Cross-Modal Reinstatement of Thalamocortical Plasticity Accelerates Ocular Dominance Plasticity in Adult Mice

Gabriela Rodríguez, Darpan Chakraborty, Katrina M. Schrode, Rinki Saha, Isabel Uribe, Amanda M Lauer, Hey-Kyoung Lee

Research output: Contribution to journalArticle

Abstract

Plasticity of thalamocortical (TC) synapses is robust during early development and becomes limited in the adult brain. We previously reported that a short duration of deafening strengthens TC synapses in the primary visual cortex (V1) of adult mice. Here, we demonstrate that deafening restores NMDA receptor (NMDAR)-dependent long-term potentiation (LTP) of TC synapses onto principal neurons in V1 layer 4 (L4), which is accompanied by an increase in NMDAR function. In contrast, deafening did not recover long-term depression (LTD) at TC synapses. Potentiation of TC synapses by deafening is absent in parvalbumin-positive (PV+) interneurons, resulting in an increase in feedforward excitation to inhibition (E/I) ratio. Furthermore, we found that a brief duration of deafening adult mice recovers rapid ocular dominance plasticity (ODP) mainly by accelerating potentiation of the open-eye responses. Our results suggest that cross-modal sensory deprivation promotes adult cortical plasticity by specifically recovering TC-LTP and increasing the E/I ratio. Plasticity of thalamocortical (TC) synapses is limited in adults. Rodríguez et al. demonstrate that a brief period of deafening adults recovers LTP at TC synapses in visual cortex and accelerates ocular dominance plasticity. These results suggest that cross-modal sensory deprivation may be an effective way to promote adult cortical plasticity.

Original languageEnglish (US)
Pages (from-to)3433-3440.e4
JournalCell Reports
Volume24
Issue number13
DOIs
StatePublished - Sep 25 2018

Fingerprint

ocular Dominance
Synapses
Plasticity
Long-Term Potentiation
Sensory Deprivation
N-Methyl-D-Aspartate Receptors
Visual Cortex
Parvalbumins
Interneurons
Neurons
Brain
Depression

Keywords

  • adult cortical plasticity
  • cross-modal plasticity
  • E/I ratio
  • NMDA receptor function
  • thalamocortical LTP
  • visual cortex

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Cross-Modal Reinstatement of Thalamocortical Plasticity Accelerates Ocular Dominance Plasticity in Adult Mice. / Rodríguez, Gabriela; Chakraborty, Darpan; Schrode, Katrina M.; Saha, Rinki; Uribe, Isabel; Lauer, Amanda M; Lee, Hey-Kyoung.

In: Cell Reports, Vol. 24, No. 13, 25.09.2018, p. 3433-3440.e4.

Research output: Contribution to journalArticle

Rodríguez, Gabriela ; Chakraborty, Darpan ; Schrode, Katrina M. ; Saha, Rinki ; Uribe, Isabel ; Lauer, Amanda M ; Lee, Hey-Kyoung. / Cross-Modal Reinstatement of Thalamocortical Plasticity Accelerates Ocular Dominance Plasticity in Adult Mice. In: Cell Reports. 2018 ; Vol. 24, No. 13. pp. 3433-3440.e4.
@article{7693a3324d4e4082bfaaec82bf79eefa,
title = "Cross-Modal Reinstatement of Thalamocortical Plasticity Accelerates Ocular Dominance Plasticity in Adult Mice",
abstract = "Plasticity of thalamocortical (TC) synapses is robust during early development and becomes limited in the adult brain. We previously reported that a short duration of deafening strengthens TC synapses in the primary visual cortex (V1) of adult mice. Here, we demonstrate that deafening restores NMDA receptor (NMDAR)-dependent long-term potentiation (LTP) of TC synapses onto principal neurons in V1 layer 4 (L4), which is accompanied by an increase in NMDAR function. In contrast, deafening did not recover long-term depression (LTD) at TC synapses. Potentiation of TC synapses by deafening is absent in parvalbumin-positive (PV+) interneurons, resulting in an increase in feedforward excitation to inhibition (E/I) ratio. Furthermore, we found that a brief duration of deafening adult mice recovers rapid ocular dominance plasticity (ODP) mainly by accelerating potentiation of the open-eye responses. Our results suggest that cross-modal sensory deprivation promotes adult cortical plasticity by specifically recovering TC-LTP and increasing the E/I ratio. Plasticity of thalamocortical (TC) synapses is limited in adults. Rodr{\'i}guez et al. demonstrate that a brief period of deafening adults recovers LTP at TC synapses in visual cortex and accelerates ocular dominance plasticity. These results suggest that cross-modal sensory deprivation may be an effective way to promote adult cortical plasticity.",
keywords = "adult cortical plasticity, cross-modal plasticity, E/I ratio, NMDA receptor function, thalamocortical LTP, visual cortex",
author = "Gabriela Rodr{\'i}guez and Darpan Chakraborty and Schrode, {Katrina M.} and Rinki Saha and Isabel Uribe and Lauer, {Amanda M} and Hey-Kyoung Lee",
year = "2018",
month = "9",
day = "25",
doi = "10.1016/j.celrep.2018.08.072",
language = "English (US)",
volume = "24",
pages = "3433--3440.e4",
journal = "Cell Reports",
issn = "2211-1247",
publisher = "Cell Press",
number = "13",

}

TY - JOUR

T1 - Cross-Modal Reinstatement of Thalamocortical Plasticity Accelerates Ocular Dominance Plasticity in Adult Mice

AU - Rodríguez, Gabriela

AU - Chakraborty, Darpan

AU - Schrode, Katrina M.

AU - Saha, Rinki

AU - Uribe, Isabel

AU - Lauer, Amanda M

AU - Lee, Hey-Kyoung

PY - 2018/9/25

Y1 - 2018/9/25

N2 - Plasticity of thalamocortical (TC) synapses is robust during early development and becomes limited in the adult brain. We previously reported that a short duration of deafening strengthens TC synapses in the primary visual cortex (V1) of adult mice. Here, we demonstrate that deafening restores NMDA receptor (NMDAR)-dependent long-term potentiation (LTP) of TC synapses onto principal neurons in V1 layer 4 (L4), which is accompanied by an increase in NMDAR function. In contrast, deafening did not recover long-term depression (LTD) at TC synapses. Potentiation of TC synapses by deafening is absent in parvalbumin-positive (PV+) interneurons, resulting in an increase in feedforward excitation to inhibition (E/I) ratio. Furthermore, we found that a brief duration of deafening adult mice recovers rapid ocular dominance plasticity (ODP) mainly by accelerating potentiation of the open-eye responses. Our results suggest that cross-modal sensory deprivation promotes adult cortical plasticity by specifically recovering TC-LTP and increasing the E/I ratio. Plasticity of thalamocortical (TC) synapses is limited in adults. Rodríguez et al. demonstrate that a brief period of deafening adults recovers LTP at TC synapses in visual cortex and accelerates ocular dominance plasticity. These results suggest that cross-modal sensory deprivation may be an effective way to promote adult cortical plasticity.

AB - Plasticity of thalamocortical (TC) synapses is robust during early development and becomes limited in the adult brain. We previously reported that a short duration of deafening strengthens TC synapses in the primary visual cortex (V1) of adult mice. Here, we demonstrate that deafening restores NMDA receptor (NMDAR)-dependent long-term potentiation (LTP) of TC synapses onto principal neurons in V1 layer 4 (L4), which is accompanied by an increase in NMDAR function. In contrast, deafening did not recover long-term depression (LTD) at TC synapses. Potentiation of TC synapses by deafening is absent in parvalbumin-positive (PV+) interneurons, resulting in an increase in feedforward excitation to inhibition (E/I) ratio. Furthermore, we found that a brief duration of deafening adult mice recovers rapid ocular dominance plasticity (ODP) mainly by accelerating potentiation of the open-eye responses. Our results suggest that cross-modal sensory deprivation promotes adult cortical plasticity by specifically recovering TC-LTP and increasing the E/I ratio. Plasticity of thalamocortical (TC) synapses is limited in adults. Rodríguez et al. demonstrate that a brief period of deafening adults recovers LTP at TC synapses in visual cortex and accelerates ocular dominance plasticity. These results suggest that cross-modal sensory deprivation may be an effective way to promote adult cortical plasticity.

KW - adult cortical plasticity

KW - cross-modal plasticity

KW - E/I ratio

KW - NMDA receptor function

KW - thalamocortical LTP

KW - visual cortex

UR - http://www.scopus.com/inward/record.url?scp=85053737795&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85053737795&partnerID=8YFLogxK

U2 - 10.1016/j.celrep.2018.08.072

DO - 10.1016/j.celrep.2018.08.072

M3 - Article

C2 - 30257205

AN - SCOPUS:85053737795

VL - 24

SP - 3433-3440.e4

JO - Cell Reports

JF - Cell Reports

SN - 2211-1247

IS - 13

ER -