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Stone, B. T.

Publications and source records attributed to Stone, B. T..

4 recordsLinked to original sources

Changes in taste palatability across the estrous cycle are modulated by hypothalamic estradiol signaling

Food intake varies across the stages of a rats estrous cycle. It is reasonable to hypothesize that this cyclic fluctuation in consumption reflects an impact of hormones on taste palatability/preference, but evidence for this hypothesis has been mixed, and critical within-subject experiments in which rats sample multiple tastes during each of the four main estrous phases (metestrus, diestrus, proestrus, and estrus) have been scarce. Here, we assayed licking for pleasant (sucrose, NaCl, saccharin) and aversive (quinine-HCl, citric acid) tastes each day for 5-10 days while tracking rats estrous cycles through vaginal cytology. Initial analyses confirmed the previously-described increased consumption of pleasant stimuli 24-48 hours following the time of high estradiol. A closer look, however, revealed this effect to reflect a general magnification of palatability--higher than normal preferences for pleasant tastes and lower than normal preferences for aversive tastes--during metestrus. We hypothesized that this phenomenon might be related to estradiol processing in the lateral hypothalamus (LH), and tested this hypothesis by inhibiting LH estrogen receptor activity with ICI182,780 during tasting. Control infusions replicated the metestrus magnification of palatability pattern; ICI infusions blocked this effect as predicted, but failed to render preferences "cycle free," instead delaying the palatability magnification until diestrus. Clearly, estrous phase mediates details of taste palatability in a manner involving hypothalamic actions of estradiol; further work will be needed to explain the lack of a flat response across the cycle with hypothalamic estradiol binding inhibited, a result which perhaps suggests dynamic interplay between brain regions or hormones. Significance StatementConsummatory behaviors are impacted by many variables, including naturally circulating hormones. While it is clear that consumption is particularly high during the stages following the high-estradiol stage of the rodents estrous (and human menstrual) cycle, it is as of yet unclear whether this phenomenon reflects cycle stage-specific palatability (i.e., whether pleasant tastes are particularly delicious, and aversive tastes particularly disgusting, at particular phases). Here we show that palatability is indeed modulated by estrous phase, and that this effect is governed, at least in part, by the action of estradiol within the lateral hypothalamus. These findings shed light on the mechanisms underlying the adverse impact on human welfare due to irregularities observed across the otherwise cyclic menstrual process.

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Experience-induced drift in the neural coding of individual differences in perception

As is true in humans, no two rodents prefer precisely the same tastes. Furthermore, no one rodent keeps precisely the same taste preferences forever. Here, we have made use of this between- and within-animal variability to generate and test novel hypotheses about the stability and malleability of neural perceptual coding. We used a brief-access task (BAT) to reveal both individual differences in taste preferences and shifting preferences within individual rats (quantified in terms of lick bout lengths). We moved on to show that these phenomena are not simply random variation: first, by demonstrating that gustatory cortical (GC) taste response dynamics, the late part of which reflect palatability, match that individual rat's BAT preferences (evaluated almost 2 weeks prior) better than canonical preference patterns; that is, individual differences in preferences reflect differences in neural taste processing. This match, however, links neural taste processing only to the most recent BAT session--GC palatability processing does not reflect performance in earlier BAT sessions. We hypothesized that any tasting experience might impact taste processing (i.e., not just BAT licking), and tested this hypothesis by adding a second session of GC taste-response recordings; palatability-epoch taste responses in this later session no longer matched the most recent pre-recording BAT session, demonstrating that responses following the first electrophysiology session had changed. Together, these data demonstrate that every tasting experience (regardless of the method of taste delivery) changes the rat's processing of those tastes.

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Early life stress impairs VTA coordination of BLA network and behavioral states

Motivated behaviors, such as social interactions, are governed by the interplay between mesocorticolimbic structures, such as the ventral tegmental area (VTA), basolateral amygdala (BLA), and medial prefrontal cortex (mPFC). Adverse childhood experiences and early life stress (ELS) can impact these networks and behaviors, which is associated with increased risk for psychiatric illnesses. While it is known that the VTA projects to both the BLA and mPFC, the influence of these inputs on local network activity which govern behavioral states - and whether ELS impacts VTA-mediated network communication - remains unknown. Our study demonstrates that VTA inputs influence BLA oscillations and mPFC activity, and that ELS weakens the ability of the VTA to coordinate BLA network states, likely due to ELS-induced impairments in dopamine signaling between the VTA and BLA. Consequently, ELS mice exhibit increased social avoidance, which can be recapitulated in control mice by inhibiting VTA-BLA communication. These data suggest that ELS impacts social reward via the VTA-BLA dopamine network.

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LiCl-induced sickness modulates spontaneous activity and response dynamics in rat gustatory cortex.

Gustatory Cortex (GC), a structure deeply involved in the making of consumption decisions, presumably performs this function by integrating information about taste, experiences, and internal states related to the animals health, such as illness. Here, we investigated this assertion, examining whether illness is represented in GC activity, and how this representation impacts taste responses and behavior. We recorded GC single-neuron activity and local field potentials (LFP) from healthy rats and (the same) rats made ill (via LiCl injection). We show (consistent with the extant literature) that the onset of illness-related behaviors arises contemporaneously with alterations in spontaneous 7-12Hz LFP power at [~]11 min following injection. This process was accompanied by reductions in single-neuron taste response magnitudes and discriminability, and with enhancements in palatability-relatedness - a result reflecting the collapse of responses toward a simple "good-bad" code arising in a specific subset of GC neurons. Overall, our data show that a state (illness) that profoundly reduces consumption changes basic properties of the sensory cortical response to tastes, in a manner that can easily explain illness impact on consumption. Significance StatementNeural responses in primary sensory cortex are often thought to faithfully represent physical stimuli, and while recent studies (including ours) have challenged this view by documenting enhancements and decrements in stimulus-induced firing related to animals internal states, there has been little work setting these changes in any sort of functional, mechanistic context. Here we show that a state (illness) that profoundly reduces consumption changes basic properties of the sensory cortical response to tastes, and then go beyond this to precisely characterize this response plasticity, connecting it to the specific perceptual changes that drive illness impact on consumption.

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