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NMDA receptor subunit composition determines the polarity of leptin-induced synaptic plasticity

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NMDA receptor subunit composition determines the polarity of leptin-induced synaptic plasticity. / Moult, Peter R.; Harvey, Jenni (Lead / Corresponding author).

In: Neuropharmacology, Vol. 61, No. 5-6, 2011, p. 924-936.

Research output: Contribution to journalArticle

Harvard

Moult, PR & Harvey, J 2011, 'NMDA receptor subunit composition determines the polarity of leptin-induced synaptic plasticity' Neuropharmacology, vol 61, no. 5-6, pp. 924-936., 10.1016/j.neuropharm.2011.06.021

APA

Moult, P. R., & Harvey, J. (2011). NMDA receptor subunit composition determines the polarity of leptin-induced synaptic plasticity. Neuropharmacology, 61(5-6), 924-936. 10.1016/j.neuropharm.2011.06.021

Vancouver

Moult PR, Harvey J. NMDA receptor subunit composition determines the polarity of leptin-induced synaptic plasticity. Neuropharmacology. 2011;61(5-6):924-936. Available from: 10.1016/j.neuropharm.2011.06.021

Author

Moult, Peter R.; Harvey, Jenni (Lead / Corresponding author) / NMDA receptor subunit composition determines the polarity of leptin-induced synaptic plasticity.

In: Neuropharmacology, Vol. 61, No. 5-6, 2011, p. 924-936.

Research output: Contribution to journalArticle

Bibtex - Download

@article{eaa0b957fb1d40c1b3fbf4d437fd39d2,
title = "NMDA receptor subunit composition determines the polarity of leptin-induced synaptic plasticity",
keywords = "Leptin, Synaptic transmission, NMDA receptor, Synaptic plasticity, PI 3-kinase, MAPK, LONG-TERM POTENTIATION, D-ASPARTATE RECEPTOR, FUNCTIONAL-PROPERTIES, HIPPOCAMPAL-NEURONS, DIFFERENTIAL ROLES, BRAIN-DEVELOPMENT, CA1 REGION, DEPRESSION, RAT, TRANSMISSION",
author = "Moult, {Peter R.} and Jenni Harvey",
year = "2011",
doi = "10.1016/j.neuropharm.2011.06.021",
volume = "61",
number = "5-6",
pages = "924--936",
journal = "Neuropharmacology",
issn = "0028-3908",

}

RIS (suitable for import to EndNote) - Download

TY - JOUR

T1 - NMDA receptor subunit composition determines the polarity of leptin-induced synaptic plasticity

A1 - Moult,Peter R.

A1 - Harvey,Jenni

AU - Moult,Peter R.

AU - Harvey,Jenni

PY - 2011

Y1 - 2011

N2 - <p>Leptin is a hormone that crosses the blood-brain barrier and regulates numerous CNS functions. The hippocampus in particular is an important site for leptin action. Indeed, leptin markedly influences excitatory synaptic transmission and synaptic plasticity in this brain region. Recent studies indicate that leptin modulation of hippocampal excitatory synaptic transmission is age-dependent however the cellular basis for this is unclear. Here we show that early in development leptin evokes a transient (P11-18) or persistent (P5-8) depression of synaptic transmission, whereas leptin evokes a long lasting increase (LIP) in synaptic strength in adulthood. The synaptic depressions induced by leptin required activation of NMDA receptor GluN2B subunits and the ERK signalling cascade. Conversely, leptin-induced LIP in adult was mediated by GluN2A subunits and involved PI 3-kinase dependent signalling. In addition, low-frequency stimulus (LFS)-evoked LTD occluded the persistent effects of leptin at P5-8 and vice versa. Similarly, synaptically-induced LIP occluded the persistent increase in synaptic transmission induced by leptin, indicating that similar expression mechanisms underlie leptin-induced LTD and LFS-induced LTD at P5-8, and leptin-induced LIP and HFS-induced LIP in adult. These findings have important implications for the role of leptin in hippocampal synaptic function during early neuronal development and in aging. (C) 2011 Elsevier Ltd. All rights reserved.</p>

AB - <p>Leptin is a hormone that crosses the blood-brain barrier and regulates numerous CNS functions. The hippocampus in particular is an important site for leptin action. Indeed, leptin markedly influences excitatory synaptic transmission and synaptic plasticity in this brain region. Recent studies indicate that leptin modulation of hippocampal excitatory synaptic transmission is age-dependent however the cellular basis for this is unclear. Here we show that early in development leptin evokes a transient (P11-18) or persistent (P5-8) depression of synaptic transmission, whereas leptin evokes a long lasting increase (LIP) in synaptic strength in adulthood. The synaptic depressions induced by leptin required activation of NMDA receptor GluN2B subunits and the ERK signalling cascade. Conversely, leptin-induced LIP in adult was mediated by GluN2A subunits and involved PI 3-kinase dependent signalling. In addition, low-frequency stimulus (LFS)-evoked LTD occluded the persistent effects of leptin at P5-8 and vice versa. Similarly, synaptically-induced LIP occluded the persistent increase in synaptic transmission induced by leptin, indicating that similar expression mechanisms underlie leptin-induced LTD and LFS-induced LTD at P5-8, and leptin-induced LIP and HFS-induced LIP in adult. These findings have important implications for the role of leptin in hippocampal synaptic function during early neuronal development and in aging. (C) 2011 Elsevier Ltd. All rights reserved.</p>

KW - Leptin

KW - Synaptic transmission

KW - NMDA receptor

KW - Synaptic plasticity

KW - PI 3-kinase

KW - MAPK

KW - LONG-TERM POTENTIATION

KW - D-ASPARTATE RECEPTOR

KW - FUNCTIONAL-PROPERTIES

KW - HIPPOCAMPAL-NEURONS

KW - DIFFERENTIAL ROLES

KW - BRAIN-DEVELOPMENT

KW - CA1 REGION

KW - DEPRESSION

KW - RAT

KW - TRANSMISSION

UR - http://www.scopus.com/inward/record.url?scp=80051784497&partnerID=8YFLogxK

U2 - 10.1016/j.neuropharm.2011.06.021

DO - 10.1016/j.neuropharm.2011.06.021

M1 - Article

JO - Neuropharmacology

JF - Neuropharmacology

SN - 0028-3908

IS - 5-6

VL - 61

SP - 924

EP - 936

ER -

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