Conditioned taste aversion in rats with excitotoxic brain lesions

@article{Yamamoto1995ConditionedTA,
  title={Conditioned taste aversion in rats with excitotoxic brain lesions},
  author={Takashi Yamamoto and Yoshiyuki Fujimoto and Tsuyoshi Shimura and Nobuyuki Sakai},
  journal={Neuroscience Research},
  year={1995},
  volume={22},
  pages={31-49}
}

Conditioned taste aversion as a learning and memory paradigm

Role of the gustatory thalamus in taste learning

Brain regions responsible for the expression of conditioned taste aversion in rats.

TLDR
Among a variety of brain regions including the parabrachial nucleus, amygdala, insular cortex, supramammillary nucleus, nucleus accumbens, and ventral pallidum that are involved in different phases of CTA expression, the enhanced taste sensitivity and hedonic shift, from positive to negative, may originate in the basolateral nucleus of the amygdala.

Involvement of the insular cortex in retention of conditioned taste aversion is not time dependent

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References

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Brain stem mechanisms of conditioned taste aversion learning in rats.

TLDR
It is concluded that the parabrachial nuclei and the adjacent reticular formation probably represent the neural substrate of the permanent CTA engram the protracted consolidation of which is disrupted by prolonged cessation of impulse which is disrupt by prolonged stopping of impulse activity in the information storing network.

Thalamocortical relations in taste aversion learning: II. Involvement of the medial ventrobasal thalamic complex in taste aversion learning.

TLDR
Results of Experiment 2 demonstrated that animals lacking VBm thalamus and the olfactory bulbs could not acquire aversions to ingested LiCl following eight conditioning trials, demonstrating that destruction of VBM thalamic nuclei is sufficient to prevent CTA learning.

Parabrachial nucleus lesions and conditioned taste aversion: evidence supporting an associative deficit.

TLDR
The results demonstrate that the disruption of CTA in lesioned rats cannot be ascribed to an inability to process either gustatory or visceral afferent information per se and suggest that PBN-lesioned rats are unable to form a specific association between gustatory and visceral cues.

Ibotenate lesions of the hippocampus enhance latent inhibition in conditioned taste aversion and increase resistance to extinction in conditioned taste preference.

TLDR
The influence of the neurotoxic lesion on LI is in the opposite direction to the effect typically found following hippocampal damage induced by traditional methods, which presents challenges for most current theories of hippocampal function.

Double dissociations of the effects of amygdala and insular cortex lesions on conditioned taste aversion, passive avoidance, and neophobia in the rat using the excitotoxin ibotenic acid.

TLDR
The results show that the insular cortex is involved in reactions to the novelty and associative salience exclusively of taste stimuli, whereas the amygdala is probably more concerned with the reaction to more general aspects of novelty in the environment and in fear-motivated behavior.
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