• M Sugita, K Yamamoto, C Hirono, and Y Shiba.
• Department of Physiology and Oral Physiology, Institute of Biomedical & Health Sciences, Hiroshima University, Kasumi 1-2-3, Minami-ku, Hiroshima 734-8553, Japan. Electronic address: sugisan@hiroshima-u.ac.jp.
• Neuroscience. 2013 Oct 10;250:166-80.

AbstractBitter reception is mediated by taste receptor cells that coexpress multiple T2Rs, a family of G-protein-coupled receptors. However, it remains elusive how bitter taste information is translated in the brain into appropriate behavioral responses. Here we used a combination of genetic tracing and electrophysiological and immunohistochemical analyses in mice to functionally characterize the neurons in the solitary tract nuclei of the medulla, which receive input from mT2R5-expressing cells. The neurons defined by a transneuronal tracer originating from mT2R5-expressing cells receive glutamatergic synaptic input via the AMPA receptor. The satiety peptide cholecystokinin increases glutamatergic transmission, suggesting an interaction between information processing of taste and the homeostatic control of feeding. Nevertheless, the tracer-labeled neuron types are heterogeneous, and can be classified into catecholamine and pro-opiomelanocortin neurons. Our data reveal that the architectural solution in the first-order central relay that processes information from mT2R5-expressing cells uses unique ensembles of neurons with different neurotransmitters.Copyright © 2013 IBRO. Published by Elsevier Ltd. All rights reserved.

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