ABSTRACT
This chapter summarizes the available data about taste receptor functions and their role in perception of food with emphasis on the human system. In addition we illuminate the widespread presence of these receptors throughout the body and discuss some of their extraoral functions. Finally, we describe clinical aspects where taste receptor signaling could be relevant.
Subject(s)
Receptors, G-Protein-Coupled/metabolism , Signal Transduction/physiology , Taste Buds/physiology , Taste/physiology , Animals , Brain/physiology , Humans , Smell/physiologyABSTRACT
Despite long and intense research, some fundamental questions regarding representation of taste information in the brain still remain unanswered. This might in part be due to shortcomings of the established methods that limit the researcher either to thorough characterization of few elements or to analyze the response of the entirety of neurons to only one stimulus. To overcome these restrictions, we evaluate the use of the immediate early gene Arc as a neuronal activity marker in the early neural structures of the taste pathway, the nodose/petrosal ganglion (NPG) and the nucleus of the solitary tract (NTS). Responses of NPG and NTS neurons were limited to substances that taste bitter to humans and are avoided by mice. Arc-expressing cells were concentrated in the rostromedial part of the dorsal NTS suggesting a role in gustatory processing. The use of Arc as a neuronal activity marker has several advantages, primarily the possibility to analyze the response of large numbers of neurons while using more than one stimulus makes Arc an interesting new tool for research in the early stages of taste processing.
Subject(s)
Aversive Agents/pharmacology , Cytoskeletal Proteins/metabolism , Gene Expression Regulation/drug effects , Nerve Tissue Proteins/metabolism , Nodose Ganglion/metabolism , Solitary Nucleus/metabolism , Taste/physiology , Animals , Brain Stem/metabolism , Brain Stem/pathology , Cytoskeletal Proteins/genetics , Image Processing, Computer-Assisted , Male , Mice , Mice, Inbred C57BL , Nerve Tissue Proteins/genetics , Nodose Ganglion/drug effects , Solitary Nucleus/drug effects , Sweetening Agents/pharmacologyABSTRACT
A region on mouse distal chromosome 1 (Chr. 1) that is highly enriched in quantitative trait loci (QTLs) controlling neural and behavioral phenotypes overlaps with the peak region of a major obesity QTL (Nob3.38), which we identified in an intercross of New Zealand Obese (NZO) mice with C57BL/6J (B6). By positional cloning we recently identified a microdeletion within this locus causing the disruption of Ifi202b that protects from adiposity by suppressing expression of 11ß-Hsd1. Here we show that the Nob3.38 segment also corresponds with the QTL rich region (Qrr1) on Chr. 1 and associates with increased voluntary running wheel activity, Rota-rod performance, decreased grip strength, and anxiety-related traits. The characterization of a subcongenic line carrying 14.2 Mbp of Nob3.38 with a polymorphic region of 4.4 Mbp indicates that the microdeletion and/or other polymorphisms in its proximity alter body weight, voluntary activity, and exploration. Since 27 out of 32 QTL were identified in crosses with B6, we hypothesized that the microdeletion and or adjacent SNPs are unique for B6 mice and responsible for some of the complex Qrr1-mediated effects. Indeed, a phylogenic study of 28 mouse strains revealed a NZO-like genotype for 22 and a B6-like genotype for NZW/LacJ and 4 other C57BL strains. Thus, we suggest that a Nob3.38 interval (173.0-177.4 Mbp) does not only modify adiposity but also neurobehavioral traits by a haplotype segregating with C57BL strains.
Subject(s)
Chromosomes, Mammalian/genetics , Obesity/genetics , Quantitative Trait Loci , Animals , Base Sequence , Behavior, Animal , Body Weight , Female , Gene Expression Regulation , Intracellular Signaling Peptides and Proteins/genetics , Male , Mice , Mice, Inbred C57BL , Mice, Obese , Molecular Sequence Data , Obesity/metabolism , Obesity/pathology , PhenotypeABSTRACT
Personal experience, learned eating behaviors, hormones, neurotransmitters, and genetic variations affect food consumption. The decision of what to eat is modulated by taste, olfaction, and oral textural perception. Taste, in particular, has an important input into food preference, permitting individuals to differentiate nutritive and harmful substances and to select nutrients. To be perceived as taste, gustatory stimuli have to contact specialized receptors and channels expressed in taste buds in the oral cavity. Gustatory information is then conveyed via afferent nerves to the central nervous system, which processes the gustatory information at different levels, resulting in stimulus recognition, integration with metabolic needs, and control of ingestive reflexes. This review discusses physiological factors influencing the decision of what to eat, spanning the bow from the recognition of the nutritive value of food in the oral cavity, over the feedback received after ingestion, to processing of gustatory information to the central nervous system.
