Brain mechanisms of taste aversion learning in the rat

Yamamoto, Takashi; Fujimoto, Yoshiyuki

doi:10.1016/0361-9230(91)90133-5

Cited by 129 publications

(78 citation statements)

References 20 publications

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“…The overall conclusions are still debated, and the results appear to depend on the type of lesion (whether surgical ablation, electrolytic, cytotoxic, or metabolic lesion), its location within the amygdala, its duration (permanent vs. transient), and its timing relative to training and testing. Although some investigations revealed no significant effects of certain amygdala lesions on CTA (Kemble et al 1979;Hatfield et al 1992;Galaverna et al 1993), in most studies, amygdala lesions, especially of the basolateral nucleus (Fitzgerald and Burton 1983;Simbayi et al 1986;Yamamoto and Fujimoto 1991;Roldan and Bures 1994;Yamamoto et al 1995), but also including the CeA (Lasiter andGlanzman 1982 1985;Roldan and Bures 1994), disrupted acquisition of CTA, its retrieval, or both. Roldan and Bures (1994) suggested that amygdaloid nuclei subserve CTA in the intact brain, but that their permanent absence can be compensated for by other brain centers.…”

Section: Discussionmentioning

confidence: 98%

Transient expression of c-Fos in rat amygdala during training is required for encoding conditioned taste aversion memory.

Lamprecht

Dudai²

1996

Learn. Mem.

136

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Local microinjection into rat amygdala of phosphorothioate modified oligodeoxynucleotides (ODNs) antisense to c-los several hours before conditioned taste aversion (CTA) training impaired taste aversion memory tested 3-5 days after conditioning. In contrast, injection of the antisense ODNs several days before training, before testing, or into the basal ganglia, or injection of c-fos sense ODNs, had no effect on CTA memory. Inhibition of translation by local microinjection of anisomycin into the amygdala shortly before as well as during CTA training, but not several days before training or shortly before testing, also impaired CTA memory. We conclude that translation in general, and c-Fos translation in particular, in the amygdala during or immediately after CTA training is essential for encoding taste aversion memory.

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Section: Discussionmentioning

confidence: 98%

Transient expression of c-Fos in rat amygdala during training is required for encoding conditioned taste aversion memory.

Lamprecht

Dudai²

1996

Learn. Mem.

136

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“…Early research favored a role for the GT in CTA acquisition (e.g., Lasiter, 1985;Loullis, Wayner, & Jolicoeur, 1978;Yamamoto, 1993;Yamamoto & Fujimoto, 1991;Yamamoto et al 1995). However, more recent research, using electrolytic lesions that caused minimal damage beyond the boundaries of the GT, finds no evidence that discrete GT lesions disrupt first-order CTA (e.g., Flynn, Grill, Schulkin, & Norgren, 1991;Grigson, Lyuboslavsky, & Tanase, 2000;Reilly & Pritchard, 1996).…”

Section: Discussionmentioning

confidence: 99%

C-fos expression in the rat brain following lithium chloride-induced illness

2007

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The present study examined c-Fos expression in selected brain areas consequent to administration of lithium chloride, the typical illness-inducing agent used in laboratory studies of conditioned taste aversion. The results replicated previous findings of significant c-Fos expression in the parabrachial nucleus, the central nucleus of the amygdala and the basolateral amygdala. New findings indicate significant lithium-induced c-Fos in the gustatory region of the thalamus and the bed nucleus of the stria terminalis but not in the insular cortex. The results are discussed with respect to the neural substrates of conditioned taste aversion.

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“…Several lines of evidence indicate that in adult rats, the amygdala plays a crucial role in both fear conditioning and odor-LiCl conditioning (Bermudez-Rattoni et al 1986;Ferry and Di Scala 1997;LeDoux 2000;Gale et al 2004;Touzani and Sclafani 2005). It should be noted that the basolateral complex of the amygdala is essential for odormalaise learning, although results are inconsistent for tastemalaise learning (Nachman and Ashe 1974;Burt and Smotherman 1980;Bermudez-Rattoni et al 1986;Dunn and Everitt 1988;Yamamoto and Fujimoto 1991;Kesner et al 1992;Sakai and Yamamoto 1999;Bahar et al 2004;Touzani and Sclafani 2005;Wilkins and Bernstein 2006).…”

Section: Amygdala Basolateral Complexmentioning

confidence: 99%

Ontogeny of odor-LiCl vs. odor-shock learning: Similar behaviors but divergent ages of functional amygdala emergence

Raineki¹,

Shionoya²,

Sander³

et al. 2009

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Both odor-preference and odor-aversion learning occur in perinatal pups before the maturation of brain structures that support this learning in adults. To characterize the development of odor learning, we compared three learning paradigms: (1) odor-LiCl (0.3M; 1% body weight, ip) and (2) odor-1.2-mA shock (hindlimb, 1sec)-both of which consistently produce odor-aversion learning throughout life and (3) odor-0.5-mA shock, which produces an odor preference in early life but an odor avoidance as pups mature. Pups were trained at postnatal day (PN) 7-8, 12-13, or 23-24, using odor-LiCl and two odor-shock conditioning paradigms of odor-0.5-mA shock and odor-1.2-mA shock. Here we show that in the youngest pups (PN7-8), odor-preference learning was associated with activity in the anterior piriform (olfactory) cortex, while odor-aversion learning was associated with activity in the posterior piriform cortex. At PN12-13, when all conditioning paradigms produced an odor aversion, the odor-0.5-mA shock, odor-1.2-mA shock, and odor-LiCl all continued producing learning-associated changes in the posterior piriform cortex. However, only odor-0.5-mA shock induced learning-associated changes within the basolateral amygdala. At weaning (PN23-24), all learning paradigms produced learning-associated changes in the posterior piriform cortex and basolateral amygdala complex. These results suggest at least two basic principles of the development of the neurobiology of learning: (1) Learning that appears similar throughout development can be supported by neural systems showing very robust developmental changes, and (2) the emergence of amygdala function depends on the learning protocol and reinforcement condition being assessed.Even in utero, infant rats rapidly learn to avoid odors paired with malaise (LiCl) as expressed by learning an odor aversion (Garcia et al. 1966(Garcia et al. , 1974Hennessey et al. 1976;Haroutunian and Campbell 1979;Smotherman 1982;Stickrod et al. 1982;Rudy and Cheatle 1983;Kucharski and Spear 1984;Smotherman and Robinson 1985, 1990;Alleva and Calamandrei 1986;Miller et al. 1990b; Best 1992, 1993;Richardson and McNally 2003;Gruest et al. 2004;Shionoya et al. 2006). In contrast to adult odor-LiCl learning, which relies on the amygdala (Touzani and Sclafani 2005), this early-life, odoraversion learning relies on the olfactory bulb until the pup approaches weaning age, when the amygdala is incorporated into the learning circuitry (Shionoya et al. 2006). In contrast, if infant rats receive an odor paired with a moderately painful stimulus (0.5-mA foot or tail shock, or tail pinch) the amygdala appears to be incorporated into this learning circuitry around postnatal day Here we expand assessment of the developing pups' odoraversion learning circuit by including the anterior and posterior piriform cortex, which have previously been demonstrated to be important for both pup and adult odor learning (Litaudon et al. 1997;Barkai and Saar 2001;Mouly et al. 2001;Mouly and Gervais 2002;Tronel and Sara 2002;Moriceau and Su...

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Brain mechanisms of taste aversion learning in the rat

Cited by 129 publications

References 20 publications

Transient expression of c-Fos in rat amygdala during training is required for encoding conditioned taste aversion memory.

Transient expression of c-Fos in rat amygdala during training is required for encoding conditioned taste aversion memory.

C-fos expression in the rat brain following lithium chloride-induced illness

Ontogeny of odor-LiCl vs. odor-shock learning: Similar behaviors but divergent ages of functional amygdala emergence

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