Brain-derived neurotrophic factor into adult neocortex strengthens a taste aversion memory

Martínez-Moreno, Araceli; Rodríguez-Durán, Luis F.; Escobar, Martha L.

doi:10.1016/j.bbr.2015.09.034

Cited by 8 publications

(2 citation statements)

References 24 publications

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“…Studies of the role of BDNF signaling in CTA acquisition, demonstrated CREB-dependent increases in the CeA and IC to occur 12 h following conditioning (Swank, 2000 ; Desmedt et al, 2003 ; Ma et al, 2011 ). BDNF infusion into the IC, previously known to revert CTA memory impairments induced by protein inhibition (Miguel-Gonzalez et al, 2008 ), was more recently shown to convert a weak CTA to a strong one when administered following training (Martinez-Moreno et al, 2016 ). The induction of BDNF transcription is thus likely to facilitate aversive taste memory formation through BLA-IC LTP, while BDNF protein expression in the IC appears to confer memory maintenance and stability of predicted CS-US associations.…”

Section: Learning and Re-learning In The Insulamentioning

confidence: 99%

The Insula and Taste Learning

Yiannakas

Rosenblum

2017

Front. Mol. Neurosci.

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The sense of taste is a key component of the sensory machinery, enabling the evaluation of both the safety as well as forming associations regarding the nutritional value of ingestible substances. Indicative of the salience of the modality, taste conditioning can be achieved in rodents upon a single pairing of a tastant with a chemical stimulus inducing malaise. This robust associative learning paradigm has been heavily linked with activity within the insular cortex (IC), among other regions, such as the amygdala and medial prefrontal cortex. A number of studies have demonstrated taste memory formation to be dependent on protein synthesis at the IC and to correlate with the induction of signaling cascades involved in synaptic plasticity. Taste learning has been shown to require the differential involvement of dopaminergic GABAergic, glutamatergic, muscarinic neurotransmission across an extended taste learning circuit. The subsequent activation of downstream protein kinases (ERK, CaMKII), transcription factors (CREB, Elk-1) and immediate early genes (c-fos, Arc), has been implicated in the regulation of the different phases of taste learning. This review discusses the relevant neurotransmission, molecular signaling pathways and genetic markers involved in novel and aversive taste learning, with a particular focus on the IC. Imaging and other studies in humans have implicated the IC in the pathophysiology of a number of cognitive disorders. We conclude that the IC participates in circuit-wide computations that modulate the interception and encoding of sensory information, as well as the formation of subjective internal representations that control the expression of motivated behaviors.

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Section: Learning and Re-learning In The Insulamentioning

confidence: 99%

The Insula and Taste Learning

Yiannakas

Rosenblum

2017

Front. Mol. Neurosci.

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“…Seventy-three male Wistar rats, weighing 360–390 g were prepared for the present study. Rats were individually caged and maintained on a 12:12 light–dark cycle at 22° C with water and food available ad libitum except where indicated (Martínez-Moreno et al, 2016 ). Experiments were performed in accordance with the Norma Oficial Mexicana and with the approval of the Animal care committee of the Faculty of Psychology of the National Autonomous University of Mexico.…”

Section: Methodsmentioning

confidence: 99%

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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