Long-Lasting Pathological Mental Fatigue After Brain Injury–A Dysfunction in Glutamate Neurotransmission?
Long-lasting mental or cognitive fatigue may be a disabling symptom after physically recovered skull trauma, stroke, infection, or inflammation in the central nervous system (CNS). It is difficult to go back to work and participate in familiar social activities, as typically the person is only able...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2022-01-01
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| Series: | Frontiers in Behavioral Neuroscience |
| Subjects: | |
| Online Access: | https://www.frontiersin.org/articles/10.3389/fnbeh.2021.791984/full |
| _version_ | 1798024783406825472 |
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| author | Lars Rönnbäck Birgitta Johansson |
| author_facet | Lars Rönnbäck Birgitta Johansson |
| author_sort | Lars Rönnbäck |
| collection | DOAJ |
| description | Long-lasting mental or cognitive fatigue may be a disabling symptom after physically recovered skull trauma, stroke, infection, or inflammation in the central nervous system (CNS). It is difficult to go back to work and participate in familiar social activities, as typically the person is only able to remain mentally active for short periods, and if mentally exhausted, the recovery time will be disproportionally long. Mental fatigue after traumatic brain injury correlates with brain information processing speed. Information processing is energy consuming and requires widespread and specific neural signaling. Glutamate signaling is essential for information processing, including learning and memory. Low levels and the fine-tuning of extracellular glutamate are necessary to maintain a high precision in information processing. The astroglial cells are responsible for the fine-tuning of the glutamate transmission, but this capacity is attenuated by substances or conditions associated with neuro-inflammation in brain pathology. In this paper, we extend our previously presented hypothesis on the cellular mechanisms underlying mental fatigue suggesting a dysfunction in the astroglial support of the glutamate transmission. Changes in other neurotransmitters such as dopamine, serotonin, norepinephrine, GABA, and acetylcholine after brain injury are also taken into consideration. |
| first_indexed | 2024-04-11T18:08:12Z |
| format | Article |
| id | doaj.art-0bf5bb7f80db4fbcb9236c8c830beafc |
| institution | Directory Open Access Journal |
| issn | 1662-5153 |
| language | English |
| last_indexed | 2024-04-11T18:08:12Z |
| publishDate | 2022-01-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Behavioral Neuroscience |
| spelling | doaj.art-0bf5bb7f80db4fbcb9236c8c830beafc2022-12-22T04:10:13ZengFrontiers Media S.A.Frontiers in Behavioral Neuroscience1662-51532022-01-011510.3389/fnbeh.2021.791984791984Long-Lasting Pathological Mental Fatigue After Brain Injury–A Dysfunction in Glutamate Neurotransmission?Lars RönnbäckBirgitta JohanssonLong-lasting mental or cognitive fatigue may be a disabling symptom after physically recovered skull trauma, stroke, infection, or inflammation in the central nervous system (CNS). It is difficult to go back to work and participate in familiar social activities, as typically the person is only able to remain mentally active for short periods, and if mentally exhausted, the recovery time will be disproportionally long. Mental fatigue after traumatic brain injury correlates with brain information processing speed. Information processing is energy consuming and requires widespread and specific neural signaling. Glutamate signaling is essential for information processing, including learning and memory. Low levels and the fine-tuning of extracellular glutamate are necessary to maintain a high precision in information processing. The astroglial cells are responsible for the fine-tuning of the glutamate transmission, but this capacity is attenuated by substances or conditions associated with neuro-inflammation in brain pathology. In this paper, we extend our previously presented hypothesis on the cellular mechanisms underlying mental fatigue suggesting a dysfunction in the astroglial support of the glutamate transmission. Changes in other neurotransmitters such as dopamine, serotonin, norepinephrine, GABA, and acetylcholine after brain injury are also taken into consideration.https://www.frontiersin.org/articles/10.3389/fnbeh.2021.791984/fullbrain injurymental fatigueastrogliaglutamate transmissiontraumatic brain injurystroke |
| spellingShingle | Lars Rönnbäck Birgitta Johansson Long-Lasting Pathological Mental Fatigue After Brain Injury–A Dysfunction in Glutamate Neurotransmission? Frontiers in Behavioral Neuroscience brain injury mental fatigue astroglia glutamate transmission traumatic brain injury stroke |
| title | Long-Lasting Pathological Mental Fatigue After Brain Injury–A Dysfunction in Glutamate Neurotransmission? |
| title_full | Long-Lasting Pathological Mental Fatigue After Brain Injury–A Dysfunction in Glutamate Neurotransmission? |
| title_fullStr | Long-Lasting Pathological Mental Fatigue After Brain Injury–A Dysfunction in Glutamate Neurotransmission? |
| title_full_unstemmed | Long-Lasting Pathological Mental Fatigue After Brain Injury–A Dysfunction in Glutamate Neurotransmission? |
| title_short | Long-Lasting Pathological Mental Fatigue After Brain Injury–A Dysfunction in Glutamate Neurotransmission? |
| title_sort | long lasting pathological mental fatigue after brain injury a dysfunction in glutamate neurotransmission |
| topic | brain injury mental fatigue astroglia glutamate transmission traumatic brain injury stroke |
| url | https://www.frontiersin.org/articles/10.3389/fnbeh.2021.791984/full |
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