of early structured noise exposure on temporal modulation in the primary auditory cortex". Proceedings of the National Academy of Sciences of the United States of America. 105 (11): 4423–8. Bibcode:2008PNAS..105.4423Z. doi:10.1073/pnas.0800009105. PMC 2393777. PMID 18332439.
  82. ^ Eugène D, Deforges S, Vibert N, Vidal PP (May 2009). "Vestibular critical period, maturation of central vestibular neurons, and locomotor control". Annals of the New York Academy of Sciences. 1164 (1): 180–7. Bibcode:2009NYASA1164..180E. doi:10.1111/j.1749-6632.2008.03727.x. PMID 19645897. S2CID 24833800.
  83. ^ Van Cleave S, Shall MS (2006). "A critical period for the impact of vestibular sensation on ferret motor development". Journal of Vestibular Research. 16 (4–5): 179–86. PMC 2034323. PMID 17538206.
  84. ^ Horn ER (May 2004). ""Critical periods" in vestibular development or adaptation of gravity sensory systems to altered gravitational conditions?". Archives Italiennes de Biologie. 142 (3): 155–74. PMID 15260375.
  85. ^ a b c d Aasebø IE, Blankvoort S, Tashiro A (March 2011). "Critical maturational period of new neurons in adult dentate gyrus for their involvement in memory formation". The European Journal of Neuroscience. 33 (6): 1094–100. doi:10.1111/j.1460-9568.2011.07608.x. PMID 21395853. S2CID 37671329.
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