Conditioned hedonic responses elicited by contextual cues paired with nausea or with internal pain.

López, Matı́as; Dwyer, Dominic M.; Gasalla, Patricia

doi:10.1037/bne0000291

Cited by 6 publications

(5 citation statements)

References 34 publications

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“…The finding that rearing durations, a measure of healthy exploratory behavior [ 2 , 70 , 71 , 78 – 80 ], drop at approximately the same time is consistent with decades of work showing that poisoning-related behaviors, and specifically those brought on by systemic nausea, emerge (depending on dose) at roughly 10 to 15 min post administration [ 2 – 4 , 78 ]. In our hands, the emergence of this LiCl-induced behavioral change closely mirrors the change in GC μ power induced by the same LiCl dose, implicating the process whereby an animal experiences illness in generation of these neural changes.…”

Section: Discussionsupporting

confidence: 70%

LiCl-induced sickness modulates rat gustatory cortical responses

et al. 2022

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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 animal’s 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 (LFPs) from healthy rats and 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 7 to 12 Hz LFP power at approximately 12 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 visible in the entire sample, but focused on 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.

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Section: Discussionsupporting

confidence: 70%

LiCl-induced sickness modulates rat gustatory cortical responses

et al. 2022

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“…In both the literature and our current data, the latency of these changes in µ are strongly correlated with the appearance of illness-related behaviors [70]. We show that rearing durations, a measure of healthy exploratory behavior [2, 64, 65, 70-72], drop starting at approximately 12min post-LiCl injection. This finding is consistent with decades of work showing that poisoning-related behaviors, and specifically those brought on by systemic nausea, emerge (depending on dose) at roughly 10min post administration [2-4, 70].…”

Section: Discussionsupporting

confidence: 60%

“…We show that rearing durations, a measure of healthy exploratory behavior [2,64,65,[70][71][72], drop starting at approximately 12min post-LiCl injection. This finding is consistent with decades of work showing that poisoning-related behaviors, and specifically those brought on by systemic nausea, emerge (depending on dose) at roughly 10min post administration [2][3][4]70].…”

Section: Illness-related Changes In Taste Coding Occur In Single Neuronsmentioning

confidence: 99%

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

Stone

Lin

Mahmood

et al. 2022

Preprint

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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 animal’s 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.

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“…Instead, they show that claims for specialisation of central processes have been based on evidence that is no longer compelling. By contrast, recent work (main text) has provided positive evidence for specialisation of peripheral processes: for both flavour and non-flavour stimuli, illness, and pain elicit very different motor outputs [48,49].…”

Section: Box 1 Taste-aversion Learningmentioning

confidence: 90%

“…However, in addition to reduced consumption when the flavours are subsequently presented alone, LiCl-induced nausea results in orofacial reactions indicative of disgust, whereas hypertonic saline-based pain results in freezing indicative of fear. Crucially, these outcome-specific responses are also displayed with non-flavour cues that were previously paired with LiCl or hypertonic saline [49]. Therefore, there is indeed something special about aversion learning.…”

Section: Taste Aversionmentioning

confidence: 97%

Sinking In: The Peripheral Baldwinisation of Human Cognition

Heyes

Chater

Dwyer

2020

Trends in Cognitive Sciences

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The Baldwin effect is a hypothetical process in which a learned response to environmental change evolves a genetic basis. Modelling has shown that the Baldwin effect offers a plausible and elegant explanation for the emergence of complex behavioural traits, but there is little direct empirical evidence for its occurrence. We highlight experimental evidence of the Baldwin effect and argue that it acts preferentially on peripheral rather than on central cognitive processes. Careful scrutiny of research on taste-aversion and fear learning, language, and imitation indicates that their efficiency depends on adaptively specialised input and output processes: analogues of scanner and printer interfaces that feed information to core inference processes and structure their behavioural expression. Sinking InWhich features of the human mind, now genetically inherited, were once the products of learning? This question relates to the Baldwin effect (see Glossary)a process in which an initially learned response to environmental change acquires a genetic basis [1][2][3][4]. This process is also known, sometimes in a misleading way [5], as organic selection [1], genetic assimilation [6], and experiential canalization [7]. Whatever it is called, Baldwin's hypothesis postulates that, at the population level, learned characteristics can 'sink in'; they can become part of what offspring inherit organically from their parents.In the following we bring empirical research from cognitive science to bear on the hypothesis that some aspects of human cognition have sunk inthat they were initially learned and are now genetically inherited. We argue that there is good empirical evidence for this hypothesis regarding peripheral cognitive mechanisms (i.e., input or perceptual systems, and output or action systems, both modulated by attention and motivation), but not for the complex and interlocking central processes, involving inference and memory, that have durable effects on the relationships between perception and action [8] (Figure 1, Key Figure).After introducing the Baldwin effect, we next focus on preparedness [9,10]. For 50 years, experimental psychologists have investigated the preparedness of mechanisms involved in learning taste aversions and fears, and how these mechanisms have been specialised by evolution to do their jobs well. We argue that this research not only provides much-needed empirical evidence of Baldwinisation but also illuminates the targets of selection. Specifically, research on preparedness suggests that, across species, Baldwinisation has had a much greater impact on peripheral than on central cognitive mechanisms [11]. There has been genetic assimilation of learning-induced changes in perception, attention, motivation, and motor controlprocesses that modulate inputs to, and outputs from, the core inference processes of the brainbut little if any change to the structure of central processors themselves. We then extend the analysis to language and imitation, human faculties that are widely thought to have been gene...

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Conditioned hedonic responses elicited by contextual cues paired with nausea or with internal pain.

Cited by 6 publications

References 34 publications

LiCl-induced sickness modulates rat gustatory cortical responses

LiCl-induced sickness modulates rat gustatory cortical responses

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

Sinking In: The Peripheral Baldwinisation of Human Cognition

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