Different disruptive effects on the acquisition and expression of conditioned taste aversion by blockades of amygdalar ionotropic and metabotropic glutamatergic receptor subtypes in rats
ABSTRACT Conditioned taste aversion (CTA) is based on the gustatory long-term memory established after association of the taste of food (conditioned stimulus, CS) with visceral signals of poisoning (unconditioned stimulus, US). After the acquisition of CTA, hedonics of the taste CS changes from positive to negative as indicated by reduced ingestive and increased aversive taste reactivities in response to re-exposures to the CS. We examined the effects of reversible and selective blockades of the amygdalar glutamate receptor subtypes, AMPA, NMDA and metabotropic glutamate receptors, on the formation of CTA. Blockades of each of the three receptor subtypes between ingestion of saccharin (CS) and malaise-inducing LiCl (US) disrupted the acquisition of CTA. After the acquisition of CTA, however, blockades of only AMPA receptors, but not NMDA or metabotropic receptors, impaired the expression of CTA. This effect was seen only during the period when the antagonistic action to AMPA receptors lasted. These results indicate that both ionotropic and metabotropic glutamate receptor subtypes in the amygdala are indispensable for the acquisition of CTA, but that the expression of acquired CTA is mediated only by AMPA receptors. The present results also suggest that the amygdalar glutamatergic neural transmission is involved in the formation and storage of long-term gustatory memory associated with the altered hedonics from positive to negative.
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ABSTRACT: Cortical glutamatergic activity is known to be important for memory formation in different learning tasks. For example, glutamate activity in the insular cortex plays an important role in aversive taste memory formation by signaling the unconditioned stimulus. However, the role of glutamate in the insular cortex in appetitive taste learning has remained poorly studied. Therefore, we considered the function of glutamate in attenuation of neophobia, a model of appetitive taste recognition memory. For this purpose, we performed infusions of vehicle, glutamate, a specific mGluR1 antagonist (AIDA) or a combination of glutamate and AIDA at 0 or 30minutes, and glutamate or vehicle at 60minutes after novel saccharin consumption. Glutamate infusion impaired appetitive taste recognition memory when infused at 0 or 30minutes, whereas, AIDA infusions produced enhanced appetitive memory at the same infusion times. Furthermore, when glutamate and AIDA were infused together no effect on attenuation of neophobia was observed. As opposed to shorter infusion times, the administration of glutamate 60minutes after the presentation of the saccharin consumption was ineffective in the impairment of the appetitive taste memory. These results are discussed in view of the effect of glutamate and its mGluR1 during the appetitive taste recognition memory formation in the insular cortex. Copyright © 2015. Published by Elsevier B.V.Behavioural Brain Research 02/2015; 284. DOI:10.1016/j.bbr.2015.02.020 · 3.39 Impact Factor
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ABSTRACT: Nerve injury induces long-term changes in neuronal activity in the primary somatosensory cortex (S1), which has often been implicated as the origin of sensory dysfunction. However, the cellular mechanisms underlying this phenomenon remain unclear. C-fos is an immediate early gene, which has been shown to play an instrumental role in plasticity. By developing a new platform to image real-time changes in gene expression in vivo, we investigated whether injury modulates the levels of c-fos in layer V of S1, since previous studies have suggested that these neurons are particularly susceptible to injury. The yellow fluorescent protein, ZsYellow1, under the regulation of the c-fos promoter, was expressed throughout the rat brain. A fiber-based confocal microscope that enabled deep brain imaging was utilized, and local field potentials were collected simultaneously. In the weeks following limb denervation in adult rats (n = 10), sensory stimulation of the intact limb induced significant increases in c-fos gene expression in cells located in S1, both contralateral (affected, 27.6 ± 3 cells) and ipsilateral (8.6 ± 3 cells) to the injury, compared to controls (n = 10, 13.4 ± 3 and 1.0 ± 1, respectively, p value <0.05). Thus, we demonstrated that injury activates cellular mechanisms that are involved in reshaping neuronal connections, and this may translate to neurorehabilitative potential.Journal of Molecular Neuroscience 06/2014; 54(4). DOI:10.1007/s12031-014-0347-y · 2.76 Impact Factor
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ABSTRACT: There are a number of experiments showing an important involvement of amygdala N-methyl-D-aspartate (NMDA) glutamate receptors on consolidation of conditioned taste aversion (CTA) memory. Interestingly, recent evidence has shown that α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamate receptors are particularly involved in CTA retrieval. Memory reconsolidation has been proposed as a destabilization and re-stabilization process induced by memory reactivation. We have recently suggested that reconsolidation could be enabled in the absence of retrieval. Hence, we decided to analyze the participation of AMPA and NMDA receptors of the central (CeA) and basolateral amygdala (BLA) in CTA memory retrieval and reconsolidation. To do so, we tested whether administrations of an AMPA receptor blocker (NBQX) or an NMDA receptor blocker (APV) 15 min before a second acquisition trial could have effects on taste aversion. We found that administration of NBQX in the BLA blocked retrieval, whereas APV blocked reconsolidation in the BLA, and consolidation in the CeA. When we administered both NBQX and APV into the BLA before the second acquisition trial, results showed impairment of both retrieval and reconsolidation. These results further support the idea that reconsolidation is independent of retrieval, since retrieval blockade in the BLA did not impair memory reconsolidation. These results suggest that glutamate receptors have different participation on retrieval and reconsolidation of CTA and further support the hypothesis that these two processes could be independent.Neurobiology of Learning and Memory 05/2014; DOI:10.1016/j.nlm.2014.03.003 · 4.04 Impact Factor