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Event: 1330

Key Event Title

A descriptive phrase which defines a discrete biological change that can be measured. More help

Decreased, neuroplasticity

Short name
The KE short name should be a reasonable abbreviation of the KE title and is used in labelling this object throughout the AOP-Wiki. More help
Decreased, neuroplasticity
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Biological Context

Structured terms, selected from a drop-down menu, are used to identify the level of biological organization for each KE. More help
Level of Biological Organization
Molecular

Cell term

The location/biological environment in which the event takes place.The biological context describes the location/biological environment in which the event takes place.  For molecular/cellular events this would include the cellular context (if known), organ context, and species/life stage/sex for which the event is relevant. For tissue/organ events cellular context is not applicable.  For individual/population events, the organ context is not applicable.  Further information on Event Components and Biological Context may be viewed on the attached pdf. More help
Cell term
neural cell

Organ term

The location/biological environment in which the event takes place.The biological context describes the location/biological environment in which the event takes place.  For molecular/cellular events this would include the cellular context (if known), organ context, and species/life stage/sex for which the event is relevant. For tissue/organ events cellular context is not applicable.  For individual/population events, the organ context is not applicable.  Further information on Event Components and Biological Context may be viewed on the attached pdf. More help
Organ term
brain

Key Event Components

The KE, as defined by a set structured ontology terms consisting of a biological process, object, and action with each term originating from one of 14 biological ontologies (Ives, et al., 2017; https://aopwiki.org/info_pages/2/info_linked_pages/7#List). Biological process describes dynamics of the underlying biological system (e.g., receptor signalling).Biological process describes dynamics of the underlying biological system (e.g., receptor signaling).  The biological object is the subject of the perturbation (e.g., a specific biological receptor that is activated or inhibited). Action represents the direction of perturbation of this system (generally increased or decreased; e.g., ‘decreased’ in the case of a receptor that is inhibited to indicate a decrease in the signaling by that receptor).  Note that when editing Event Components, clicking an existing Event Component from the Suggestions menu will autopopulate these fields, along with their source ID and description.  To clear any fields before submitting the event component, use the 'Clear process,' 'Clear object,' or 'Clear action' buttons.  If a desired term does not exist, a new term request may be made via Term Requests.  Event components may not be edited; to edit an event component, remove the existing event component and create a new one using the terms that you wish to add.  Further information on Event Components and Biological Context may be viewed on the attached pdf. More help

Key Event Overview

AOPs Including This Key Event

All of the AOPs that are linked to this KE will automatically be listed in this subsection. This table can be particularly useful for derivation of AOP networks including the KE.Clicking on the name of the AOP will bring you to the individual page for that AOP. More help
AOP Name Role of event in AOP Point of Contact Author Status OECD Status
Network of SSRIs KeyEvent Lyle Burgoon (send email) Open for adoption
Mental stress to depression KeyEvent Lyle Burgoon (send email) Open for adoption
Mental stress to agitation KeyEvent Lyle Burgoon (send email) Open for adoption
Serotonin transporter activation to agitation KeyEvent Lyle Burgoon (send email) Open for adoption
Serotonin transporter activation to depression KeyEvent Lyle Burgoon (send email) Open for adoption
Binding of Alpha 1-Adrenergics to Antagonists Leading to Depression KeyEvent LUANA GOMES (send email) Under development: Not open for comment. Do not cite

Taxonomic Applicability

Latin or common names of a species or broader taxonomic grouping (e.g., class, order, family) that help to define the biological applicability domain of the KE.In many cases, individual species identified in these structured fields will be those for which the strongest evidence used in constructing the AOP was available in relation to this KE. More help
Term Scientific Term Evidence Link
human Homo sapiens High NCBI
rat Rattus norvegicus High NCBI
mouse Mus musculus High NCBI

Life Stages

An indication of the the relevant life stage(s) for this KE. More help
Life stage Evidence
During brain development, adulthood and aging High

Sex Applicability

An indication of the the relevant sex for this KE. More help
Term Evidence
Mixed High

Key Event Description

A description of the biological state being observed or measured, the biological compartment in which it is measured, and its general role in the biology should be provided. More help
  • Neuroplasticity, also known as synaptic or brain plasticity, is a mechanism by which the brain undergoes structural and functional changes. It is defined as the brain’s ability to modify its activity in response to extrinsic and intrinsic stimuli, enabling the reorganization of its structure and function — for example, following brain injury. (Puderbaugh et al; 2023)
  • The biochemical processes that occur and are associated with synapses and other components of the brain form the foundation of neuroplasticity. These processes involve both functional and structural changes in the brain, enabling adaptation to the environment, learning, memory formation, and rehabilitation following brain injury. (Gulyaeva 2017)
  • Basically, neuroplasticity can be defined primarily as the modification of the structure or function of the nervous system in response to environmental changes. (Stee & Peigneux, 2021)

  • Synaptic plasticity is time-dependent. (Johson et al; 2023) 

  • It is suggested that neuroplasticity is also associated with neurogenesis. (Stee et al., 2021)

  • Recently, neuroplastic changes have also been found in the thickness of the myelin sheath and in the diameter of the axon. (Fields, 2015; Xin e Chan, 2020; Tramblay et al., 2021) 

  • Although the initial description of neuroplasticity focused solely on the brain, it actually occurs throughout the entire central nervous system. (Liu & Chambers, 1958)

  • In basic research, it has been observed that chronic stress leads to impaired neuroplasticity, resulting in neuronal atrophy and synaptic loss in the medial prefrontal cortex (mPFC) and the hippocampus. Structural alterations and changes in specific neural circuits are associated with performance deficits observed in depressed patients during cognitive and neuropsychological tasks. Such deficits are consistent with a reduced ability to interact flexibly with stimuli and to engage in goal-directed cognition efficiently. (Price & Duman, 2020)

How It Is Measured or Detected

A description of the type(s) of measurements that can be employed to evaluate the KE and the relative level of scientific confidence in those measurements.These can range from citation of specific validated test guidelines, citation of specific methods published in the peer reviewed literature, or outlines of a general protocol or approach (e.g., a protein may be measured by ELISA). Do not provide detailed protocols. More help

The main approaches to detect and measure the reduction of neural plasticity include:

Biochemical and protein markers: altered levels of brain-derived neurotrophic factor (BDNF) are associated with impaired synaptic plasticity, as well as imbalances between excitatory and inhibitory neuronal signaling. (Sarriés-Serrano et al., 2025) 

Neuroimaging or electrophysiological techniques: studies using EEG or fMRI can identify structural and functional changes that may reflect reduced synaptic plasticity. (Herzberg et al., 2024)

Animal models demonstrating reduced synaptic activity: for instance, studies have shown that dopamine depletion induces alterations in hippocampal synaptic plasticity in mice. (Kim et al., 2023)

Behavioral and cognitive/neuropsychological performance assays: deficits in tasks requiring cognitive effort, learning, or memory may indicate altered neuroplasticity and serve as an indirect measurement method. 

Use of indirect biomarkers: peripheral biomarkers, such as those found in blood or saliva, can also serve as indicators of changes related to brain plasticity. (Mougeot et al., 2016)

Domain of Applicability

A description of the scientific basis for the indicated domains of applicability and the WoE calls (if provided).  More help

Neuroplasticity is well characterized in vertebrates. Animal models such as rats and mice are well established as tools for studying neural plasticity. More recently, zebrafish (Danio rerio) have also been used as an experimental model to investigate neuroplasticity. (De Jager et al., 2024; Hall & Tropepe, 2018., Calvo‑Ochoa & Byrd‑Jacobs, 2019) 

References

List of the literature that was cited for this KE description. More help

Puderbaugh, M. and P. D. Emmady (2023), Neuroplasticity, Hennepin Healthcare and UNC School of Medicine, Atrium Health, last updated 1 May 2023. 

Gulyaeva, N. V. (2017). Molecular mechanisms of neuroplasticity: An expanding universe. Biochemistry (Moscow), 82(3), 237–245. https://doi.org/10.1134/S0006297917030014 

Stee, W., & Peigneux. (2021). Post-learning micro- and macro-structural neuroplasticity changes with time and sleep. Biochemical Pharmacology, 191, 114369. https://doi.org/10.1016/j.bcp.2020.114369 

Fields, R.D. (2015). A new mechanism of nervous system plasticity: activity-dependent myelination. Nature Reviews Neuroscience, 16(12), 756–767. https://doi.org/10.1038/nrn4023 

Xin, W., & Chan, J.R. (2020). Myelin plasticity: sculpting circuits in learning and memory. Nature Reviews Neuroscience, 21, 682–694. https://doi.org/10.1038/s41583-020-00379-8 

Tremblay, S.A., Jäger, A.-T., Huck, J., Giacosa, C., Beram, S., Schneider, U., Grahl, S., Villringer, A., Tardif, C.L., Bazin, P.-L., Steele, C.J., & Gauthier, C.J. (2021). White matter microstructural changes in short-term learning of a continuous visuomotor sequence. Brain Structure and Function, 226, 2061–2077. https://doi.org/10.1007/s00429-021-02267-y 

Liu, C.N., & Chambers, W.W. (1958). Intraspinal sprouting of dorsal root axons: development of new collaterals and preterminals following partial denervation of the spinal cord in the cat. AMA Archives of Neurology and Psychiatry, 79(1), 46–61. https://doi.org/10.1001/archneurpsyc.1958.02340010050005 

Price, R.B., & Duman, R. (2020). Neuroplasticity in cognitive and psychological mechanisms of depression: an integrative model. Molecular Psychiatry, 25, 530–543. https://doi.org/10.1038/s41380-019-0615-x

Sarriés-Serrano, U., Miquel-Rio, L., Santana, N., Paz, V., Sancho-Alonso, M., Callado, L.F., Meana, J.J., & Bortolozzi, A. (2025). Impaired unfolded protein response, BDNF and synuclein markers in the dorsolateral prefrontal cortex and caudate nucleus postmortem of patients with depression and Parkinson’s disease. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 128, 111299. https://doi.org/10.1016/j.pnpbp.2025.111299 

Herzberg, M.P., Nielsen, A.N., Luby, J., & Sylvester, C.M. (2024). Measuring neuroplasticity in human development: the potential to guide the type and timing of mental health interventions. Neuropsychopharmacology. Published online August 5, 2024. https://doi.org/10.1038/s41386-024-01947-7 

Kim, B., Kim, J.-S., Youn, B., & Changjong, L. (2023). Dopamine depletion alters neuroplasticity-related signaling in the rat hippocampus. Experimental Neurobiology, 32(6), 557–567. https://doi.org/10.1080/19768354.2023.2294308 

Mougeot, J.-L.C., Hirsch, M.A., Stevens, C.B., & Mougeot, F.K.B. (2016). Oral biomarkers in exercise-induced neuroplasticity in Parkinson’s disease. Oral Diseases, 22(8), 745–753. https://doi.org/10.1111/odi.12463 

De Jager, J.E., Boesjes, R., Roelandt, G.H.J., Koliaki, I., Sommer, Í.E.C., Schoevers, R.A., & Nuninga, J.O. (2024). Shared effects of electroconvulsive shocks and ketamine on neuroplasticity: a systematic review of animal models of depression. Neuroscience & Biobehavioral Reviews, (105796). https://doi.org/10.1016/j.neubiorev.2024.105796 

Hall, Z.J., & Tropepe, V. (2018). Movement maintains forebrain neurogenesis via peripheral neural feedback in larval zebrafish. eLife, 7, e31045. https://doi.org/10.7554/eLife.31045 

Calvo‑Ochoa, E., & Byrd‑Jacobs, C.A. (2019). The olfactory system of zebrafish as a model for the study of neurotoxicity and injury: implications for neuroplasticity and disease. International Journal of Molecular Sciences, 20(7), 1639. https://doi.org/10.3390/ijms20071639