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Interplay between glucose and leptin signalling determines the strength of GABAergic synapses at POMC neurons

Author

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  • Dong Kun Lee

    (Albert Einstein College of Medicine of Yeshiva University)

  • Jae Hoon Jeong

    (Albert Einstein College of Medicine of Yeshiva University)

  • Sung-Kun Chun

    (Albert Einstein College of Medicine of Yeshiva University)

  • Streamson Chua Jr.

    (Albert Einstein College of Medicine of Yeshiva University)

  • Young-Hwan Jo

    (Albert Einstein College of Medicine of Yeshiva University
    Albert Einstein College of Medicine of Yeshiva University)

Abstract

Regulation of GABAergic inhibitory inputs and alterations in POMC neuron activity by nutrients and adiposity signals regulate energy and glucose homeostasis. Thus, understanding how POMC neurons integrate these two signal molecules at the synaptic level is important. Here we show that leptin’s action on GABA release to POMC neurons is influenced by glucose levels. Leptin stimulates the JAK2–PI3K pathway in both presynaptic GABAergic terminals and postsynaptic POMC neurons. Inhibition of AMPK activity in presynaptic terminals decreases GABA release at 10 mM glucose. However, postsynaptic TRPC channel opening by the PI3K–PLC signalling pathway in POMC neurons enhances spontaneous GABA release via activation of presynaptic MC3/4 and mGlu receptors at 2.5 mM glucose. High-fat feeding blunts AMPK-dependent presynaptic inhibition, whereas PLC-mediated GABAergic feedback inhibition remains responsive to leptin. Our data indicate that the interplay between glucose and leptin signalling in glutamatergic POMC neurons is critical for determining the strength of inhibitory tone towards POMC neurons.

Suggested Citation

  • Dong Kun Lee & Jae Hoon Jeong & Sung-Kun Chun & Streamson Chua Jr. & Young-Hwan Jo, 2015. "Interplay between glucose and leptin signalling determines the strength of GABAergic synapses at POMC neurons," Nature Communications, Nature, vol. 6(1), pages 1-12, May.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms7618
    DOI: 10.1038/ncomms7618
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