Medial temporal lobe structures participate differentially in consolidation of safe and aversive taste memories

Cruz, Vanesa De la; Rodriguez‐Ortiz, Carlos J.; Balderas, Israela; Bermúdez-Rattoni, Federico

doi:10.1111/j.1460-9568.2008.06432.x

Cited by 36 publications

(22 citation statements)

References 40 publications

(45 reference statements)

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“…The IC is suggested to be important in recognition whether the taste is familiar or novel (Gutiérrez et al, 2003; Bahar et al, 2004b). More recent studies suggested that attenuation of neophobia depends not only on the IC (Rodriguez-Ortiz et al, 2005), but also hippocampus and perirhinal cortex (De la Cruz et al, 2008). …”

Section: Flavor Preferencementioning

confidence: 99%

Brain Mechanisms of Flavor Learning

Yamamoto¹,

Ueji²

2011

Front. Syst. Neurosci.

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Once the flavor of the ingested food (conditioned stimulus, CS) is associated with a preferable (e.g., good taste or nutritive satisfaction) or aversive (e.g., malaise with displeasure) signal (unconditioned stimulus, US), animals react to its subsequent exposure by increasing or decreasing ingestion to the food. These two types of association learning (preference learning vs. aversion learning) are known as classical conditioned reactions which are basic learning and memory phenomena, leading selection of food and proper food intake. Since the perception of flavor is generated by interaction of taste and odor during food intake, taste and/or odor are mainly associated with bodily signals in the flavor learning. After briefly reviewing flavor learning in general, brain mechanisms of conditioned taste aversion is described in more detail. The CS–US association leading to long-term potentiation in the amygdala, especially in its basolateral nucleus, is the basis of establishment of conditioned taste aversion. The novelty of the CS detected by the cortical gustatory area may be supportive in CS–US association. After the association, CS input is conveyed through the amygdala to different brain regions including the hippocampus for contextual fear formation, to the supramammillary and thalamic paraventricular nuclei for stressful anxiety or memory dependent fearful or stressful emotion, to the reward system to induce aversive expression to the CS, or hedonic shift from positive to negative, and to the CS-responsive neurons in the gustatory system to enhance the responsiveness to facilitate to detect the harmful stimulus.

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Section: Flavor Preferencementioning

confidence: 99%

Brain Mechanisms of Flavor Learning

Yamamoto¹,

Ueji²

2011

Front. Syst. Neurosci.

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“…This is in line with its unique anatomical connections (Figure 1), through which it receives multimodal sensory inputs, including visceral, gustatory, and somatosensory information from sensory thalamic nuclei (Fujita et al, 2010). However, other brain regions, such as the basolateral amygdala (Bla) and dorsal hippocampus, have been shown to be activated during novel taste processing (Yefet et al, 2006; Doron and Rosenblum, 2010), and also to be necessary for safe taste–memory consolidation (De la Cruz et al, 2008). Most of the studies of the molecular mechanisms underlying taste memory were performed in mice and rats, therefore, the present review will focus on these studies.…”

Section: Introductionmentioning

confidence: 99%

Molecular Mechanisms Underlying Memory Consolidation of Taste Information in the Cortex

Gal-Ben-Ari¹,

Rosenblum²

2012

Front. Behav. Neurosci.

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The senses of taste and odor are both chemical senses. However, whereas an organism can detect an odor at a relatively long distance from its source, taste serves as the ultimate proximate gatekeeper of food intake: it helps in avoiding poisons and consuming beneficial substances. The automatic reaction to a given taste has been developed during evolution and is well adapted to conditions that may occur with high probability during the lifetime of an organism. However, in addition to this automatic reaction, animals can learn and remember tastes, together with their positive or negative values, with high precision and in light of minimal experience. This ability of mammalians to learn and remember tastes has been studied extensively in rodents through application of reasonably simple and well defined behavioral paradigms. The learning process follows a temporal continuum similar to those of other memories: acquisition, consolidation, retrieval, relearning, and reconsolidation. Moreover, inhibiting protein synthesis in the gustatory cortex (GC) specifically affects the consolidation phase of taste memory, i.e., the transformation of short- to long-term memory, in keeping with the general biochemical definition of memory consolidation. This review aims to present a general background of taste learning, and to focus on recent findings regarding the molecular mechanisms underlying taste–memory consolidation in the GC. Specifically, the roles of neurotransmitters, neuromodulators, immediate early genes, and translation regulation are addressed.

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“…: Martinez et al ,1981; Davis & Squire, 1984; Dudai, 2002; Kandel, 2001; Alberini, 2008; Gold, 2008; Desgranges et al , 2008; De la Cruz, et al , 2008). Previous results show that intra-amygdala injections of anisomycin impair synaptic plasticity within the amygdala (Huang & Kandel, 2007) and impair fear conditioning (Schafe & Ledoux, 2000; Parsons et al , 2006; Maren et al , 2003).…”

Section: Discussionmentioning

confidence: 99%

“…The findings of experiments in which protein synthesis inhibitors injected directly into the amygdala impair memory have generally been interpreted as revealing a role for training-initiated protein synthesis important for the formation of new memories (Duvarci et al , 2005; Nader et al , 2000a,b; Milekic et al , 2007; Cammarota et al , 2004; Izquierdo et al , 2002; Schafe & LeDoux, 2000; Chai et al , 2006), an interpretation common to similar tests of other brain areas as well (Rossato et al , 2007; De la Cruz et al , 2008; Desgranges et al , 2008; Izquierdo et al , 1992; Morris et al , 2006). When trained on fear conditioning tasks in particular, the interpretation is often that protein synthesis is necessary at a primary site of neural plasticity essential for memory formation (Duvarci et al , 2005; Maren et al , 2003; Nader, 2003; Nader et al , 2003a,b); Schafe & LeDoux, 2000), although the evidence for the amygdala as the primary site of memory storage for fear conditioning appears to be unconvincing (Weinberger, 2010).…”

Section: Discussionmentioning

confidence: 99%

Lidocaine attenuates anisomycin-induced amnesia and release of norepinephrine in the amygdala

Sadowski

Canal

Gold

2011

Neurobiology of Learning and Memory

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When administered near the time of training, protein synthesis inhibitors such as anisomycin impair later memory. A common interpretation of these findings is that memory consolidation requires new protein synthesis initiated by training. However, recent findings support an alternative interpretation that abnormally large increases in neurotransmitter release after injections of anisomycin may be responsible for producing amnesia. In the present study, a local anesthetic was administered prior to anisomycin injections in an attempt to mitigate neurotransmitter actions and thereby attenuate the resulting amnesia. Rats received lidocaine and anisomycin injections into the amygdala 130 and 120 min, respectively, prior to inhibitory avoidance training. Memory tests 48 hr later revealed that lidocaine attenuated anisomycin-induced amnesia. In other rats, in vivo microdialysis was performed at the site of amygdala infusion of lidocaine and anisomycin. As seen previously, anisomycin injections produced large increases in release of norepinephrine in the amygdala. Lidocaine attenuated the anisomycin-induced increase in release of norepinephrine but did not reverse anisomycin inhibition of protein synthesis, as assessed by c-Fos immunohistochemistry. These findings are consistent with past evidence suggesting that anisomycin causes amnesia by initiating abnormal release of neurotransmitters in response to the inhibition of protein synthesis.

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Medial temporal lobe structures participate differentially in consolidation of safe and aversive taste memories

Cited by 36 publications

References 40 publications

Brain Mechanisms of Flavor Learning

Brain Mechanisms of Flavor Learning

Molecular Mechanisms Underlying Memory Consolidation of Taste Information in the Cortex

Lidocaine attenuates anisomycin-induced amnesia and release of norepinephrine in the amygdala

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