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Regarding humans, developmental plasticity is a general term referring to changes in neural connections during development as a result of environmental interactions as well as neural changes induced by learning.[1] Much like neuroplasticity, or brain plasticity, developmental plasticity is specific to the change in neurons and synaptic connections as a consequence of developmental processes. A child creates most of these connections from birth to early childhood. There are three primary methods by which this may occur as the brain develops,[2] but critical periods determine when lasting changes may form. Developmental plasticity may also be used in place of the term phenotypic plasticity when an organism in an embryonic or larval stage can alter its phenotype based on environmental factors.[3] However, a main difference between the two is that phenotypic plasticity experienced during adulthood can be reversible, whereas traits that are considered developmentally plastic set foundations during early development that remain throughout the life of the organism.[4]

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Mechanisms

During development, the central nervous system acquires information via endogenous or exogenous factors as well as learning experiences. In acquiring and storing such information, the plastic nature of the central nervous system allows for the adaptation of existing neural connections in order to accommodate new information and experiences, resulting in developmental plasticity. This form of plasticity that occurs during development is the result of three predominant mechanisms: synaptic and homeostatic plasticity, and learning.[2]

Synaptic plasticity

The underlying principle of synaptic plasticity is that synapses undergo an activity-dependent and selective strengthening or weakening so that new information can be stored.[5] Synaptic plasticity depends on numerous factors including the threshold of the presynaptic stimulus in addition to the relative concentrations of neurotransmitter molecules. Synaptic plasticity has long been implicated for its role in memory storage and is thought to play a key role in learning.[6] However, during developmental periods, synaptic plasticity is of particular importance, as changes in the network of synaptic connections can ultimately lead to changes in developmental milestones. For instance, the initial overproduction of synapses during development is key to plasticity that occurs in the visual and auditory cortices.[7] In experiments conducted by Hubel and Wiesel, the visual cortex of kittens exhibits synaptic plasticity in the refinement of neural connections following visual inputs. Correspondingly, in the absence of such inputs during development, the visual field fails to develop properly and can lead to abnormal structures and behavior.[8] Furthermore, research suggests that this initial overproduction of synapses during developmental periods provides the foundation by which many synaptic connections can be formed, thus resulting in more synaptic plasticity. In the same way that synapses are abundant during development, there are also refining mechanisms that assist in the maturation of synapses in neural circuits. This regulatory process allows the strengthening of important or frequently used synaptic connections while reducing the amount of weak connections.[9]

Homeostatic plasticity

In order to maintain balance, homeostatic controls exist to regulate the overall activity of neural circuits, specifically by regulating the destabilizing effects of developmental and learning processes that result in changes of synaptic strength. Homeostatic plasticity also helps regulate prolonged excitatory responses, which lead to a reduction in all of a neuron's synaptic responses.[10] Numerous pathways have recently been associated with homeostatic plasticity, though there is still no clear molecular mechanism. Synaptic scaling is one method that serves as a type of autoregulation, as neurons can recognize their own firing rates and notice when there are alterations; calcium-dependent signals control the levels of glutamate receptors at synaptic sites in response. Homeostatic mechanisms may be local or network-wide.[11]

Learning

While synaptic plasticity is considered to be a by-product of learning, learning involves interaction with the environment to acquire the new information or behavior; synaptic plasticity merely represents the change in strength or configuration of neural circuits.[12] Learning is crucial, as there is considerable interaction with the environment, which is when the potential for acquiring new information is greatest. By depending largely upon selective experiences, neural connections are altered and strengthened in a manner that is unique to those experiences.[13] Experimentally, this can be seen when rats are raised in an environment that allows ample social interaction, resulting in increased brain weight and cortical thickness. In contrast, the inverse is seen following rearing in an environment devoid of interaction.[14] Also, learning plays a considerable role in the selective acquisition of information and is markedly demonstrated when children develop one language instead of another. Another example of such experience-dependent plasticity that is critical during development is the occurrence of imprinting. This occurs as a result of a young child or animal being exposed to a novel stimulus and rapidly implementing a certain behavior in response.[15]




Environmental Cues

Environmental cues in either the mother's or the developing embryo's environment can result in changes in the embryo. Embryonic development is a sensitive process and can be impacted by cues from predators,[16] light,[17] and/or temperature.[18] For example, in Daphnia, neonates exposed to predator cues had higher expression of genes related to digestion, reproductive function, and defense. It was hypothesized that this increase in gene expression would allow the Daphnia to defend itself, and that an increase in growth would result in a larger investment in future offspring.[16] Subsequent generations saw a similar pattern, despite not being exposed to any predator cues, suggesting an inheritance of epigenetic expression factors.[16] An organism's sensitivity to light during to development could be useful in predicting what phenotype would be the most beneficial in the future, based on the foliage that will be present in the future. Several species, including alligators and tortoises have temperature dependent sex determination, where the sex of the organism is dependent on the temperature during a crucial thermosensitive period.[18] The mechanics of temperature sex determination is an active area research, and has been hypothesized to be associated with the methylation of specific genes.[18]

References

  1. ^ Kolb, Bryan; Gibb, Robbin (2011). "Brain plasticity and behaviour in the developing brain". Journal of the Canadian Academy of Child and Adolescent Psychiatry = Journal De l'Academie Canadienne De Psychiatrie De L'enfant Et De L'adolescent. 20 (4): 265–276. ISSN 2293-6122. PMC 3222570. PMID 22114608.
  2. ^ a b Kania, Bogdan Feliks; Wrońska, Danuta; Zięba, Dorota (2017-02-06). "Introduction to Neural Plasticity Mechanism". Journal of Behavioral and Brain Science. 7 (2): 41–49. doi:10.4236/jbbs.2017.72005.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  3. ^ Gilbert, Scott F. (2015). Ecological developmental biology : the environmental regulation of development, health, and evolution. David Epel (2nd ed.). Sunderland, Massachusetts, U.S.A. ISBN 978-1-60535-344-9. OCLC 905089531.{{cite book}}: CS1 maint: location missing publisher (link)
  4. ^ Lafuente, Elvira; Beldade, Patrícia (2019). "Genomics of Developmental Plasticity in Animals". Frontiers in Genetics. 10. doi:10.3389/fgene.2019.00720. ISSN 1664-8021. PMC 6709652. PMID 31481970.{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link)
  5. ^ Foehring RC, Lorenzon NM (March 1999). "Neuromodulation, development and synaptic plasticity". Canadian Journal of Experimental Psychology. 53 (1): 45–61. doi:10.1037/h0087299. PMID 10389489.
  6. ^ Black JE (1998). "How a child builds its brain: some lessons from animal studies of neural plasticity". Preventive Medicine. 27 (2): 168–171. doi:10.1006/pmed.1998.0271. PMID 9578989.
  7. ^ Phillips, Deborah; Shonkoff, Jack P. (2000). From neurons to neighborhoods : the science of early childhood development. ISBN 978-0-309-06988-5. OCLC 927036965.
  8. ^ Baudry M, Thompson RF, Davis JL (1994). "Synaptic Plasticity: Molecular, Cellular, and Functional Aspects". The Quarterly Review of Biology. 69 (4): 553–554. doi:10.1086/418827.
  9. ^ Tau, Gregory Z.; Peterson, Bradley S. (2010). "Normal Development of Brain Circuits". Neuropsychopharmacology. 35 (1): 147–168. doi:10.1038/npp.2009.115. ISSN 1740-634X. PMC 3055433. PMID 19794405.{{cite journal}}: CS1 maint: PMC format (link)
  10. ^ Butz M, Wörgötter F, van Ooyen A (May 2009). "Activity-dependent structural plasticity". Brain Research Reviews. 60 (2): 287–305. doi:10.1016/j.brainresrev.2008.12.023. PMID 19162072. S2CID 18230052.
  11. ^ Turrigiano, G. (2012-01-01). "Homeostatic Synaptic Plasticity: Local and Global Mechanisms for Stabilizing Neuronal Function". Cold Spring Harbor Perspectives in Biology. 4 (1): a005736–a005736. doi:10.1101/cshperspect.a005736. ISSN 1943-0264. PMC 3249629. PMID 22086977.{{cite journal}}: CS1 maint: PMC format (link)
  12. ^ Kennedy, Mary B. (2013-12-30). "Synaptic Signaling in Learning and Memory". Cold Spring Harbor Perspectives in Biology. 8 (2): a016824. doi:10.1101/cshperspect.a016824. ISSN 1943-0264. PMC 4743082. PMID 24379319.
  13. ^ Fox, Sharon E.; Levitt, Pat; Nelson III, Charles A. (2010-01). "How the Timing and Quality of Early Experiences Influence the Development of Brain Architecture". Child Development. 81 (1): 28–40. doi:10.1111/j.1467-8624.2009.01380.x. PMC 2846084. PMID 20331653. {{cite journal}}: Check date values in: |date= (help)CS1 maint: PMC format (link)
  14. ^ Bennett EL, Diamond MC, Krech D, Rosenzweig MR (October 1964). "Chemical and Anatomical Plasticity of Brain". Science. 146 (3644): 610–619. Bibcode:1964Sci...146..610B. doi:10.1126/science.146.3644.610. PMID 14191699.
  15. ^ D., Breed, Michael (2015). Animal behavior. ISBN 978-0-12-801532-2. OCLC 943254906.{{cite book}}: CS1 maint: multiple names: authors list (link)
  16. ^ a b c Hales, Nicole R.; Schield, Drew R.; Andrew, Audra L.; Card, Daren C.; Walsh, Matthew R.; Castoe, Todd A. (2017). "Contrasting gene expression programs correspond with predator-induced phenotypic plasticity within and across generations in Daphnia". Molecular Ecology. 26 (19): 5003–5015. doi:10.1111/mec.14213.
  17. ^ Zambre, Amod Mohan; Burns, Linnea; Suresh, Jayanti; Hegeman, Adrian D.; Snell-Rood, Emilie C. (2022). "Developmental plasticity in multimodal signals: light environment produces novel signalling phenotypes in a butterfly". Biology Letters. 18 (8): 20220099. doi:10.1098/rsbl.2022.0099. ISSN 1744-957X. PMC 9382452. PMID 35975631.{{cite journal}}: CS1 maint: PMC format (link)
  18. ^ a b c Bock, Samantha L.; Smaga, Christopher R.; McCoy, Jessica A.; Parrott, Benjamin B. (2022). "Genome‐wide DNA methylation patterns harbour signatures of hatchling sex and past incubation temperature in a species with environmental sex determination". Molecular Ecology. 31 (21): 5487–5505. doi:10.1111/mec.16670. ISSN 0962-1083. PMC 9826120. PMID 35997618.{{cite journal}}: CS1 maint: PMC format (link)
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