Once Bitten, Twice Shy: What Happens in the Brain When We Have Bad Experiences With Food

Summary: With the help of snails, researchers investigate the neural processes at work when we develop food aversions after eating a bad meal.

Source: University of Sussex

A negative experience with food usually leaves us unable to stomach the thought of eating that particular dish again. Using sugar-loving snails as models, researchers at the University of Sussex believe these bad experiences could be causing a switch in our brains, which impacts our future eating habits.

Like many other animals, snails like sugar and usually start feeding on it as soon as it is presented to them. But through aversive training which involved tapping the snails gently on the head when sugar appeared, the snails’ behaviour was altered and they refused to feed on the sugar, even when hungry.

When the team of Sussex Neuroscience researchers led by Dr Ildiko Kemenes looked a little closer, they discovered a neuronal mechanism that effectively reversed the snails’ usual response to sugar after the conditioning training had taken place.

Dr Ildiko Kemenes, Reader in Neuroscience in the University of Sussex’s School of Life Sciences, explained: “There’s a neuron in the snail’s brain which normally suppresses the feeding circuit. This is important, as the network is prone to becoming spontaneously activated, even in the absence of any food. By suppressing the feeding circuit, it ensures that the snail doesn’t just eat everything and anything. But when sugar or other food stimulus is present, this neuron becomes inhibited so that feeding can commence.

“After the aversive training, we found that this neuron reverses its electrical response to sugar and becomes excited instead of inhibited by it. Effectively, a switch has been flipped in the brain which means the snail no longer eats the sugar when presented with it, because sugar now suppresses rather than activates feeding.”

When researchers presented the trained snails with a piece of cucumber instead, they found that the animal was still happy to eat the healthy option – showing that the taps were associated with only the particular type of food they were trained to reject.

George Kemenes, Professor of Neuroscience at the University of Sussex and a senior member of the investigator team, added: “Snails provide us with a similar yet exceptionally basic model of how human brains work.

This shows a rotten, furry cheese burger
A negative experience with food usually leaves us unable to stomach the thought of eating that particular dish again. Image is in the public domain

“The effect of the inhibitory neuron which suppresses the feeding circuit in the snail is quite similar to how, in the human brain, cortical networks are under inhibitory control to avoid ‘runaway’ activation which may lead to overeating resulting in obesity.

“In our research, the negative experience the snail had with the sugar could be likened to eating a bad takeaway curry which then puts us off that particular dish in future.

“We believe that in a human brain, a similar switch could be happening where particular groups of neurons reverse their activity in line with the negative association of a particular food. “

The research, funded by the Biotechnology and Biological Sciences Research Council (BBSRC) and published in Current Biology, also revealed that when the neuron was removed entirely from trained snails, they returned to eating sugar again.

Dr Ildiko Kemenes said: “This suggests that the neuron is necessary for the expression of the learned behaviour and for altering the response to sugar.

“However, we cannot rule out that the sugar-activated sensory pathway also undergoes some changes, so we don’t make the assumption that this is all that’s happening in the brain.”

About this neuroscience research news

Source: University of Sussex
Contact: Stephanie Allen – University of Sussex
Image: The image is in the public domain

Original Research: Open access.
Interneuronal mechanisms for learning-induced switch in a sensory response that anticipates changes in behavioral outcomes” by Ildiko Kemenes et al. Current Biology


Interneuronal mechanisms for learning-induced switch in a sensory response that anticipates changes in behavioral outcomes


  • Anticipation of an aversive outcome reverses the behavioral response to food.
  • The switching mechanism relies on an interneuron extrinsic to the feeding network.
  • Aversive learning causes persistent physiological change in this interneuron.


Sensory cues in the natural environment predict reward or punishment, important for survival. For example, the ability to detect attractive tastes indicating palatable food is essential for foraging while the recognition of inedible substrates prevents harm. While some of these sensory responses are innate, they can undergo fundamental changes due to prior experience associated with the stimulus. However, the mechanisms underlying such behavioral switching of an innate sensory response at the neuron and network levels require further investigation. We used the model learning system of Lymnaea stagnalis to address the question of how an anticipated aversive outcome reverses the behavioral response to a previously effective feeding stimulus, sucrose. Key to the switching mechanism is an extrinsic inhibitory interneuron of the feeding network, PlB (pleural buccal), which is inhibited by sucrose to allow a feeding response. After multi-trial aversive associative conditioning, pairing sucrose with strong tactile stimuli to the head, PlB’s firing rate increases in response to sucrose application to the lips and the feeding response is suppressed; this learned response is reversed by the photoinactivation of a single PlB. A learning-induced persistent change in the cellular properties of PlB that results in an increase rather than a decrease in its firing rate in response to sucrose provides a neurophysiological mechanism for this behavioral switch. A key interneuron, PeD12 (Pedal-Dorsal 12), of the defensive withdrawal network does not mediate the conditioned suppression of feeding, but its facilitated output contributes to the sensitization of the withdrawal response.

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