Conditioned taste aversion prevents the long-lasting BDNF-induced enhancement of synaptic transmission in the insular cortex: A metaplastic effect

Rivera-Olvera, Alejandro; Rodríguez-Durán, Luis F.; Escobar, Martha L.

doi:10.1016/j.nlm.2016.01.014

Cited by 17 publications

(8 citation statements)

References 56 publications

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“…Electrophysiological recordings were performed in anesthetized rats as previously described (Escobar et al, 1998a ; Rodríguez-Durán et al, 2011 ; Rivera-Olvera et al, 2016 ). Briefly, rats were anesthetized with pentobarbital (50 mg/kg i.p.).…”

Section: Methodsmentioning

confidence: 99%

“…As previously described (Rivera-Olvera et al, 2016 ), 7 days after surgery animals were trained to drink water twice a day from a graduated cylinder, during 10 min trials for 3 days. On the acquisition session, water was replaced by a saccharin solution 0.1% (Sigma, St. Louis, MO), and 10 min later, animals were intraperitoneally injected with LiCl (0.15 M; 7.5 ml/kg).…”

Section: Methodsmentioning

confidence: 99%

“…The insular cortex (IC) is a region of the temporal neocortex implicated in the acquisition and storage of conditioned taste aversion (CTA). CTA is a well-established learning and memory paradigm in which an animal acquires aversion to a novel taste when it is associated with nausea (Bernstein and Koh, 2007 ; Bermúdez-Rattoni, 2014 ; Rivera-Olvera et al, 2016 ). Previous studies demonstrated that high frequency stimulation of the basolateral amygdaloid nucleus (Bla) elicits LTP in the IC (Escobar et al, 1998a , b ; Jones et al, 1999 ).…”

Section: Introductionmentioning

confidence: 99%

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CaMKII Requirement for in Vivo Insular Cortex LTP Maintenance and CTA Memory Persistence

2017

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Calcium-calmodulin/dependent protein kinase II (CaMKII) plays an essential role in LTP induction, but since it has the capacity to remain persistently activated even after the decay of external stimuli it has been proposed that it can also be necessary for LTP maintenance and therefore for memory persistence. It has been shown that basolateral amygdaloid nucleus (Bla) stimulation induces long-term potentiation (LTP) in the insular cortex (IC), a neocortical region implicated in the acquisition and retention of conditioned taste aversion (CTA). Our previous studies have demonstrated that induction of LTP in the Bla-IC pathway before CTA training increased the retention of this task. Although it is known that IC-LTP induction and CTA consolidation share similar molecular mechanisms, little is known about the molecular actors that underlie their maintenance. The purpose of the present study was to evaluate the role of CaMKII in the maintenance of in vivo Bla-IC LTP as well as in the persistence of CTA long-term memory (LTM). Our results show that acute microinfusion of myr-CaMKIINtide, a selective inhibitor of CaMKII, in the IC of adult rats during the late-phase of in vivo Bla-IC LTP blocked its maintenance. Moreover, the intracortical inhibition of CaMKII 24 h after CTA acquisition impairs CTA-LTM persistence. Together these results indicate that CaMKII is a central key component for the maintenance of neocortical synaptic plasticity as well as for persistence of CTA-LTM.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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CaMKII Requirement for in Vivo Insular Cortex LTP Maintenance and CTA Memory Persistence

2017

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“…The neural plasticity mechanisms related to taste learning, including CTA, also involve other molecular sequences. The expression of brain-derived neurotrophic factor (BDNF) in the gustatory insular cortex (and the basolateral amygdala) induces long-term synaptic plasticity, and the acquisition of taste aversions seems to block the long-lasting BDNF-induced strengthening of synaptic plasticity [71]. These findings point to the BDNF gene expression in the gustatory insular cortex as one of the molecular mechanisms critically involved in the long-term synaptic plasticity processes related to taste memory.…”

Section: Molecular Mechanisms Of Ctamentioning

confidence: 99%

“…Thus, taste learning and taste memory consolidation have been related to specific protein expression in the gustatory insular cortex [65][66][67]. Gene expression of BDNF in the gustatory insular cortex and basolateral amygdala has been described during the long-term synaptic plasticity associated with taste aversion memory [71]. Receptor expression is another plasticity process necessary for the acquisition of CTA.…”

Section: Molecular Mechanisms Of Ctamentioning

confidence: 99%

Taste Processing: Insights from Animal Models

Molero‐Chamizo

Rivera-Urbina

2020

Molecules

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Taste processing is an adaptive mechanism involving complex physiological, motivational and cognitive processes. Animal models have provided relevant data about the neuroanatomical and neurobiological components of taste processing. From these models, two important domains of taste responses are described in this review. The first part focuses on the neuroanatomical and neurophysiological bases of olfactory and taste processing. The second part describes the biological and behavioral characteristics of taste learning, with an emphasis on conditioned taste aversion as a key process for the survival and health of many species, including humans.

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Tongue−Brain‐Transported ZnO Nanoparticles Induce Abnormal Taste Perception

Chen

Wang

Kang

et al. 2023

Adv Healthcare Materials

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Nanoparticles (NPs) can be transported to the brain, especially through nerves, because of their small size and high biological activity. Previous studies confirmed that zinc oxide (ZnO) NPs can enter the brain through the tongue−brain pathway, but it is unclear whether they will further affect synaptic transmission and brain perception. In this study, it is found that tongue−brain‐transported ZnO NPs can cause a decrease in taste sensitivity and taste aversion learning ability, indicating abnormal taste perception. Moreover, the release of miniature excitatory postsynaptic currents, the frequency of action potential release, and the expression of c‐fos are decreased, suggesting that the synaptic transmission is reduced. To further explore the mechanism, protein chip detection of inflammatory factors is carried out and it is found that neuroinflammation occurs. Importantly, it is found that neuroinflammation originated from neurons. The JAK‐STAT signaling pathway is activated, which inhibits the Neurexin1‐PSD95‐Neurologigin1 pathway and c‐fos expression. Blocking the activation of the JAK‐STAT pathway prevents neuroinflammation and the reduction in Neurexin1‐PSD95‐Neurologigin1. These results indicate that ZnO NPs can be transported by the tongue−brain pathway and lead to abnormal taste perception by neuroinflammation‐induced deficits in synaptic transmission. The study reveals the influence of ZnO NPs on neuronal function and provides a novel mechanism.

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Conditioned taste aversion prevents the long-lasting BDNF-induced enhancement of synaptic transmission in the insular cortex: A metaplastic effect

Cited by 17 publications

References 56 publications

CaMKII Requirement for in Vivo Insular Cortex LTP Maintenance and CTA Memory Persistence

CaMKII Requirement for in Vivo Insular Cortex LTP Maintenance and CTA Memory Persistence

Taste Processing: Insights from Animal Models

Tongue−Brain‐Transported ZnO Nanoparticles Induce Abnormal Taste Perception

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