Sweet-bitter and umami-bitter taste interactions in single parabrachial neurons in C57BL/6J mice

Abstract

We investigated sweet-bitter and umami-bitter mixture taste interactions by presenting sucrose or umami stimuli mixed with quinine hydrochloride (QHCl) while recording single-unit activity of neurons in the parabrachial nucleus (PbN) of urethane-anesthetized C57BL/6J mice. A total of 70 taste-responsive neurons were classified according to which stimulus evoked the greatest net response (36 sucrose-best, 19 NaCl-best, 6 citric acid-best, and 9 QHCl-best). Although no neurons responded best to monopotassium glutamate (MPG) or inosine 5'-monophosphate (IMP), the combination of these two stimuli evoked a synergistic response (i.e., response > 120% of the sum of the component responses) in all sucrose-best and some NaCl-best neurons (n = 43). Adding QHCl to sucrose or MPG + IMP resulted in suppression of the response (responses to mixture < responses to the more effective component) in 41 of 43 synergistic neurons. Neurons showing QHCl suppression were classified into two types: an "MS1" type (n = 27) with suppressed responses both to sucrose and MPG + IMP and an "MS2" type (n = 14) that showed suppressed responses only to sucrose. No neuron displayed suppressed responses to MPG or IMP alone. The suppression ratio (1 - mixture response/sucrose or MPG + IMP response) of sucrose and MPG + IMP in MS1 neurons had a weak positive correlation (r = 0.36). The pattern of reconstructed recording sites of neuron types suggested chemotopic organization in the PbN. Although a peripheral basis for QHCl suppression has been demonstrated, our results suggest that convergence in the PbN plays a role in shaping responses to taste mixtures.

Why do we like sweet taste: A bitter tale?

“…As an example of central interactions between sweet and bitter taste, Kroeze & Bartoshuk [66] used a clever split tongue psychophysical technique to show that suppression of quinine hydrochloride bitterness by sucrose was due to interactions occurring in the brain. However, based on physiological evidence, Talavera et al [67] suggested that quinine hydrochloride is capable of suppressing sweet neural responses in mice by inhibiting currents that are necessary for the depolarization of taste receptor cells, suggesting a possible peripheral role for bitter suppression of sweet taste (see also [68–70]).…”

The Role of the Melanocortin System in Metabolic Disease: New Developments and Advances

“…The lateral PBN has been implicated in taste [93, 94], learned taste aversion [95], and appetite suppression in response to illness or nausea [96–99]. Inhibiting CGRP neurons reduces nausea and increases food intake during illness but does not increase feeding under standard conditions [55, 100].…”

Topographic organizations of taste-responsive neurons in the parabrachial nucleus of C57BL/6J mice: An electrophysiological mapping study

“…In two previous single-unit recording studies from our lab (Tokita et al, 2012; Tokita and Boughter, 2012) we collected taste responses from 52 and 70 PbN neurons, respectively. These sample sizes are similar to the other few published studies of mouse taste brainstem (NST) physiology using in vivo methods (e.g.…”

“…We combined these data with 122 neurons collected in our previous studies (Tokita et al, 2012; Tokita and Boughter, 2012). We included the fifth basic taste umami as one of the stimuli used in the present study, including both individual stimuli and a synergistic mix, as umami was typically omitted in previous electrophysiological mapping studies in the rat and hamster.…”