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孕早期吃什么水果

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For environmental enrichment for captive animals, see behavioral enrichment.
A rodent is not stimulated by the environment in a wire cage, and this affects its brain negatively, particularly the complexity of its synaptic connections
百度 预计未来，浙江西湖高等研究院将拥有200名教授，近2000名科研人员。

Environmental enrichment is the stimulation of the brain by its physical and social surroundings. Brains in richer, more stimulating environments have higher rates of synaptogenesis and more complex dendrite arbors, leading to increased brain activity. This effect takes place primarily during neurodevelopment, but also during adulthood to a lesser degree. With extra synapses there is also increased synapse activity, leading to an increased size and number of glial energy-support cells. Environmental enrichment also enhances capillary vasculation, providing the neurons and glial cells with extra energy. The neuropil (neurons, glial cells, capillaries, combined) expands, thickening the cortex. Research on rodent brains suggests that environmental enrichment may also lead to an increased rate of neurogenesis.

Research on animals finds that environmental enrichment could aid the treatment and recovery of numerous brain-related dysfunctions, including Alzheimer's disease and those connected to aging, whereas a lack of stimulation might impair cognitive development. Moreover, this research also suggests that environmental enrichment leads to a greater level of cognitive reserve, the brain's resilience to the effects of conditions such as aging and dementia.

Research on humans suggests that lack of stimulation delays and impairs cognitive development. Research also finds that attaining and engaging in higher levels of education, environments in which people participate in more challenging cognitively stimulating activities, results in greater cognitive reserve.

Early research

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Donald O. Hebb in 1947 found that rats raised as pets performed better on problem solving tests than rats raised in cages.[1] His research, however, did not investigate the brain nor use standardized impoverished and enriched environments. Research doing this first was started in 1960 at the University of California, Berkeley by Mark Rosenzweig, who compared single rats in normal cages, and those placed in ones with toys, ladders, tunnels, running wheels in groups. This found that growing up in enriched environments affected enzyme cholinesterase activity.[2] This work led in 1962 to the discovery that environmental enrichment increased cerebral cortex volume.[3] In 1964, it was found that this was due to increased cerebral cortex thickness and greater synapse and glial numbers.[4][5]

Also starting around 1960, Harry Harlow studied the effects of maternal and social deprivation on rhesus monkey infants (a form of environmental stimulus deprivation). This established the importance of social stimulation for normal cognitive and emotional development.[6]

Synapses

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Synaptogenesis

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Rats raised with environmental enrichment have thicker cerebral cortices (3.3–7%) that contain 25% more synapses.[5][7] This effect of environmental richness upon the brain occurs whether it is experienced immediately following birth,[8] after weaning,[5][7][9] or during maturity.[10] When synapse numbers increase in adults, they can remain high in number even when the adults are returned to impoverished environment for 30 days[10] suggesting that such increases in synapse numbers are not necessarily temporary. However, the increase in synapse numbers has been observed generally to reduce with maturation.[11][12] Stimulation affects not only synapses upon pyramidal neurons (the main projecting neurons in the cerebral cortex) but also stellate ones (that are usually interneurons).[13] It can also affect neurons outside the brain, such as those in the retina.[14]

Dendrite complexity

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Environmental enrichment affects the complexity and length of the dendrite arbors (upon which synapses form). Higher-order dendrite branch complexity is increased in enriched environments,[13][15] as can the length, in young animals, of distal branches.[16] Environmental enrichment rescues harmful effects of stress on dendritic complexity.[17]

Activity and energy consumption

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Animals in enriched environments show evidence of increased synapse activation.[18] Synapses tend to also be much larger.[19] Gamma oscillations become larger in amplitude in the hippocampus.[20] This increased energy consumption is reflected in glial and local capillary vasculation that provides synapses with extra energy.

  • Glial cell numbers per neuron increase 12–14%[5][7]
  • The direct apposition area of glial cells with synapses expands by 19%[21]
  • The volume of glial cell nuclei for each synapse is higher by 37.5%[18]
  • The mean volume of mitochondria per neuron is 20% greater[18]
  • The volume of glial cell nuclei for each neuron is 63% higher[18]
  • Capillary density is increased.[22]
  • Capillaries are wider (4.35 μm compared to 4.15 μm in controls)[18]
  • Shorter distance exist between any part of the neuropil and a capillary (27.6 μm compared to 34.6 μm)[18]

These energy related changes to the neuropil are responsible for increasing the volume of the cerebral cortex (the increase in synapse numbers contributes in itself hardly any extra volume).

Motor learning stimulation

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Part of the effect of environmental enrichment is providing opportunities to acquire motor skills. Research on rats learning an “acrobatic” skill shows that such learning activity leads to increased synapse count.[23][24]

Maternal transmission

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Environmental enrichment during pregnancy has effects upon the fetus, such as accelerating his or her retinal development.[25]

Neurogenesis

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Environmental enrichment can also lead to the formation of neurons (at least in rats)[26] and reverse both the loss of neurons in the hippocampus and memory impairment from chronic stress.[27] However, its relevance has been questioned for the behavioral effects of enriched environments.[28]

Mechanisms

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Enriched environments affect the expression of genes that determine neuronal structure in the cerebral cortex and hippocampus.[29] At the molecular level, this occurs through increased concentrations of the neurotrophins NGF, NT-3,[30][31] and changes in BDNF.[14][32] This alters the activation of cholinergic neurons,[31] 5-HT,[33] and beta-adrenolin.[34] Another effect is to increase proteins such as synaptophysin and PSD-95 in synapses.[35] Changes in Wnt signaling have also been found to mimic in adult mice the effects of environmental enrichment upon synapses in the hippocampus.[36] Increase in neurons numbers could be linked to changes in VEGF.[37]

Rehabilitation and resilience

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Research in animals suggests that environmental enrichment aids recovery from certain neurological disorders and cognitive impairments. There are two mains areas of focus: neurological rehabilitation and cognitive reserve, the brain's resistance to the effects of exposure to physical, natural, and social threats. Although most of these experiments used animal subjects, mainly rodents, researchers have pointed to the affected areas of animal brains to which human brains are most similar and used their findings as evidence to show that humans would have comparable reactions to enriched environments. The tests done on animals are thus meant to represent human simulations for the following list of conditions.

Neurological rehabilitation

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Autism

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A study conducted in 2011 led to the conclusion that environmental enrichment vastly improves the cognitive ability of children with autism. The study found that autistic children who receive olfactory and tactile stimulation along with exercises that stimulated other paired sensory modalities clinically improved by 42 percent while autistic children not receiving this treatment clinically improved by just 7 percent.[38] The same study also showed that there was significant clinical improvement in autistic children exposed to enriched sensorimotor environments, and a vast majority of parents reported that their child's quality of life was much better with the treatment.[38] A second study confirmed its effectiveness. The second study also found after 6 months of sensory enrichment therapy, 21% of the children who initially had been given an autism classification, using the Autism Diagnostic Observation Schedule, improved to the point that, although they remained on the autism spectrum, they no longer met the criteria for classic autism. None of the standard care controls reached an equivalent level of improvement.[39] The therapy using the methodologies is titled Sensory Enrichment Therapy.[40][41]

Alzheimer's disease

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Through environmental enrichment, researchers were able to enhance and partially repair memory deficits in mice between ages of 2 to 7 months with characteristics of Alzheimer's disease. Mice in enriched environments performed significantly better on object recognition tests and the Morris Water Maze than they had when they were in standard environments. It was thus concluded that environmental enrichment enhances visual and learning memory for those with Alzheimer's.[42] Furthermore, it has been found that mouse models of Alzheimer's disease that were exposed to enriched environment before amyloid onset (at 3 months of age) and then returned to their home cage for over 7 months, showed preserved spatial memory and reduced amyloid deposition at 13 months old, when they are supposed to show dramatic memory deficits and amyloid plaque load. These findings reveal the preventive, and long-lasting effects of early life stimulating experience on Alzheimer-like pathology in mice and likely reflect the capacity of enriched environment to efficiently stimulate the cognitive reserve.[43] A human study suggests that enriched gardens contribute to better cognitive function and independence in activities of daily living, compared to conventional sensory gardens.[44]

Huntington's disease

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Research has indicated that environmental enrichment can help relieve motor and psychiatric deficits caused by Huntington's disease. It also improves lost protein levels for those with the disease, and prevents striatal and hippocampal deficits in the BDNF, located in the hippocampus.[45] These findings have led researchers to suggest that environmental enrichment has a potential to be a possible form of therapy for those with Huntington's.[45]

Parkinson's disease

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Multiple studies have reported that environmental enrichment for adult mice helps relieve neuronal death, which is particularly beneficial to those with Parkinson's disease.[46] A more recent study shows that environmental enrichment particularly affects the nigrostriatal pathway, which is important for managing dopamine and acetylcholine levels, critical for motor deficits.[47] Moreover, it was found that environmental enrichment has beneficial effects for the social implications of Parkinson's disease.[47]

Stroke

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Research done in animals has shown that subjects recovering in an enriched environment 15 days after having a stroke had significantly improved neurobehavioral function. In addition these same subjects showed greater capability of learning and larger infarct post-intervention than those who were not in an enriched environment. It was thus concluded that environmental enrichment had a considerable beneficial effect on the learning and sensorimotor functions on animals post-stroke.[48] A 2013 study also found that environmental enrichment socially benefits patients recovering from stroke. Researchers in that study concluded that stroke patients in enriched environments in assisted-care facilities are much more likely to be engaging with other patients during normal social hours instead of being alone or sleeping.[49]

Rett syndrome

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A 2008 study found that environmental enrichment was significant in aiding recovery of motor coordination and some recovery of BDNF levels in female mice with conditions similar to those of Rett syndrome. Over the course of 30 weeks female mice in enriched environments showed superior ability in motor coordination to those in standard conditions.[50] Although they were unable to have full motor capability, they were able to prevent a more severe motor deficit by living in an enriched environment. These results combined with increased levels of BDNF in the cerebellum led researchers to conclude that an enriched environment that stimulates areas of the motor cortex and areas of the cerebellum having to do with motor learning is beneficial in aiding mice with Rett syndrome.[50]

Amblyopia

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A recent study found that adult rats with amblyopia improved visual acuity two weeks after being placed into an enriched environment.[51] The same study showed that another two weeks after ending environmental enrichment, the rats retained their visual acuity improvement. Conversely, rats in a standard environment showed no improvement in visual acuity. It was thus concluded that environmental enrichment reduces GABA inhibition and increases BDNF expression in the visual cortex. As a result, the growth and development of neurons and synapses in the visual cortex were much improved due to the enriched environment.[51]

Sensory deprivation

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Studies have shown that with the help of environmental enrichment the effects of sensory deprivation can be corrected. For example, a visual impairment known as "dark-rearing" in the visual cortex can be prevented and rehabilitated. In general, an enriched environment will improve, if not repair, the sensory systems animals possess.[52]

Lead poisoning

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During development, gestation is one of the most critical periods for exposure to any lead. Exposure to high levels of lead at this time can lead to inferior spatial learning performance. Studies have shown that environmental enrichment can overturn damage to the hippocampus induced by lead exposure.[53] Learning and spatial memory that are dependent on the long-term potentiation of the hippocampus are vastly improve as subjects in an enriched environments had lower levels of lead concentration in their hippocampi. The findings also showed that enriched environments result in some natural protection of lead-induced brain deficits.[53]

Chronic spinal cord injuries

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Research has indicated that animals suffering from spinal cord injuries showed significant improvement in motor capabilities even with a long delay in treatment after the injury when exposed to environmental enrichment.[54] Social interactions, exercise, and novelty all play major roles in aiding the recovery of an injured subject. This has led to some suggestions that the spinal cord has a continued plasticity and all efforts must be made for enriched environments to stimulate this plasticity in order to aid recovery.[54]

Maternal deprivation stress

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Maternal deprivation can be caused by the abandonment by a nurturing parent at a young age. In rodents or nonhuman primates, this leads to a higher vulnerability for stress-related illness.[55] Research suggests that environmental enrichment can reverse the effects of maternal separation on stress reactivity, possibly by affecting the hippocampus, the amygdala and the prefrontal cortex.[55][17]

Child neglect

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In all children, maternal care is one of the significant influences for hippocampal development, providing the foundation for stable and individualized learning and memory. However, this is not the case for those who have experienced child neglect. Researchers determined that through environmental enrichment, a neglected child can partially receive the same hippocampal development and stability, albeit not at the same level as that of the presence of a parent or guardian.[56] The results were comparable to those of child intervention programs, rendering environmental enrichment a useful method for dealing with child neglect.[56][failed verification]

Cognitive reserve

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Aging

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Decreased hippocampal neurogenesis is a characteristic of aging. Environmental enrichment increases neurogenesis in aged rodents by potentiating neuronal differentiation and new cell survival.[57] As a result, subjects exposed to environmental enrichment aged better due to superior ability in retaining their levels of spatial and learning memory.[57]

Prenatal and perinatal cocaine exposure

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Research has shown that mice exposed to environmental enrichment are less affected by the consequences of cocaine exposure in comparison with those in standard environments. Although the levels of dopamine in the brains of both sets of mice were relatively similar, when both subjects were exposed to the cocaine injection, mice in enriched environment were significantly less responsive than those in standard environments.[58] It was thus concluded that both the activating and rewarding effects are suppressed by environmental enrichment and early exposure to environmental enrichment can help prevent drug addiction.[58]

Humans

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Though environmental enrichment research has been mostly done upon rodents, similar effects occur in primates,[59] and are likely to affect the human brain. However, direct research upon human synapses and their numbers is limited since this requires histological study of the brain. A link, however, has been found between educational level and greater dendritic branch complexity following autopsy removal of the brain.[60]

Localized cerebral cortex changes

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MRI detects localized cerebral cortex expansion after people learn complex tasks such as mirror reading (in this case in the right occipital cortex),[61] three-ball juggling (bilateral mid-temporal area and left posterior intraparietal sulcus),[62] and when medical students intensively revise for exams (bilaterally in the posterior and lateral parietal cortex).[63] Such changes in gray matter volume can be expected to link to changes in synapse numbers due to the increased numbers of glial cells and the expanded capillary vascularization needed to support their increased energy consumption.

Institutional deprivation

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Children that receive impoverished stimulation due to being confined to cots without social interaction or reliable caretakers in low quality orphanages show severe delays in cognitive and social development.[64] 12% of them if adopted after 6 months of age show autistic or mildly autistic traits later at four years of age.[65] Some children in such impoverished orphanages at two and half years of age still fail to produce intelligible words, though a year of foster care enabled such children to catch up in their language in most respects.[66] Catch-up in other cognitive functioning also occurs after adoption, though problems continue in many children if this happens after the age of 6 months.[67]

Such children show marked differences in their brains, consistent with research upon experiment animals, compared to children from normally stimulating environments. They have reduced brain activity in the orbital prefrontal cortex, amygdala, hippocampus, temporal cortex, and brain stem.[68] They also showed less developed white matter connections between different areas in their cerebral cortices, particularly the uncinate fasciculus.[69]

Conversely, enriching the experience of preterm infants with massage quickens the maturation of their electroencephalographic activity and their visual acuity. Moreover, as with enrichment in experimental animals, this associates with an increase in IGF-1.[70]

Cognitive reserve and resilience

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Another source of evidence for the effect of environment stimulation upon the human brain is cognitive reserve (a measure of the brain's resilience to cognitive impairment) and the level of a person's education. Not only is higher education linked to a more cognitively demanding educational experience, but it also correlates with a person's general engagement in cognitively demanding activities.[71] The more education a person has received, the less the effects of aging,[72][73] dementia,[74] white matter hyperintensities,[75] MRI-defined brain infarcts,[76] Alzheimer's disease,[77][78] and traumatic brain injury.[79] Also, aging and dementia are less in those that engage in complex cognitive tasks.[80] The cognitive decline of those with epilepsy could also be affected by the level of a person's education.[81]

See also

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Notes

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  1. ^ Hebb DO (1947). "The effects of early experience on problem solving at maturity". American Psychologist. 2 (8): 306–7. doi:10.1037/h0063667.
  2. ^ Krech D, Rosenzweig MR, Bennett EL (December 1960). "Effects of environmental complexity and training on brain chemistry". J Comp Physiol Psychol. 53 (6): 509–19. doi:10.1037/h0045402. PMID 13754181.
  3. ^ Rosenzweig MR, Krech D, Bennett EL, Diamond MC (August 1962). "Effects of environmental complexity and training on brain chemistry and anatomy: a replication and extension". J Comp Physiol Psychol. 55 (4): 429–37. doi:10.1037/h0041137. PMID 14494091.
  4. ^ Altman J, Das GD (December 1964). "Autoradiographic Examination of the Effects of Enriched Environment on the Rate of Glial Multiplication in the Adult Rat Brain". Nature. 204 (4964): 1161–3. Bibcode:1964Natur.204.1161A. doi:10.1038/2041161a0. PMID 14264369. S2CID 29794121.
  5. ^ a b c d Diamond MC, Krech D, Rosenzweig MR (August 1964). "The Effects of an Enriched Environment on the Histology of the Rat Cerebral Cortex". J. Comp. Neurol. 123: 111–20. doi:10.1002/cne.901230110. PMID 14199261. S2CID 30997263.
  6. ^ Harlow HF, Rowland GL, Griffin GA (December 1964). "The Effect of Total Social Deprivation on the Development of Monkey Behavior". Psychiatr Res Rep Am Psychiatr Assoc. 19: 116–35. PMID 14232649.
  7. ^ a b c Diamond MC, Law F, Rhodes H, et al. (September 1966). "Increases in cortical depth and glia numbers in rats subjected to enriched environment". J. Comp. Neurol. 128 (1): 117–26. doi:10.1002/cne.901280110. PMID 4165855. S2CID 32351844.
  8. ^ Schapiro S, Vukovich KR (January 1970). "Early experience effects upon cortical dendrites: a proposed model for development". Science. 167 (3916): 292–4. Bibcode:1970Sci...167..292S. doi:10.1126/science.167.3916.292. PMID 4188192. S2CID 10057164.
  9. ^ Bennett EL, Diamond MC, Krech D, Rosenzweig MR (October 1964). "Chemical and Anatomical Plasticity Brain". Science. 146 (3644): 610–9. Bibcode:1964Sci...146..610B. doi:10.1126/science.146.3644.610. PMID 14191699.
  10. ^ a b Briones TL, Klintsova AY, Greenough WT (August 2004). "Stability of synaptic plasticity in the adult rat visual cortex induced by complex environment exposure". Brain Res. 1018 (1): 130–5. doi:10.1016/j.brainres.2004.06.001. PMID 15262214. S2CID 22709746.
  11. ^ Holtmaat AJ, Trachtenberg JT, Wilbrecht L, et al. (January 2005). "Transient and persistent dendritic spines in the neocortex in vivo". Neuron. 45 (2): 279–91. doi:10.1016/j.neuron.2005.01.003. PMID 15664179. S2CID 13320649.
  12. ^ Zuo Y, Lin A, Chang P, Gan WB (April 2005). "Development of long-term dendritic brain stability in diverse regions of cerebral cortex". Neuron. 46 (2): 181–9. doi:10.1016/j.neuron.2005.04.001. PMID 15848798. S2CID 16232150.
  13. ^ a b Greenough WT, Volkmar FR (August 1973). "Pattern of dendritic branching in occipital cortex of rats reared in complex environments". Exp. Neurol. 40 (2): 491–504. doi:10.1016/0014-4886(73)90090-3. PMID 4730268.
  14. ^ a b Landi S, Sale A, Berardi N, Viegi A, Maffei L, Cenni MC (January 2007). "Retinal functional development is sensitive to environmental enrichment: a role for BDNF". FASEB J. 21 (1): 130–9. doi:10.1096/fj.06-6083com. PMID 17135370. S2CID 8897589.
  15. ^ Volkmar FR, Greenough WT (June 1972). "Rearing complexity affects branching of dendrites in the visual cortex of the rat". Science. 176 (4042): 1445–7. Bibcode:1972Sci...176.1445V. doi:10.1126/science.176.4042.1445. PMID 5033647. S2CID 35027584.
  16. ^ Wallace CS, Kilman VL, Withers GS, Greenough WT (July 1992). "Increases in dendritic length in occipital cortex after 4 days of differential housing in weanling rats". Behav. Neural Biol. 58 (1): 64–8. doi:10.1016/0163-1047(92)90937-Y. PMID 1417672.
  17. ^ a b Koe, A; Ashokan, A; Mitra, R (2016). "Short environmental enrichment in adulthood reverses anxiety and basolateral amygdala hypertrophy induced by maternal separation". Transl Psychiatry. 6 (2): e729. doi:10.1038/tp.2015.217. PMC 4872421. PMID 26836417.
  18. ^ a b c d e f Sirevaag AM, Greenough WT (October 1987). "Differential rearing effects on rat visual cortex synapses. III. Neuronal and glial nuclei, boutons, dendrites, and capillaries". Brain Res. 424 (2): 320–32. doi:10.1016/0006-8993(87)91477-6. PMID 3676831. S2CID 20782513.
  19. ^ Sirevaag AM, Greenough WT (April 1985). "Differential rearing effects on rat visual cortex synapses. II. Synaptic morphometry". Brain Res. 351 (2): 215–26. doi:10.1016/0165-3806(85)90193-2. PMID 3995348.
  20. ^ Shinohara Y, Hosoya A, Hirase H (April 2013). "Experience enhances gamma oscillations and interhemispheric asymmetry in the hippocampus". Nat Commun. 4 (4): 1652. Bibcode:2013NatCo...4.1652S. doi:10.1038/ncomms2658. PMC 3644069. PMID 23552067.
  21. ^ Jones TA, Greenough WT (January 1996). "Ultrastructural evidence for increased contact between astrocytes and synapses in rats reared in a complex environment". Neurobiol Learn Mem. 65 (1): 48–56. doi:10.1006/nlme.1996.0005. PMID 8673406. S2CID 45890185.
  22. ^ Borowsky IW, Collins RC (October 1989). "Metabolic anatomy of brain: a comparison of regional capillary density, glucose metabolism, and enzyme activities". J. Comp. Neurol. 288 (3): 401–13. doi:10.1002/cne.902880304. PMID 2551935. S2CID 37188261.
  23. ^ Black JE, Isaacs KR, Anderson BJ, Alcantara AA, Greenough WT (July 1990). "Learning causes synaptogenesis, whereas motor activity causes angiogenesis, in cerebellar cortex of adult rats". Proc. Natl. Acad. Sci. U.S.A. 87 (14): 5568–72. Bibcode:1990PNAS...87.5568B. doi:10.1073/pnas.87.14.5568. PMC 54366. PMID 1695380.
  24. ^ Kleim JA, Hogg TM, VandenBerg PM, Cooper NR, Bruneau R, Remple M (January 2004). "Cortical synaptogenesis and motor map reorganization occur during late, but not early, phase of motor skill learning". J. Neurosci. 24 (3): 628–33. doi:10.1523/JNEUROSCI.3440-03.2004. PMC 6729261. PMID 14736848.
  25. ^ Sale A, Cenni MC, Ciucci F, Putignano E, Chierzi S, Maffei L (2007). Reh T (ed.). "Maternal Enrichment during Pregnancy Accelerates Retinal Development of the Fetus". PLOS ONE. 2 (11): e1160. Bibcode:2007PLoSO...2.1160S. doi:10.1371/journal.pone.0001160. PMC 2063464. PMID 18000533. Open access icon
  26. ^ Fan Y, Liu Z, Weinstein PR, Fike JR, Liu J (January 2007). "Environmental enrichment enhances neurogenesis and improves functional outcome after cranial irradiation". Eur. J. Neurosci. 25 (1): 38–46. doi:10.1111/j.1460-9568.2006.05269.x. PMID 17241265. S2CID 43259184.
  27. ^ Veena J, Srikumar BN, Mahati K, Bhagya V, Raju TR, Shankaranarayana Rao BS (March 2009). "Enriched environment restores hippocampal cell proliferation and ameliorates cognitive deficits in chronically stressed rats". J. Neurosci. Res. 87 (4): 831–43. doi:10.1002/jnr.21907. PMID 19006089. S2CID 21765537.
  28. ^ Meshi D, Drew MR, Saxe M, et al. (June 2006). "Hippocampal neurogenesis is not required for behavioral effects of environmental enrichment". Nat. Neurosci. 9 (6): 729–31. doi:10.1038/nn1696. PMID 16648847. S2CID 11043203.
  29. ^ Rampon C, Jiang CH, Dong H, et al. (November 2000). "Effects of environmental enrichment on gene expression in the brain". Proc. Natl. Acad. Sci. U.S.A. 97 (23): 12880–4. Bibcode:2000PNAS...9712880R. doi:10.1073/pnas.97.23.12880. PMC 18858. PMID 11070096.
  30. ^ Ickes BR, Pham TM, Sanders LA, Albeck DS, Mohammed AH, Granholm AC (July 2000). "Long-term environmental enrichment leads to regional increases in neurotrophin levels in rat brain". Exp. Neurol. 164 (1): 45–52. doi:10.1006/exnr.2000.7415. PMID 10877914. S2CID 24876134.
  31. ^ a b Torasdotter M, Metsis M, Henriksson BG, Winblad B, Mohammed AH (June 1998). "Environmental enrichment results in higher levels of nerve growth factor mRNA in the rat visual cortex and hippocampus". Behav. Brain Res. 93 (1–2): 83–90. doi:10.1016/S0166-4328(97)00142-3. PMID 9659990. S2CID 4022222.
  32. ^ Zhu SW, Codita A, Bogdanovic N, et al. (February 2009). "Influence of environmental manipulation on exploratory behaviour in male BDNF knockout mice". Behav. Brain Res. 197 (2): 339–46. doi:10.1016/j.bbr.2008.09.032. PMID 18951926. S2CID 46218238.
  33. ^ Rasmuson S, Olsson T, Henriksson BG, et al. (January 1998). "Environmental enrichment selectively increases 5-HT1A receptor mRNA expression and binding in the rat hippocampus". Brain Res. Mol. Brain Res. 53 (1–2): 285–90. doi:10.1016/S0169-328X(97)00317-3. PMID 9473697.
  34. ^ Escorihuela RM, Fernández-Teruel A, Tobe?a A, et al. (July 1995). "Early environmental stimulation produces long-lasting changes on beta-adrenoceptor transduction system". Neurobiol Learn Mem. 64 (1): 49–57. doi:10.1006/nlme.1995.1043. PMID 7582812. S2CID 26095038.
  35. ^ Nithianantharajah J, Levis H, Murphy M (May 2004). "Environmental enrichment results in cortical and subcortical changes in levels of synaptophysin and PSD-95 proteins". Neurobiol Learn Mem. 81 (3): 200–10. doi:10.1016/j.nlm.2004.02.002. PMID 15082021. S2CID 27246269.
  36. ^ Gogolla N, Galimberti I, Deguchi Y, Caroni P (May 2009). "Wnt signaling mediates experience-related regulation of synapse numbers and mossy fiber connectivities in the adult hippocampus". Neuron. 62 (4): 510–25. doi:10.1016/j.neuron.2009.04.022. PMID 19477153. S2CID 17085834.
  37. ^ During MJ, Cao L (February 2006). "VEGF, a mediator of the effect of experience on hippocampal neurogenesis". Curr Alzheimer Res. 3 (1): 29–33. doi:10.2174/156720506775697133. PMID 16472200. Archived from the original on 2025-08-06.
  38. ^ a b Woo CC, Leon M (March 2011). "Environmental Enrichment as an Effective Treatment for Autism: A Randomized Controlled Trial". Behav Neurosci. 127 (4): 487–97. doi:10.1037/a0033010. PMID 23688137.
  39. ^ Woo, Cynthia C.; Donnelly, Joseph H.; Steinberg-Epstein, Robin; Leon, Michael (Aug 2015). "Environmental enrichment as a therapy for autism: A clinical trial replication and extension". Behavioral Neuroscience. 129 (4): 412–422. doi:10.1037/bne0000068. PMC 4682896. PMID 26052790.
  40. ^ Mary Brophy Marcus (June 5, 2013). "'Sensory-Focused' Autism Therapy Shows Early Promise". webmd.com.
  41. ^ Nkoyo Iyamba (October 9, 2014). "Autism treatment gives Utah family hope". ksl.com. Archived from the original on September 25, 2015.
  42. ^ Berardi N, Braschi C, Capsoni S, Cattaneo A, Maffei L (June 2007). "Environmental enrichment delays the onset of memory deficits and reduces neuropathological hallmarks in a mouse model of Alzheimer-like neurodegeneration". J. Alzheimers Dis. 11 (3): 359–70. doi:10.3233/JAD-2007-11312. PMID 17851186. Archived from the original on 2025-08-06.
  43. ^ Verret L, Krezymon A, Halley H, Trouche S, Zerwas M, Lazouret M, Lassalle JM, Rampon C (Jan 2013). "Transient enriched housing before amyloidosis onset sustains cognitive improvement in Tg2576 mice". Neurobiology of Aging. 34 (1): 211–25. doi:10.1016/j.neurobiolaging.2012.05.013. PMID 22727275. S2CID 28453351.
  44. ^ Bourdon E, Belmin J (Jun 2021). "Enriched gardens improve cognition and independence of nursing home residents with dementia: a pilot controlled trial". Alzheimer's Research & Therapy. 13 (1): 116. doi:10.1186/s13195-021-00849-w. PMC 8207740. PMID 34134758. S2CID 235454186.
  45. ^ a b Spires TL, Grote HE, Varshney NK, et al. (March 2004). "Environmental enrichment rescues protein deficits in a mouse model of Huntington's disease, indicating a possible disease mechanism". J. Neurosci. 24 (9): 2270–6. doi:10.1523/JNEUROSCI.1658-03.2004. PMC 6730435. PMID 14999077.
  46. ^ Faherty CJ, Raviie Shepherd K, Herasimtschuk A, Smeyne RJ (March 2005). "Environmental enrichment in adulthood eliminates neuronal death in experimental Parkinsonism". Brain Res. Mol. Brain Res. 134 (1): 170–9. doi:10.1016/j.molbrainres.2004.08.008. PMID 15790541.
  47. ^ a b Goldberg, NR; Fields, V; Pflibsen, L; Salvatore, MF; Meshul, CK (March 2012). "Social enrichment attenuates nigrostriatal lesioning and reverses motor impairment in a progressive 1-methyl-2-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson's disease". Neurobiology of Disease. 45 (3): 1051–67. doi:10.1016/j.nbd.2011.12.024. PMID 22198503. S2CID 32701524.
  48. ^ Janssen H, Bernhardt J, Collier JM, Sena ES, McElduff P, Attia J, Pollack M, Howells DW, Nilsson M, Calford MB, Spratt NJ (12 September 2010). "An Enriched Environment Improves Sensorimotor Function Post-Ischemic Stroke" (PDF). Neurorehabilitation and Neural Repair. 24 (9): 802–813. doi:10.1177/1545968310372092. hdl:20.500.11820/302d9858-29ae-4a10-b684-e5f54bdb7ed9. PMID 20834046. S2CID 12755512.
  49. ^ Janssen, Heidi; Ada, Louise; Bernhardt, Julie; McElduff, Patrick; Pollack, Michael; Nilsson, Michael; Spratt, Neil J. (29 April 2013). "An enriched environment increases activity in stroke patients undergoing rehabilitation in a mixed rehabilitation unit: a pilot non-randomized controlled trial". Disability and Rehabilitation. 36 (3): 255–262. doi:10.3109/09638288.2013.788218. PMID 23627534. S2CID 40609997.
  50. ^ a b Kondo M, Gray LJ, Pelka GJ, Christodoulou J, Tam PP, Hannan AJ (June 2008). "Environmental enrichment ameliorates a motor coordination deficit in a mouse model of Rett syndrome--Mecp2 gene dosage effects and BDNF expression". Eur. J. Neurosci. 27 (12): 3342–50. doi:10.1111/j.1460-9568.2008.06305.x. PMID 18557922. S2CID 15401209.
  51. ^ a b Sale A, Maya Vetencourt JF, Medini P, et al. (June 2007). "Environmental enrichment in adulthood promotes amblyopia recovery through a reduction of intracortical inhibition". Nat. Neurosci. 10 (6): 679–81. doi:10.1038/nn1899. PMID 17468749. S2CID 37390442.
  52. ^ Argando?a EG, Bengoetxea H, Lafuente JV (2009). "Physical exercise is required for environmental enrichment to offset the quantitative effects of dark-rearing on the S-100β astrocytic density in the rat visual cortex". Journal of Anatomy. 215 (2): 132–140. doi:10.1111/j.1469-7580.2009.01103.x. PMC 2740960. PMID 19500177.
  53. ^ a b Cao, Xiujing; Huang, Shenghai; Ruan, Diyun (April 2008). "Enriched environment restores impaired hippocampal long-term potentiation and water maze performance induced by developmental lead exposure in rats". Developmental Psychobiology. 50 (3): 307–313. doi:10.1002/dev.20287. PMID 18335502.
  54. ^ a b Fischer FR, Peduzzi JD (2007). "Functional Recovery in Rats With Chronic Spinal Cord Injuries After Exposure to an Enriched Environment". J Spinal Cord Med. 30 (2): 147–55. doi:10.1080/10790268.2007.11753926. PMC 2031947. PMID 17591227.
  55. ^ a b Francis DD, Diorio J, Plotsky PM, Meaney MJ (September 2002). "Environmental enrichment reverses the effects of maternal separation on stress reactivity". J. Neurosci. 22 (18): 7840–3. doi:10.1523/JNEUROSCI.22-18-07840.2002. PMC 6758090. PMID 12223535.
  56. ^ a b Bredy TW, Humpartzoomian RA, Cain DP, Meaney MJ (2003). "Partial reversal of the effect of maternal care on cognitive function through environmental enrichment". Neuroscience. 118 (2): 571–6. doi:10.1016/S0306-4522(02)00918-1. PMID 12699791. S2CID 46611492.
  57. ^ a b Speisman, RB; Kumar, A; Rani, A; Pastoriza, JM; Severance, JE; Foster, TC; Ormerod, BK (January 2013). "Environmental enrichment restores neurogenesis and rapid acquisition in aged rats". Neurobiology of Aging. 34 (1): 263–74. doi:10.1016/j.neurobiolaging.2012.05.023. PMC 3480541. PMID 22795793.
  58. ^ a b Solinas M, Thiriet N, El Rawas R, Lardeux V, Jaber M (April 2009). "Environmental enrichment during early stages of life reduces the behavioral, neurochemical, and molecular effects of cocaine". Neuropsychopharmacology. 34 (5): 1102–11. doi:10.1038/npp.2008.51. PMID 18463628.
  59. ^ Kozorovitskiy Y, Gross CG, Kopil C, et al. (November 2005). "Experience induces structural and biochemical changes in the adult primate brain". Proc. Natl. Acad. Sci. U.S.A. 102 (48): 17478–82. Bibcode:2005PNAS..10217478K. doi:10.1073/pnas.0508817102. PMC 1297690. PMID 16299105.
  60. ^ Jacobs B, Schall M, Scheibel AB (January 1993). "A quantitative dendritic analysis of Wernicke's area in humans. II. Gender, hemispheric, and environmental factors". J. Comp. Neurol. 327 (1): 97–111. doi:10.1002/cne.903270108. PMID 8432910. S2CID 2084006.
  61. ^ Ilg R, Wohlschl?ger AM, Gaser C, et al. (April 2008). "Gray matter increase induced by practice correlates with task-specific activation: a combined functional and morphometric magnetic resonance imaging study". J. Neurosci. 28 (16): 4210–5. doi:10.1523/JNEUROSCI.5722-07.2008. PMC 6670304. PMID 18417700.
  62. ^ Draganski B, Gaser C, Busch V, Schuierer G, Bogdahn U, May A (January 2004). "Neuroplasticity: changes in grey matter induced by training". Nature. 427 (6972): 311–2. Bibcode:2004Natur.427..311D. doi:10.1038/427311a. PMID 14737157. S2CID 4421248.
  63. ^ Draganski B, Gaser C, Kempermann G, et al. (June 2006). "Temporal and spatial dynamics of brain structure changes during extensive learning". J. Neurosci. 26 (23): 6314–7. doi:10.1523/JNEUROSCI.4628-05.2006. PMC 6675198. PMID 16763039.
  64. ^ Kaler SR, Freeman BJ (May 1994). "Analysis of environmental deprivation: cognitive and social development in Romanian orphans". J Child Psychol Psychiatry. 35 (4): 769–81. doi:10.1111/j.1469-7610.1994.tb01220.x. PMID 7518826.
  65. ^ Rutter M, Andersen-Wood L, Beckett C, et al. (May 1999). "Quasi-autistic patterns following severe early global privation. English and Romanian Adoptees (ERA) Study Team". J Child Psychol Psychiatry. 40 (4): 537–49. doi:10.1017/S0021963099003935. PMID 10357161.
  66. ^ Windsor J, Glaze LE, Koga SF (October 2007). "Language acquisition with limited input: Romanian institution and foster care". J. Speech Lang. Hear. Res. 50 (5): 1365–81. doi:10.1044/1092-4388(2007/095). PMID 17905917.
  67. ^ Beckett C, Maughan B, Rutter M, et al. (2006). "Do the effects of early severe deprivation on cognition persist into early adolescence? Findings from the English and Romanian adoptees study". Child Dev. 77 (3): 696–711. doi:10.1111/j.1467-8624.2006.00898.x. PMID 16686796.
  68. ^ Chugani HT, Behen ME, Muzik O, Juhász C, Nagy F, Chugani DC (December 2001). "Local brain functional activity following early deprivation: a study of postinstitutionalized Romanian orphans". NeuroImage. 14 (6): 1290–301. doi:10.1006/nimg.2001.0917. PMID 11707085. S2CID 30892.
  69. ^ Eluvathingal TJ, Chugani HT, Behen ME, et al. (June 2006). "Abnormal brain connectivity in children after early severe socioemotional deprivation: a diffusion tensor imaging study". Pediatrics. 117 (6): 2093–100. doi:10.1542/peds.2005-1727. PMID 16740852. S2CID 30359252.
  70. ^ Guzzetta A, Baldini S, Bancale A, et al. (May 2009). "Massage accelerates brain development and the maturation of visual function". J. Neurosci. 29 (18): 6042–51. doi:10.1523/JNEUROSCI.5548-08.2009. PMC 6665233. PMID 19420271.
  71. ^ Wilson R, Barnes L, Bennett D (August 2003). "Assessment of lifetime participation in cognitively stimulating activities". J Clin Exp Neuropsychol. 25 (5): 634–42. doi:10.1076/jcen.25.5.634.14572. PMID 12815501. S2CID 11877167.
  72. ^ Corral M, Rodríguez M, Amenedo E, Sánchez JL, Díaz F (2006). "Cognitive reserve, age, and neuropsychological performance in healthy participants". Dev Neuropsychol. 29 (3): 479–91. doi:10.1207/s15326942dn2903_6. PMID 16671863. S2CID 27689165.
  73. ^ Fritsch T, McClendon MJ, Smyth KA, Lerner AJ, Friedland RP, Larsen JD (June 2007). "Cognitive functioning in healthy aging: the role of reserve and lifestyle factors early in life". Gerontologist. 47 (3): 307–22. doi:10.1093/geront/47.3.307. PMID 17565095.
  74. ^ Hall CB, Derby C, LeValley A, Katz MJ, Verghese J, Lipton RB (October 2007). "Education delays accelerated decline on a memory test in persons who develop dementia". Neurology. 69 (17): 1657–64. doi:10.1212/01.wnl.0000278163.82636.30. PMID 17954781. S2CID 33173284.
  75. ^ Nebes RD, Meltzer CC, Whyte EM, et al. (2006). "The relation of white matter hyperintensities to cognitive performance in the normal old: education matters". Neuropsychol Dev Cogn B Aging Neuropsychol Cogn. 13 (3–4): 326–40. doi:10.1080/138255890969294. PMID 16887777. S2CID 20341312.
  76. ^ Elkins JS, Longstreth WT, Manolio TA, Newman AB, Bhadelia RA, Johnston SC (August 2006). "Education and the cognitive decline associated with MRI-defined brain infarct". Neurology. 67 (3): 435–40. doi:10.1212/01.wnl.0000228246.89109.98. PMID 16894104. S2CID 44570701.
  77. ^ Koepsell TD, Kurland BF, Harel O, Johnson EA, Zhou XH, Kukull WA (May 2008). "Education, cognitive function, and severity of neuropathology in Alzheimer disease". Neurology. 70 (19 Pt 2): 1732–9. doi:10.1212/01.wnl.0000284603.85621.aa. PMID 18160675. S2CID 31439417.
  78. ^ Roe CM, Mintun MA, D'Angelo G, Xiong C, Grant EA, Morris JC (November 2008). "Alzheimer's and Cognitive Reserve: Education Effect Varies with 11CPIB Uptake". Arch. Neurol. 65 (11): 1467–71. doi:10.1001/archneur.65.11.1467. PMC 2752218. PMID 19001165.
  79. ^ Kesler SR, Adams HF, Blasey CM, Bigler ED (2003). "Premorbid intellectual functioning, education, and brain size in traumatic brain injury: an investigation of the cognitive reserve hypothesis". Appl Neuropsychol. 10 (3): 153–62. doi:10.1207/S15324826AN1003_04. PMID 12890641. S2CID 23635493.
  80. ^ Fratiglioni L, Paillard-Borg S, Winblad B (June 2004). "An active and socially integrated lifestyle in late life might protect against dementia". Lancet Neurol. 3 (6): 343–53. doi:10.1016/S1474-4422(04)00767-7. PMID 15157849. S2CID 8818506.
  81. ^ Pai MC, Tsai JJ (2005). "Is cognitive reserve applicable to epilepsy? The effect of educational level on the cognitive decline after onset of epilepsy". Epilepsia. 46 (Suppl 1): 7–10. doi:10.1111/j.0013-9580.2005.461003.x. PMID 15816971. S2CID 24313873.

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