Leptin induces a novel form of NMDA receptor-dependent LTP at hippocampal termporoammonic-CA1 synapses

Xiao Luo, Gemma McGregor, Andrew J. Irving, Jenni Harvey (Lead / Corresponding author)

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    Abstract

    It is well documented that the hormone leptin regulates many central functions and that hippocampal CA1 pyramidal neurons are a key target for leptin action. Indeed, leptin modulates excitatory synaptic transmission and synaptic plasticity at the Schaffer-collateral (SC) input to CA1 neurons. However the impact of leptin on the direct temporoammonic (TA) input to CA1 neurons is not known. Here we show that leptin evokes a long lasting increase (LTP) in excitatory synaptic transmission at TA-CA1 synapses in rat juvenile hippocampus. Leptin-induced LTP was NMDA receptor-dependent and specifically involved the activation of GluN2B subunits. The signalling pathways underlying leptin-induced LTP involve the activation of PI 3-kinase, but were independent of the ERK signalling cascade. Moreover, insertion of GluA2-lacking AMPA receptors was required for leptin-induced LTP as prior application of philanthotoxin prevented the effects of leptin. In addition, synaptic-induced LTP occluded the persistent increase in synaptic efficacy induced by leptin. In conclusion, these data indicate that leptin induces a novel form of NMDA receptor-dependent LTP at juvenile TA-CA1 synapses, which has important implications for the role of leptin in modulating hippocampal synaptic function in health and disease.
    Original languageEnglish
    Number of pages17
    JournaleNeuro
    Volume2
    Issue number3
    DOIs
    Publication statusPublished - 26 May 2015

    Keywords

    • Leptin
    • Synaptic plasticity
    • Hippocampus
    • NMDA

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