Regulation of glutamate receptor trafficking by leptin

Peter R. Moult, Jenni Harvey

    Research output: Contribution to journalArticle

    17 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 UP (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 (alpha-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
    DOIs
    Publication statusPublished - Dec 2009

    Keywords

    • alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor (AMPA receptor)
    • hippocampus
    • leptin
    • N-methyl-n-aspartate receptor (NMDA receptor)
    • synaptic plasticity
    • trafficking
    • LONG-TERM POTENTIATION
    • HIPPOCAMPAL SYNAPTIC PLASTICITY
    • GLUR2-LACKING AMPA RECEPTORS
    • NMDA RECEPTORS
    • MESSENGER-RNA
    • CA1 SYNAPSES
    • RAT-BRAIN
    • PHOSPHORYLATION
    • DEPOTENTIATION
    • EXPRESSION

    Cite this

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    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 UP (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 (alpha-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.",
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    Regulation of glutamate receptor trafficking by leptin. / Moult, Peter R.; Harvey, Jenni.

    In: Biochemical Society Transactions, Vol. 37, 12.2009, p. 1364-1368.

    Research output: Contribution to journalArticle

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    AU - Moult, Peter R.

    AU - Harvey, Jenni

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    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 UP (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 (alpha-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.

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    KW - NMDA RECEPTORS

    KW - MESSENGER-RNA

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    JF - Biochemical Society Transactions

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