Symmetric and Asymmetric Synapses Driving Neurodegenerative Disorders
In 1959, E. G. Gray described two different types of synapses in the brain for the first time: symmetric and asymmetric. Later on, symmetric synapses were associated with inhibitory terminals, and asymmetric synapses to excitatory signaling. The balance between these two systems is critical to maint...
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| Format: | Article |
| Language: | English |
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MDPI AG
2021-12-01
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| Series: | Symmetry |
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| Online Access: | https://www.mdpi.com/2073-8994/13/12/2333 |
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| author | Daniel Romaus-Sanjurjo Antía Custodia Marta Aramburu-Núñez Adrián Posado-Fernández Laura Vázquez-Vázquez Javier Camino-Castiñeiras Yago Leira Juan Manuel Pías-Peleteiro José Manuel Aldrey Alberto Ouro Tomás Sobrino |
| author_facet | Daniel Romaus-Sanjurjo Antía Custodia Marta Aramburu-Núñez Adrián Posado-Fernández Laura Vázquez-Vázquez Javier Camino-Castiñeiras Yago Leira Juan Manuel Pías-Peleteiro José Manuel Aldrey Alberto Ouro Tomás Sobrino |
| author_sort | Daniel Romaus-Sanjurjo |
| collection | DOAJ |
| description | In 1959, E. G. Gray described two different types of synapses in the brain for the first time: symmetric and asymmetric. Later on, symmetric synapses were associated with inhibitory terminals, and asymmetric synapses to excitatory signaling. The balance between these two systems is critical to maintain a correct brain function. Likewise, the modulation of both types of synapses is also important to maintain a healthy equilibrium. Cerebral circuitry responds differently depending on the type of damage and the timeline of the injury. For example, promoting symmetric signaling following ischemic damage is beneficial only during the acute phase; afterwards, it further increases the initial damage. Synapses can be also altered by players not directly related to them; the chronic and long-term neurodegeneration mediated by tau proteins primarily targets asymmetric synapses by decreasing neuronal plasticity and functionality. Dopamine represents the main modulating system within the central nervous system. Indeed, the death of midbrain dopaminergic neurons impairs locomotion, underlying the devastating Parkinson’s disease. Herein, we will review studies on symmetric and asymmetric synapses plasticity after three different stressors: symmetric signaling under acute damage—ischemic stroke; asymmetric signaling under chronic and long-term neurodegeneration—Alzheimer’s disease; symmetric and asymmetric synapses without modulation—Parkinson’s disease. |
| first_indexed | 2024-03-10T03:59:59Z |
| format | Article |
| id | doaj.art-6c422d50a45d4ded863a973f38700c11 |
| institution | Directory Open Access Journal |
| issn | 2073-8994 |
| language | English |
| last_indexed | 2024-03-10T03:59:59Z |
| publishDate | 2021-12-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Symmetry |
| spelling | doaj.art-6c422d50a45d4ded863a973f38700c112023-11-23T10:45:36ZengMDPI AGSymmetry2073-89942021-12-011312233310.3390/sym13122333Symmetric and Asymmetric Synapses Driving Neurodegenerative DisordersDaniel Romaus-Sanjurjo0Antía Custodia1Marta Aramburu-Núñez2Adrián Posado-Fernández3Laura Vázquez-Vázquez4Javier Camino-Castiñeiras5Yago Leira6Juan Manuel Pías-Peleteiro7José Manuel Aldrey8Alberto Ouro9Tomás Sobrino10NeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratories (LINCs), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratories (LINCs), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratories (LINCs), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratories (LINCs), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratories (LINCs), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratories (LINCs), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratories (LINCs), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratories (LINCs), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratories (LINCs), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratories (LINCs), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainNeuroAging Group (NEURAL), Clinical Neurosciences Research Laboratories (LINCs), Health Research Institute of Santiago de Compostela (IDIS), 15706 Santiago de Compostela, SpainIn 1959, E. G. Gray described two different types of synapses in the brain for the first time: symmetric and asymmetric. Later on, symmetric synapses were associated with inhibitory terminals, and asymmetric synapses to excitatory signaling. The balance between these two systems is critical to maintain a correct brain function. Likewise, the modulation of both types of synapses is also important to maintain a healthy equilibrium. Cerebral circuitry responds differently depending on the type of damage and the timeline of the injury. For example, promoting symmetric signaling following ischemic damage is beneficial only during the acute phase; afterwards, it further increases the initial damage. Synapses can be also altered by players not directly related to them; the chronic and long-term neurodegeneration mediated by tau proteins primarily targets asymmetric synapses by decreasing neuronal plasticity and functionality. Dopamine represents the main modulating system within the central nervous system. Indeed, the death of midbrain dopaminergic neurons impairs locomotion, underlying the devastating Parkinson’s disease. Herein, we will review studies on symmetric and asymmetric synapses plasticity after three different stressors: symmetric signaling under acute damage—ischemic stroke; asymmetric signaling under chronic and long-term neurodegeneration—Alzheimer’s disease; symmetric and asymmetric synapses without modulation—Parkinson’s disease.https://www.mdpi.com/2073-8994/13/12/2333Alzheimer’s diseaseasymmetric synapsesdopamineGABAergic transmissionglutamatergic transmissionParkinson’s disease |
| spellingShingle | Daniel Romaus-Sanjurjo Antía Custodia Marta Aramburu-Núñez Adrián Posado-Fernández Laura Vázquez-Vázquez Javier Camino-Castiñeiras Yago Leira Juan Manuel Pías-Peleteiro José Manuel Aldrey Alberto Ouro Tomás Sobrino Symmetric and Asymmetric Synapses Driving Neurodegenerative Disorders Symmetry Alzheimer’s disease asymmetric synapses dopamine GABAergic transmission glutamatergic transmission Parkinson’s disease |
| title | Symmetric and Asymmetric Synapses Driving Neurodegenerative Disorders |
| title_full | Symmetric and Asymmetric Synapses Driving Neurodegenerative Disorders |
| title_fullStr | Symmetric and Asymmetric Synapses Driving Neurodegenerative Disorders |
| title_full_unstemmed | Symmetric and Asymmetric Synapses Driving Neurodegenerative Disorders |
| title_short | Symmetric and Asymmetric Synapses Driving Neurodegenerative Disorders |
| title_sort | symmetric and asymmetric synapses driving neurodegenerative disorders |
| topic | Alzheimer’s disease asymmetric synapses dopamine GABAergic transmission glutamatergic transmission Parkinson’s disease |
| url | https://www.mdpi.com/2073-8994/13/12/2333 |
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