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Changes in Prefrontal Cortex–Thalamic Circuitry after Acoustic Trauma
In the adult auditory system, loss of input resulting from peripheral deafferentation is well known to lead to plasticity in the central nervous system, manifested as reorganization of cortical maps and altered activity throughout the central auditory pathways. The auditory system also has strong af...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7829915/ https://www.ncbi.nlm.nih.gov/pubmed/33466899 http://dx.doi.org/10.3390/biomedicines9010077 |
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author | Barry, Kristin M. Robertson, Donald Mulders, Wilhelmina H. A. M. |
author_facet | Barry, Kristin M. Robertson, Donald Mulders, Wilhelmina H. A. M. |
author_sort | Barry, Kristin M. |
collection | PubMed |
description | In the adult auditory system, loss of input resulting from peripheral deafferentation is well known to lead to plasticity in the central nervous system, manifested as reorganization of cortical maps and altered activity throughout the central auditory pathways. The auditory system also has strong afferent and efferent connections with cortico-limbic circuitry including the prefrontal cortex and the question arises whether this circuitry is also affected by loss of peripheral input. Recent studies in our laboratory showed that PFC activation can modulate activity of the auditory thalamus or medial geniculate nucleus (MGN) in normal hearing rats. In addition, we have shown in rats that cochlear trauma resulted in altered spontaneous burst firing in MGN. However, whether the PFC influence on MGN is changed after cochlear trauma is unknown. We investigated the effects of electrical stimulation of PFC on single neuron activity in the MGN in anaesthetized Wistar rats 2 weeks after acoustic trauma or sham surgery. Electrical stimulation of PFC showed a variety of effects in MGN neurons both in sham and acoustic trauma groups but inhibitory responses were significantly larger in the acoustic trauma animals. These results suggest an alteration in functional connectivity between PFC and MGN after cochlear trauma. This change may be a compensatory mechanism increasing sensory gating after the development of altered spontaneous activity in MGN, to prevent altered activity reaching the cortex and conscious perception. |
format | Online Article Text |
id | pubmed-7829915 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-78299152021-01-26 Changes in Prefrontal Cortex–Thalamic Circuitry after Acoustic Trauma Barry, Kristin M. Robertson, Donald Mulders, Wilhelmina H. A. M. Biomedicines Article In the adult auditory system, loss of input resulting from peripheral deafferentation is well known to lead to plasticity in the central nervous system, manifested as reorganization of cortical maps and altered activity throughout the central auditory pathways. The auditory system also has strong afferent and efferent connections with cortico-limbic circuitry including the prefrontal cortex and the question arises whether this circuitry is also affected by loss of peripheral input. Recent studies in our laboratory showed that PFC activation can modulate activity of the auditory thalamus or medial geniculate nucleus (MGN) in normal hearing rats. In addition, we have shown in rats that cochlear trauma resulted in altered spontaneous burst firing in MGN. However, whether the PFC influence on MGN is changed after cochlear trauma is unknown. We investigated the effects of electrical stimulation of PFC on single neuron activity in the MGN in anaesthetized Wistar rats 2 weeks after acoustic trauma or sham surgery. Electrical stimulation of PFC showed a variety of effects in MGN neurons both in sham and acoustic trauma groups but inhibitory responses were significantly larger in the acoustic trauma animals. These results suggest an alteration in functional connectivity between PFC and MGN after cochlear trauma. This change may be a compensatory mechanism increasing sensory gating after the development of altered spontaneous activity in MGN, to prevent altered activity reaching the cortex and conscious perception. MDPI 2021-01-14 /pmc/articles/PMC7829915/ /pubmed/33466899 http://dx.doi.org/10.3390/biomedicines9010077 Text en © 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Barry, Kristin M. Robertson, Donald Mulders, Wilhelmina H. A. M. Changes in Prefrontal Cortex–Thalamic Circuitry after Acoustic Trauma |
title | Changes in Prefrontal Cortex–Thalamic Circuitry after Acoustic Trauma |
title_full | Changes in Prefrontal Cortex–Thalamic Circuitry after Acoustic Trauma |
title_fullStr | Changes in Prefrontal Cortex–Thalamic Circuitry after Acoustic Trauma |
title_full_unstemmed | Changes in Prefrontal Cortex–Thalamic Circuitry after Acoustic Trauma |
title_short | Changes in Prefrontal Cortex–Thalamic Circuitry after Acoustic Trauma |
title_sort | changes in prefrontal cortex–thalamic circuitry after acoustic trauma |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7829915/ https://www.ncbi.nlm.nih.gov/pubmed/33466899 http://dx.doi.org/10.3390/biomedicines9010077 |
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