Leptin excites enteric neurons of guinea-pig submucous and myenteric plexus

Authors

Errata

This article is corrected by:

  1. Errata: Corrigendum Volume 23, Issue 7, 691, Article first published online: 17 June 2011

Address for Correspondence
Michael Schemann, Lehrstuhl für Humanbiologie, Technische Universität München, Liesel-Beckmann-Straße 4, 85350 Freising-Weihenstephan, Germany.
Tel: +49 (0) 8161 71 54 83; fax: +49 (0) 8161 71 57 85;
e-mail: schemann@wzw.tum.de

Abstract

Background  Leptin, one of the most prominent mediators released from adipocytes, influences neuronal activity in the central nervous system. The enteric nervous system (ENS) expresses leptin receptors but consequence of activation of these receptors on enteric neuron activity has not been systematically studied. An adipocyte-ENS axis is suggested by close apposition between enteric nerves and adipocytes. The aim of this study was to investigate the effects of leptin on guinea-pig submucous and myenteric neurons.

Methods  Using voltage sensitive dye imaging, we recorded neural responses to application of leptin (0.0625 nmol L−1) in myenteric and submucous neurons, nicotine (10 μmol L−1) served as a reference for neuronal excitation. Mucosal ion secretion and muscle activity were measured in vitro with Ussing and organ bath techniques, respectively.

Key Results  Leptin induced spike discharge in 13.6% of submucous neurons and in 8.2% of myenteric neurons (1.1 ± 0.9 and 1.2 ± 1.0 Hz, respectively). Although there was an overlap of nicotine and leptin responses, 38.5% of submucous and 25% of myenteric neurons activated by leptin did not respond to nicotine. Leptin did not inhibit ongoing spike discharge or fast excitatory postsynaptic potentials. Leptin (0.0625 nmol L−1) did not affect mucosal secretion or muscle activity suggesting a subtle modulatory action of leptin at the level of the ENS.

Conclusions & Inferences  Leptin activates submucous and myenteric neurons indicating relevance for adipocyte-ENS signaling. These results set the basis for further studies to reveal the functional correlate of the neural action of leptin in the ENS.

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