Acute suppression, but not chronic genetic deficiency, of c-
            <i>fos</i>
            gene expression impairs long-term memory in aversive taste learning

Yasoshima, Yasunobu; Sako, Noritaka; Senba, Emiko; Yamamoto, Takashi

doi:10.1073/pnas.0600869103

Cited by 69 publications

(71 citation statements)

References 48 publications

(52 reference statements)

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“…However, the consensus is that GC is necessary for an effective acquisition of CTA (12). Approaches aimed to unravel the molecular machinery of taste learning established that GC is fundamental for the formation of short-and long-term aversion memories (35)(36)(37)(38)(39)(40). The changes we observed in the saccharin activated patterns between the control and the CTA rats might therefore be explained by a long-term retention of saccharin aversion.…”

Section: Discussionmentioning

confidence: 66%

Internal body state influences topographical plasticity of sensory representations in the rat gustatory cortex

Accolla

Carleton²

2008

Proc. Natl. Acad. Sci. U.S.A.

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Primary sensory cortices are remarkably organized in spatial maps according to specific sensory features of the stimuli. These cortical maps can undergo plastic rearrangements after changes in afferent (''bottom-up'') sensory inputs such as peripheral lesions or passive sensory experience. However, much less is known about the influence of ''top-down'' factors on cortical plasticity. Here, we studied the effect of a visceral malaise on taste representations in the gustatory cortex (GC). Using in vivo optical imaging, we showed that inducing conditioned taste aversion (CTA) to a sweet and pleasant stimulus induced plastic rearrangement of its cortical representation, becoming more similar to a bitter and unpleasant taste representation. Using a behavior task, we showed that changes in hedonic perception are directly related to the maps plasticity in the GC. Indeed imaging the animals after CTA extinction indicated that sweet and bitter representations were dissimilar. In conclusion, we showed that an internal state of malaise induces plastic reshaping in the GC associated to behavioral shift of the stimulus hedonic value. We propose that the GC not only encodes taste modality, intensity, and memory but extends its integrative properties to process also the stimulus hedonic value.chemical senses ͉ map plasticity ͉ taste coding

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Section: Discussionmentioning

confidence: 66%

Internal body state influences topographical plasticity of sensory representations in the rat gustatory cortex

Accolla

Carleton²

2008

Proc. Natl. Acad. Sci. U.S.A.

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“…Acute inhibition of Fos attenuates learning in mice and in invertebrate models such as Drosophila; AP-1 positively regulates developmental plasticity of motor neurons (Swank and Bernstein 1994;Sanyal et al 2002;Yasoshima et al 2006). Essential to the understanding of AP-1 activity in neurons is the knowledge of other proteins that influence AP-1 function or are downstream transcriptional targets.…”

Section: Discussionmentioning

confidence: 99%

“…Experimental demonstrations in diverse systems have verified the central role of AP-1 in controlling the development, growth, survival, and plasticity of neurons. These include learning behavior in rodents, developmental plasticity in insect models, and cocaine addiction in mammals, to name a few (Sanyal et al 2002;McClung and Nestler 2003;Yasoshima et al 2006). Despite this obvious centrality of AP-1 function in neurons, additional proteins that interact with and modulate AP-1 function in neurons remain largely unknown.…”

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confidence: 99%

Overexpression Screen in Drosophila Identifies Neuronal Roles of GSK-3β/shaggyas a Regulator of AP-1-Dependent Developmental Plasticity

et al. 2008

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AP-1, an immediate-early transcription factor comprising heterodimers of the Fos and Jun proteins, has been shown in several animal models, including Drosophila, to control neuronal development and plasticity. In spite of this important role, very little is known about additional proteins that regulate, cooperate with, or are downstream targets of AP-1 in neurons. Here, we outline results from an overexpression/misexpression screen in Drosophila to identify potential regulators of AP-1 function at third instar larval neuromuscular junction (NMJ) synapses. First, we utilize .4000 enhancer and promoter (EP) and EPgy2 lines to screen a large subset of Drosophila genes for their ability to modify an AP-1-dependent eye-growth phenotype. Of 303 initially identified genes, we use a set of selection criteria to arrive at 25 prioritized genes from the resulting collection of putative interactors. Of these, perturbations in 13 genes result in synaptic phenotypes. Finally, we show that one candidate, the GSK-3b-kinase homolog, shaggy, negatively influences AP-1-dependent synaptic growth, by modulating the Jun-Nterminal kinase pathway, and also regulates presynaptic neurotransmitter release at the larval neuromuscular junction. Other candidates identified in this screen provide a useful starting point to investigate genes that interact with AP-1 in vivo to regulate neuronal development and plasticity.

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“…Recruited downstream of Ca 2ϩ -dependent signaling pathways (7), Fos and Jun are required for encoding persistent forms of behavioral plasticity including aspects of drug addiction and memory (2,3,8,9). Indeed, stable expression of a Fos isoform in the striatum, observed after repeated cocaine exposure, underlies long-term sensitization to cocaine (3,8).…”

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confidence: 99%

Fos and Jun potentiate individual release sites and mobilize the reserve synaptic-vesicle pool at the Drosophila larval motor synapse

Kim

Kumar²,

Lin³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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In all nervous systems, short-term enhancement of transmitter release is achieved by increasing the weights of unitary synapses; in contrast, long-term enhancement, which requires nuclear gene expression, is generally thought to be mediated by the addition of new synaptic vesicle release sites. In Drosophila motor neurons, induction of AP-1, a heterodimer of Fos and Jun, induces cAMP-and CREB-dependent forms of presynaptic enhancement. Light and electron microscopic studies indicate that this synaptic enhancement is caused by increasing the weight of unitary synapses and not through the insertion of additional release sites. Electrophysiological and optical measurements of vesicle dynamics demonstrate that enhanced neurotransmitter release is accompanied by an increase in the actively cycling synaptic vesicle pool at the expense of the reserve pool. Finally, the observation that AP-1 mediated enhancement eliminates tetanus-induced forms of presynaptic potentiation suggests: (i) that reserve-pool mobilization is required for tetanus-induced short-term synaptic plasticity; and (ii) that long-term synaptic plasticity may, in some instances, be accomplished by stable recruitment of mechanisms that normally underlie short-term synaptic change. neuromuscular junction ͉ facilitation ͉ augmentation ͉ posttetanic potentiation

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Acute suppression, but not chronic genetic deficiency, of c- fos gene expression impairs long-term memory in aversive taste learning

Abstract: antisense oligodeoxynucleotide ͉ c-fos knockout mice ͉ amygdala ͉ conditioned taste aversion ͉ zif268

Cited by 69 publications

References 48 publications

Internal body state influences topographical plasticity of sensory representations in the rat gustatory cortex

Internal body state influences topographical plasticity of sensory representations in the rat gustatory cortex

Overexpression Screen in Drosophila Identifies Neuronal Roles of GSK-3β/shaggyas a Regulator of AP-1-Dependent Developmental Plasticity

Fos and Jun potentiate individual release sites and mobilize the reserve synaptic-vesicle pool at the Drosophila larval motor synapse

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