Rescue of inhibitory synapse strength following developmental hearing loss.

Inhibitory synapse dysfunction may contribute to many developmental brain disorders, including the secondary consequences of sensory deprivation. In fact, developmental hearing loss leads to a profound reduction in the strength of inhibitory postsynaptic currents (IPSCs) in the auditory cortex, and...

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Autores principales:	Vibhakar C Kotak, Anne E Takesian, Patricia C MacKenzie, Dan H Sanes
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/c20929455f864b3a92d664e1d2b3e160
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spelling	oai:doaj.org-article:c20929455f864b3a92d664e1d2b3e1602021-11-18T08:01:51ZRescue of inhibitory synapse strength following developmental hearing loss.1932-620310.1371/journal.pone.0053438https://doaj.org/article/c20929455f864b3a92d664e1d2b3e1602013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23326429/?tool=EBIhttps://doaj.org/toc/1932-6203Inhibitory synapse dysfunction may contribute to many developmental brain disorders, including the secondary consequences of sensory deprivation. In fact, developmental hearing loss leads to a profound reduction in the strength of inhibitory postsynaptic currents (IPSCs) in the auditory cortex, and this deficit persists into adulthood. This finding is consistent with the general theory that the emergence of mature synaptic properties requires activity during development. Therefore, we tested the prediction that inhibitory strength can be restored following developmental hearing loss by boosting GABAergic transmission in vivo. Conductive or sensorineural hearing loss was induced surgically in gerbils prior to hearing onset and GABA agonists were then administered for one week. IPSCs were subsequently recorded from pyramidal neurons in a thalamocortical brain slice preparation. Administration of either a GABA(A) receptor a1 subunit specific agonist (zolpidem), or a selective GABA reuptake inhibitor (SGRI), rescued IPSC amplitude in hearing loss animals. Furthermore, this restoration persisted in adults, long after drug treatment ended. In contrast, a GABA(B) receptor agonist baclofen did not restore inhibitory strength. IPSCs could also be restored when SGRI administration began 3 weeks after sensory deprivation. Together, these results demonstrate long-lasting restoration of cortical inhibitory strength in the absence of normal experience. This suggests that in vivo GABA(A) receptor activation is sufficient to promote maturation, and this principle may extend to other developmental disorders associated with diminished inhibitory function.Vibhakar C KotakAnne E TakesianPatricia C MacKenzieDan H SanesPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 1, p e53438 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Vibhakar C Kotak Anne E Takesian Patricia C MacKenzie Dan H Sanes Rescue of inhibitory synapse strength following developmental hearing loss.
description	Inhibitory synapse dysfunction may contribute to many developmental brain disorders, including the secondary consequences of sensory deprivation. In fact, developmental hearing loss leads to a profound reduction in the strength of inhibitory postsynaptic currents (IPSCs) in the auditory cortex, and this deficit persists into adulthood. This finding is consistent with the general theory that the emergence of mature synaptic properties requires activity during development. Therefore, we tested the prediction that inhibitory strength can be restored following developmental hearing loss by boosting GABAergic transmission in vivo. Conductive or sensorineural hearing loss was induced surgically in gerbils prior to hearing onset and GABA agonists were then administered for one week. IPSCs were subsequently recorded from pyramidal neurons in a thalamocortical brain slice preparation. Administration of either a GABA(A) receptor a1 subunit specific agonist (zolpidem), or a selective GABA reuptake inhibitor (SGRI), rescued IPSC amplitude in hearing loss animals. Furthermore, this restoration persisted in adults, long after drug treatment ended. In contrast, a GABA(B) receptor agonist baclofen did not restore inhibitory strength. IPSCs could also be restored when SGRI administration began 3 weeks after sensory deprivation. Together, these results demonstrate long-lasting restoration of cortical inhibitory strength in the absence of normal experience. This suggests that in vivo GABA(A) receptor activation is sufficient to promote maturation, and this principle may extend to other developmental disorders associated with diminished inhibitory function.
format	article
author	Vibhakar C Kotak Anne E Takesian Patricia C MacKenzie Dan H Sanes
author_facet	Vibhakar C Kotak Anne E Takesian Patricia C MacKenzie Dan H Sanes
author_sort	Vibhakar C Kotak
title	Rescue of inhibitory synapse strength following developmental hearing loss.
title_short	Rescue of inhibitory synapse strength following developmental hearing loss.
title_full	Rescue of inhibitory synapse strength following developmental hearing loss.
title_fullStr	Rescue of inhibitory synapse strength following developmental hearing loss.
title_full_unstemmed	Rescue of inhibitory synapse strength following developmental hearing loss.
title_sort	rescue of inhibitory synapse strength following developmental hearing loss.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/c20929455f864b3a92d664e1d2b3e160
work_keys_str_mv	AT vibhakarckotak rescueofinhibitorysynapsestrengthfollowingdevelopmentalhearingloss AT anneetakesian rescueofinhibitorysynapsestrengthfollowingdevelopmentalhearingloss AT patriciacmackenzie rescueofinhibitorysynapsestrengthfollowingdevelopmentalhearingloss AT danhsanes rescueofinhibitorysynapsestrengthfollowingdevelopmentalhearingloss
_version_	1718422630511411200

Rescue of inhibitory synapse strength following developmental hearing loss.

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