Sensorimotor stroke alters hippocampo-thalamic network activity

Abstract Many stroke survivors experience persisting episodic memory disturbances. Since hippocampal and para-hippocampal areas are usually spared from the infarcted area, alterations of memory processing networks remote from the ischemic brain region might be responsible for the observed clinical s...

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Autores principales: Philipp Baumgartner, Mohamad El Amki, Oliver Bracko, Andreas R. Luft, Susanne Wegener
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Lenguaje:EN
Publicado: Nature Portfolio 2018
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Acceso en línea:https://doaj.org/article/e56c1c86ab1b464aba0467c7bfa15ad7
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spelling oai:doaj.org-article:e56c1c86ab1b464aba0467c7bfa15ad72021-12-02T15:08:25ZSensorimotor stroke alters hippocampo-thalamic network activity10.1038/s41598-018-34002-92045-2322https://doaj.org/article/e56c1c86ab1b464aba0467c7bfa15ad72018-10-01T00:00:00Zhttps://doi.org/10.1038/s41598-018-34002-9https://doaj.org/toc/2045-2322Abstract Many stroke survivors experience persisting episodic memory disturbances. Since hippocampal and para-hippocampal areas are usually spared from the infarcted area, alterations of memory processing networks remote from the ischemic brain region might be responsible for the observed clinical symptoms. To pinpoint changes in activity of hippocampal connections and their role in post-stroke cognitive impairment, we induced ischemic stroke by occlusion of the middle cerebral artery (MCAO) in adult rats and analyzed the functional and structural consequences using activity-dependent manganese (Mn2+) enhanced MRI (MEMRI) along with behavioral and histopathological analysis. MCAO caused stroke lesions of variable extent along with sensorimotor and cognitive deficits. Direct hippocampal injury occurred in some rats, but was no prerequisite for cognitive impairment. In healthy rats, injection of Mn2+ into the entorhinal cortex resulted in distribution of the tracer within the hippocampal subfields into the lateral septal nuclei. In MCAO rats, Mn2+ accumulated in the ipsilateral thalamus. Histopathological analysis revealed secondary thalamic degeneration 28 days after stroke. Our findings provide in vivo evidence that remote sensorimotor stroke modifies the activity of hippocampal-thalamic networks. In addition to potentially reversible alterations in signaling of these connections, structural damage of the thalamus likely reinforces dysfunction of hippocampal-thalamic circuitries.Philipp BaumgartnerMohamad El AmkiOliver BrackoAndreas R. LuftSusanne WegenerNature PortfolioarticleSensorimotor StrokeMiddle Cerebral Artery Occlusion (MCAO)Lateral Septal NucleusPost-stroke Cognitive ImpairmentEntorhinal Cortex (EC)MedicineRScienceQENScientific Reports, Vol 8, Iss 1, Pp 1-11 (2018)
institution DOAJ
collection DOAJ
language EN
topic Sensorimotor Stroke
Middle Cerebral Artery Occlusion (MCAO)
Lateral Septal Nucleus
Post-stroke Cognitive Impairment
Entorhinal Cortex (EC)
Medicine
R
Science
Q
spellingShingle Sensorimotor Stroke
Middle Cerebral Artery Occlusion (MCAO)
Lateral Septal Nucleus
Post-stroke Cognitive Impairment
Entorhinal Cortex (EC)
Medicine
R
Science
Q
Philipp Baumgartner
Mohamad El Amki
Oliver Bracko
Andreas R. Luft
Susanne Wegener
Sensorimotor stroke alters hippocampo-thalamic network activity
description Abstract Many stroke survivors experience persisting episodic memory disturbances. Since hippocampal and para-hippocampal areas are usually spared from the infarcted area, alterations of memory processing networks remote from the ischemic brain region might be responsible for the observed clinical symptoms. To pinpoint changes in activity of hippocampal connections and their role in post-stroke cognitive impairment, we induced ischemic stroke by occlusion of the middle cerebral artery (MCAO) in adult rats and analyzed the functional and structural consequences using activity-dependent manganese (Mn2+) enhanced MRI (MEMRI) along with behavioral and histopathological analysis. MCAO caused stroke lesions of variable extent along with sensorimotor and cognitive deficits. Direct hippocampal injury occurred in some rats, but was no prerequisite for cognitive impairment. In healthy rats, injection of Mn2+ into the entorhinal cortex resulted in distribution of the tracer within the hippocampal subfields into the lateral septal nuclei. In MCAO rats, Mn2+ accumulated in the ipsilateral thalamus. Histopathological analysis revealed secondary thalamic degeneration 28 days after stroke. Our findings provide in vivo evidence that remote sensorimotor stroke modifies the activity of hippocampal-thalamic networks. In addition to potentially reversible alterations in signaling of these connections, structural damage of the thalamus likely reinforces dysfunction of hippocampal-thalamic circuitries.
format article
author Philipp Baumgartner
Mohamad El Amki
Oliver Bracko
Andreas R. Luft
Susanne Wegener
author_facet Philipp Baumgartner
Mohamad El Amki
Oliver Bracko
Andreas R. Luft
Susanne Wegener
author_sort Philipp Baumgartner
title Sensorimotor stroke alters hippocampo-thalamic network activity
title_short Sensorimotor stroke alters hippocampo-thalamic network activity
title_full Sensorimotor stroke alters hippocampo-thalamic network activity
title_fullStr Sensorimotor stroke alters hippocampo-thalamic network activity
title_full_unstemmed Sensorimotor stroke alters hippocampo-thalamic network activity
title_sort sensorimotor stroke alters hippocampo-thalamic network activity
publisher Nature Portfolio
publishDate 2018
url https://doaj.org/article/e56c1c86ab1b464aba0467c7bfa15ad7
work_keys_str_mv AT philippbaumgartner sensorimotorstrokealtershippocampothalamicnetworkactivity
AT mohamadelamki sensorimotorstrokealtershippocampothalamicnetworkactivity
AT oliverbracko sensorimotorstrokealtershippocampothalamicnetworkactivity
AT andreasrluft sensorimotorstrokealtershippocampothalamicnetworkactivity
AT susannewegener sensorimotorstrokealtershippocampothalamicnetworkactivity
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