Regulation of glutamate receptor trafficking by leptin

Peter R. Moult, Jenni Harvey

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

It is well established that leptin is a circulating hormone that enters the brain and regulates food intake and body weight via its hypothalamic actions. However, it is also known that leptin receptors are widely expressed in the CNS (central nervous system), and evidence is accumulating that leptin modulates many neuronal functions. In particular, recent studies have indicated that leptin plays an important role in the regulation of hippocampal synaptic plasticity. Indeed leptin-insensitive rodents display impairments in hippocampal synaptic plasticity and defects in spatial memory tasks. We have also shown that leptin facilitates the induction of hippocampal LTP (long-term potentiation) via enhancing NMDA (N-methyl-D-aspartate) receptor function and that leptin has the ability to evoke a novel form of NMDA receptor-dependent LTD (long-term depression). In addition, leptin promotes rapid alterations in hippocampal dendritic morphology and synaptic density, which are likely to contribute to the effects of this hormone on excitatory synaptic strength. Recent studies have demonstrated that trafficking of AMPA (α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid) receptors is pivotal for activity-dependent hippocampal synaptic plasticity. However, little is known about how AMPA receptor trafficking processes are regulated by hormonal systems. In the present paper, we discuss evidence that leptin rapidly alters the trafficking of AMPA receptors to and away from hippocampal CA1 synapses. The impact of these leptin-driven changes on hippocampal excitatory synaptic function are discussed.
Original languageEnglish
Pages (from-to)1364-1368
Number of pages5
JournalBiochemical Society Transactions
Volume37
Issue number6
DOIs
Publication statusPublished - Dec 2009

Fingerprint

Glutamate Receptors
Leptin
Neuronal Plasticity
Plasticity
N-Methyl-D-Aspartate Receptors
Hormones
Leptin Receptors
Aptitude
Long-Term Potentiation
Neurology
Synapses
Rodentia
Brain
Central Nervous System
Eating
Body Weight
Depression
Data storage equipment
Defects

Cite this

Moult, Peter R. ; Harvey, Jenni. / Regulation of glutamate receptor trafficking by leptin. In: Biochemical Society Transactions. 2009 ; Vol. 37, No. 6. pp. 1364-1368.
@article{cd50970b698b44379262e2c31e2d11d9,
title = "Regulation of glutamate receptor trafficking by leptin",
abstract = "It is well established that leptin is a circulating hormone that enters the brain and regulates food intake and body weight via its hypothalamic actions. However, it is also known that leptin receptors are widely expressed in the CNS (central nervous system), and evidence is accumulating that leptin modulates many neuronal functions. In particular, recent studies have indicated that leptin plays an important role in the regulation of hippocampal synaptic plasticity. Indeed leptin-insensitive rodents display impairments in hippocampal synaptic plasticity and defects in spatial memory tasks. We have also shown that leptin facilitates the induction of hippocampal LTP (long-term potentiation) via enhancing NMDA (N-methyl-D-aspartate) receptor function and that leptin has the ability to evoke a novel form of NMDA receptor-dependent LTD (long-term depression). In addition, leptin promotes rapid alterations in hippocampal dendritic morphology and synaptic density, which are likely to contribute to the effects of this hormone on excitatory synaptic strength. Recent studies have demonstrated that trafficking of AMPA (α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid) receptors is pivotal for activity-dependent hippocampal synaptic plasticity. However, little is known about how AMPA receptor trafficking processes are regulated by hormonal systems. In the present paper, we discuss evidence that leptin rapidly alters the trafficking of AMPA receptors to and away from hippocampal CA1 synapses. The impact of these leptin-driven changes on hippocampal excitatory synaptic function are discussed.",
author = "Moult, {Peter R.} and Jenni Harvey",
year = "2009",
month = "12",
doi = "10.1042/BST0371364",
language = "English",
volume = "37",
pages = "1364--1368",
journal = "Biochemical Society Transactions",
issn = "0300-5127",
publisher = "Portland Press Ltd.",
number = "6",

}

Regulation of glutamate receptor trafficking by leptin. / Moult, Peter R.; Harvey, Jenni.

In: Biochemical Society Transactions, Vol. 37, No. 6, 12.2009, p. 1364-1368.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Regulation of glutamate receptor trafficking by leptin

AU - Moult, Peter R.

AU - Harvey, Jenni

PY - 2009/12

Y1 - 2009/12

N2 - It is well established that leptin is a circulating hormone that enters the brain and regulates food intake and body weight via its hypothalamic actions. However, it is also known that leptin receptors are widely expressed in the CNS (central nervous system), and evidence is accumulating that leptin modulates many neuronal functions. In particular, recent studies have indicated that leptin plays an important role in the regulation of hippocampal synaptic plasticity. Indeed leptin-insensitive rodents display impairments in hippocampal synaptic plasticity and defects in spatial memory tasks. We have also shown that leptin facilitates the induction of hippocampal LTP (long-term potentiation) via enhancing NMDA (N-methyl-D-aspartate) receptor function and that leptin has the ability to evoke a novel form of NMDA receptor-dependent LTD (long-term depression). In addition, leptin promotes rapid alterations in hippocampal dendritic morphology and synaptic density, which are likely to contribute to the effects of this hormone on excitatory synaptic strength. Recent studies have demonstrated that trafficking of AMPA (α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid) receptors is pivotal for activity-dependent hippocampal synaptic plasticity. However, little is known about how AMPA receptor trafficking processes are regulated by hormonal systems. In the present paper, we discuss evidence that leptin rapidly alters the trafficking of AMPA receptors to and away from hippocampal CA1 synapses. The impact of these leptin-driven changes on hippocampal excitatory synaptic function are discussed.

AB - It is well established that leptin is a circulating hormone that enters the brain and regulates food intake and body weight via its hypothalamic actions. However, it is also known that leptin receptors are widely expressed in the CNS (central nervous system), and evidence is accumulating that leptin modulates many neuronal functions. In particular, recent studies have indicated that leptin plays an important role in the regulation of hippocampal synaptic plasticity. Indeed leptin-insensitive rodents display impairments in hippocampal synaptic plasticity and defects in spatial memory tasks. We have also shown that leptin facilitates the induction of hippocampal LTP (long-term potentiation) via enhancing NMDA (N-methyl-D-aspartate) receptor function and that leptin has the ability to evoke a novel form of NMDA receptor-dependent LTD (long-term depression). In addition, leptin promotes rapid alterations in hippocampal dendritic morphology and synaptic density, which are likely to contribute to the effects of this hormone on excitatory synaptic strength. Recent studies have demonstrated that trafficking of AMPA (α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid) receptors is pivotal for activity-dependent hippocampal synaptic plasticity. However, little is known about how AMPA receptor trafficking processes are regulated by hormonal systems. In the present paper, we discuss evidence that leptin rapidly alters the trafficking of AMPA receptors to and away from hippocampal CA1 synapses. The impact of these leptin-driven changes on hippocampal excitatory synaptic function are discussed.

U2 - 10.1042/BST0371364

DO - 10.1042/BST0371364

M3 - Article

VL - 37

SP - 1364

EP - 1368

JO - Biochemical Society Transactions

JF - Biochemical Society Transactions

SN - 0300-5127

IS - 6

ER -