Traumatic brain injury causes long-term behavioral changes related to region-specific increases of cerebral blood flow

Autor: Bruno Pöttker, Franziska Stöber, Michael K. E. Schäfer, Konstantin Radyushkin, Frank Angenstein, Jürgen Goldschmidt, Regina Hummel
Rok vydání: 2017
Předmět:
0301 basic medicine
Neurology
metabolism [Interleukin-6]
Interleukin-1beta
genetics [Interleukin-1beta]
Morris water navigation task
Hippocampus
Mice
Epilepsy
0302 clinical medicine
chemically induced [Seizures]
Brain Injuries
Traumatic
Conditioning
Psychological
Trauma Severity Indices
Mental Disorders
General Neuroscience
Fear
Magnetic Resonance Imaging
Cerebral blood flow
Lcn2 protein
mouse
Cerebrovascular Circulation
diagnostic imaging [Seizures]
Anatomy
medicine.symptom
physiology [Conditioning
Psychological]
Psychology
etiology [Mental Disorders]
medicine.medical_specialty
diagnostic imaging [Brain Injuries
Traumatic]
Histology
Traumatic brain injury
metabolism [Lipocalin-2]
genetics [Interleukin-6]
Brain damage
physiology [Cerebrovascular Circulation]
03 medical and health sciences
metabolism [Interleukin-1beta]
physiology [Maze Learning]
Lipocalin-2
Seizures
Spect imaging
Glial Fibrillary Acidic Protein
medicine
Animals
ddc:610
Maze Learning
Tomography
Emission-Computed
Single-Photon
complications [Brain Injuries
Traumatic]
toxicity [Pentylenetetrazole]
Interleukin-6
metabolism [Glial Fibrillary Acidic Protein]
medicine.disease
Mice
Inbred C57BL
Disease Models
Animal
030104 developmental biology
IL1B protein
mouse
Pentylenetetrazole
Neuroscience
physiology [Fear]
Psychomotor Performance
030217 neurology & neurosurgery
Zdroj: Brain structure & function 222(9), 4005-4021 (2017). doi:10.1007/s00429-017-1452-9
ISSN: 1863-2661
1863-2653
DOI: 10.1007/s00429-017-1452-9
Popis: Traumatic brain injury (TBI) is a leading cause of disability and death and survivors often suffer from long-lasting motor impairment, cognitive deficits, anxiety disorders and epilepsy. Few experimental studies have investigated long-term sequelae after TBI and relations between behavioral changes and neural activity patterns remain elusive. We examined these issues in a murine model of TBI combining histology, behavioral analyses and single-photon emission computed tomography (SPECT) imaging of regional cerebral blood flow (CBF) as a proxy for neural activity. Adult C57Bl/6N mice were subjected to unilateral cortical impact injury and investigated at early (15-57 days after lesion, dal) and late (184-225 dal) post-traumatic time points. TBI caused pronounced tissue loss of the parietal cortex and subcortical structures and enduring neurological deficits. Marked perilesional astro- and microgliosis was found at 57 dal and declined at 225 dal. Motor and gait pattern deficits occurred at early time points after TBI and improved over the time. In contrast, impaired performance in the Morris water maze test and decreased anxiety-like behavior persisted together with an increased susceptibility to pentylenetetrazole-induced seizures suggesting alterations in neural activity patterns. Accordingly, SPECT imaging of CBF indicated asymmetric hemispheric baseline neural activity patterns. In the ipsilateral hemisphere, increased baseline neural activity was found in the amygdala. In the contralateral hemisphere, homotopic to the structural brain damage, the hippocampus and distinct cortex regions displayed increased baseline neural activity. Thus, regionally elevated CBF along with behavioral alterations indicate that increased neural activity is critically involved in the long-lasting consequences of TBI.
Databáze: OpenAIRE
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