An N-methyl-d-aspartate-receptor dependent, late-phase long-term depression in middle-aged mice identifies no GluN2-subunit bias

Tariq Ahmed, V. Sabanov, R. D'Hooge, D. Balschun

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Late-phase long-term depression (L-LTD) in middle-aged mice has been difficult to achieve and maintain. Here we report an electrically induced, homosynaptic, input-specific form of LTD that could be stably maintained for at least 4 h in the CA1 area of hippocampal slices of 10-14 months old mice. This form of L-LTD was similar in magnitude in aged, middle-aged and young mice and was blocked by high concentrations of broad-spectrum N-methyl-d-aspartate receptor (NMDAR) antagonists such as d(-)-2-amino-5-phospho-pentanoic acid (d-AP5) and (R)-3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid (CPP). Extracellular and whole cell recordings revealed a decreased sensitivity to d-AP5 with age, without any differences in NMDAR conductance between the age groups tested. This L-LTD could be inhibited neither by common doses of NMDA-subunit specific antagonists like zinc, ifenprodil and Ro-25-6981, nor by various co-applications of these compounds. In addition to the lack of any GluN2 subunit bias, L-LTD did not show any discernible involvement of L-type voltage-gated calcium channels. In conclusion, our results do not support any specific role of NMDAR subunits in LTD.

Original languageEnglish
Pages (from-to)27-38
Number of pages12
JournalNeuroscience
Volume185
DOIs
Publication statusPublished - 30 Jun 2011
Externally publishedYes

Fingerprint

Pentanoic Acids
Patch-Clamp Techniques
N-Methylaspartate
Calcium Channels
Zinc
Age Groups
aspartic acid receptor
3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid
ifenprodil
Ro 25-6981

Keywords

  • Hippocampal cA1-region
  • In vitro
  • Long term depression
  • Synaptic plasticity

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

An N-methyl-d-aspartate-receptor dependent, late-phase long-term depression in middle-aged mice identifies no GluN2-subunit bias. / Ahmed, Tariq; Sabanov, V.; D'Hooge, R.; Balschun, D.

In: Neuroscience, Vol. 185, 30.06.2011, p. 27-38.

Research output: Contribution to journalArticle

@article{6c3cbfec1f054dc0a813b5cd5201492e,
title = "An N-methyl-d-aspartate-receptor dependent, late-phase long-term depression in middle-aged mice identifies no GluN2-subunit bias",
abstract = "Late-phase long-term depression (L-LTD) in middle-aged mice has been difficult to achieve and maintain. Here we report an electrically induced, homosynaptic, input-specific form of LTD that could be stably maintained for at least 4 h in the CA1 area of hippocampal slices of 10-14 months old mice. This form of L-LTD was similar in magnitude in aged, middle-aged and young mice and was blocked by high concentrations of broad-spectrum N-methyl-d-aspartate receptor (NMDAR) antagonists such as d(-)-2-amino-5-phospho-pentanoic acid (d-AP5) and (R)-3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid (CPP). Extracellular and whole cell recordings revealed a decreased sensitivity to d-AP5 with age, without any differences in NMDAR conductance between the age groups tested. This L-LTD could be inhibited neither by common doses of NMDA-subunit specific antagonists like zinc, ifenprodil and Ro-25-6981, nor by various co-applications of these compounds. In addition to the lack of any GluN2 subunit bias, L-LTD did not show any discernible involvement of L-type voltage-gated calcium channels. In conclusion, our results do not support any specific role of NMDAR subunits in LTD.",
keywords = "Hippocampal cA1-region, In vitro, Long term depression, Synaptic plasticity",
author = "Tariq Ahmed and V. Sabanov and R. D'Hooge and D. Balschun",
year = "2011",
month = "6",
day = "30",
doi = "10.1016/j.neuroscience.2011.04.006",
language = "English",
volume = "185",
pages = "27--38",
journal = "Neuroscience",
issn = "0306-4522",
publisher = "Elsevier Limited",

}

TY - JOUR

T1 - An N-methyl-d-aspartate-receptor dependent, late-phase long-term depression in middle-aged mice identifies no GluN2-subunit bias

AU - Ahmed, Tariq

AU - Sabanov, V.

AU - D'Hooge, R.

AU - Balschun, D.

PY - 2011/6/30

Y1 - 2011/6/30

N2 - Late-phase long-term depression (L-LTD) in middle-aged mice has been difficult to achieve and maintain. Here we report an electrically induced, homosynaptic, input-specific form of LTD that could be stably maintained for at least 4 h in the CA1 area of hippocampal slices of 10-14 months old mice. This form of L-LTD was similar in magnitude in aged, middle-aged and young mice and was blocked by high concentrations of broad-spectrum N-methyl-d-aspartate receptor (NMDAR) antagonists such as d(-)-2-amino-5-phospho-pentanoic acid (d-AP5) and (R)-3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid (CPP). Extracellular and whole cell recordings revealed a decreased sensitivity to d-AP5 with age, without any differences in NMDAR conductance between the age groups tested. This L-LTD could be inhibited neither by common doses of NMDA-subunit specific antagonists like zinc, ifenprodil and Ro-25-6981, nor by various co-applications of these compounds. In addition to the lack of any GluN2 subunit bias, L-LTD did not show any discernible involvement of L-type voltage-gated calcium channels. In conclusion, our results do not support any specific role of NMDAR subunits in LTD.

AB - Late-phase long-term depression (L-LTD) in middle-aged mice has been difficult to achieve and maintain. Here we report an electrically induced, homosynaptic, input-specific form of LTD that could be stably maintained for at least 4 h in the CA1 area of hippocampal slices of 10-14 months old mice. This form of L-LTD was similar in magnitude in aged, middle-aged and young mice and was blocked by high concentrations of broad-spectrum N-methyl-d-aspartate receptor (NMDAR) antagonists such as d(-)-2-amino-5-phospho-pentanoic acid (d-AP5) and (R)-3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid (CPP). Extracellular and whole cell recordings revealed a decreased sensitivity to d-AP5 with age, without any differences in NMDAR conductance between the age groups tested. This L-LTD could be inhibited neither by common doses of NMDA-subunit specific antagonists like zinc, ifenprodil and Ro-25-6981, nor by various co-applications of these compounds. In addition to the lack of any GluN2 subunit bias, L-LTD did not show any discernible involvement of L-type voltage-gated calcium channels. In conclusion, our results do not support any specific role of NMDAR subunits in LTD.

KW - Hippocampal cA1-region

KW - In vitro

KW - Long term depression

KW - Synaptic plasticity

UR - http://www.scopus.com/inward/record.url?scp=79956268764&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=79956268764&partnerID=8YFLogxK

U2 - 10.1016/j.neuroscience.2011.04.006

DO - 10.1016/j.neuroscience.2011.04.006

M3 - Article

C2 - 21504782

AN - SCOPUS:79956268764

VL - 185

SP - 27

EP - 38

JO - Neuroscience

JF - Neuroscience

SN - 0306-4522

ER -