Different disruptive effects on the acquisition and expression of conditioned taste aversion by blockades of amygdalar ionotropic and metabotropic glutamatergic receptor subtypes in rats

Yasoshima, Yasunobu; Morimoto, Tadatsugu; Yamamoto, Takashi

doi:10.1016/s0006-8993(00)02397-0

Cited by 90 publications

(65 citation statements)

References 47 publications

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“…The results are very similar to our results obtained with independent groups (each stimulus measured in different animals); i.e., an increase in glutamate release only after the visceral stimulation (injection of LiCl) but not after saccharin drinking presentation in the two structures analyzed. These data are in agreement with other reports which suggest that the amygdala seems to be important during the latest associative phase between the gustatory and visceral stimulus in CTA (12,(20)(21)(22)(23)28). For instance, amygdala inactivation by tetrodotoxin before the gustatory stimulus presentation failed to prevent CTA acquisition, but its inactivation after the gustatory stimulus, or before the visceral stimulus presentation, disrupted the CTA (16).…”

Section: Discussionsupporting

confidence: 93%

“…However, tetrodotoxin inactivation of the amygdala after the gustatory stimulus, or before the visceral stimulus presentation, disrupts CTA memory formation (16). These results suggest that the amygdala does not play an important role in the initial processing of the taste signaling, but seems to be indispensable for processing the visceral stimulus (16,19).The finding that pharmacological manipulations, such as the injection of N-methyl-D-aspartate (NMDA) receptor antagonists into the IC or amygdala, disrupts CTA (2,12,(20)(21)(22)(23) suggests that glutamate release in these structures may be critically involved in taste aversion memory formation. However, these results provide only indirect evidence for the involvement of IC and amygdala glutamatergic activity in taste memory formation.…”

mentioning

confidence: 99%

“…The finding that pharmacological manipulations, such as the injection of N-methyl-D-aspartate (NMDA) receptor antagonists into the IC or amygdala, disrupts CTA (2,12,(20)(21)(22)(23) suggests that glutamate release in these structures may be critically involved in taste aversion memory formation. However, these results provide only indirect evidence for the involvement of IC and amygdala glutamatergic activity in taste memory formation.…”

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confidence: 99%

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Glutamatergic activity in the amygdala signals visceral input during taste memory formation

Miranda

Ferreira

Ramı́rez-Lugo

et al. 2002

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

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Conditioned taste aversion (CTA) is a learning paradigm in which an animal avoids a taste (conditioned stimulus) previously associated with visceral toxic effects [or unconditioned stimulus (US)]. Although many studies have implicated glutamate-mediated neurotransmission in memory consolidation of different types of learning tasks, including CTA, the exact role of this neurotransmitter system in memory formation is not known. Thus, we set out to determine whether glutamate mediates signaling of the US in CTA. We present evidence obtained by in vivo microdialysis that the US (i.p. injection of lithium chloride) induced a dramatic increase in glutamate release in the amygdala and a modest but significant release in the insular cortex. Moreover, CTA can be elicited by intra-amygdalar microinjections of glutamate; consequently, when glutamate is administered just before the presentation of a weak US, a clear CTA is induced. In contrast, the injection of glutamate alone or glutamate 2 h after the suboptimal US did not have any effect on the acquisition of CTA. These results indicate that glutamate activation of the amygdala can partially substitute the US in CTA, thus providing a clear indication that the amygdala conveys visceral information for this kind of memory.A number of studies (1-5) have implicated glutamatemediated transmission in consolidation of memory for different types of training, such as inhibitory avoidance, Morris water maze, and conditioned taste aversion (CTA). CTA is a learning paradigm in which the novel taste of food or drink (conditioned stimulus, CS) is paired with visceral signals of poisoning (unconditioned stimulus, US). Consequently, the animals avoid consuming the food or drink previously associated with toxic effects. CTA has unique properties; it is established after a single trial, permits long delays between stimuli presentation, and lasts for very long periods of time, even weeks. This feature makes it possible to separate the acquisition process into phases-CS presentation and US presentation-which can be studied independently under different experimental treatments (6).CTA is established by the interaction of brainstem, limbic, and neocortical structures underlying different phases of the acquisition storage and retrieval of gustatory memory (7). Among the structures involved in the initial phases of taste memory formation are the gustatory neocortex and amygdala (8). Thus, damage to either the gustatory insular cortex (IC) or amygdala in adult rats leads to impaired acquisition of CTA (6,7,[9][10][11][12][13][14][15][16][17]. However, the functional roles of IC and amygdala seem to be different during the phases of taste memory formation. Functional blockade of IC before taste presentation, but not between taste presentation and lithium chloride (LiCl) injection, blocks CTA (16, 18), suggesting that the gustatory cortex is involved in taste processing and͞or memory but is not necessary for processing the visceral signals of poisoning. Conversely, amygdala functional inactivation...

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Section: Discussionsupporting

confidence: 93%

mentioning

confidence: 99%

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confidence: 99%

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Glutamatergic activity in the amygdala signals visceral input during taste memory formation

Miranda

Ferreira

Ramı́rez-Lugo

et al. 2002

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

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“…In addition, the 2B subunit of the NMDA receptor in the gustatory cortex undergoes tyrosine phosphorylation when rats drink a novel taste solution (Rosenblum et al, 1997), suggesting that posttranslational modification of NMDA receptor may also be important during the association of a novel taste and a toxic effect. Although the amygdala is also a critical site for CTA function, blockade of NMDA receptor in the amygdala does not attenuate CTA learning as consistently as blockade in the gustatory cortex (Ferry and Di Scala, 2000;Hatfield and Gallagher, 1995;Tucci et al, 1998;Yasoshima et al, 2000).…”

Section: Introductionmentioning

confidence: 94%

d-Cycloserine enhances conditioned taste aversion learning in rats

Nunnink

Davenport

Ortega

et al. 2007

Pharmacology Biochemistry and Behavior

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Conditioned taste aversion (CTA) is a form of associative learning in which the pairing of a taste with a toxin causes an animal to avoid the taste. NMDA receptor mediated neurotransmission has been implicated in CTA, but the role of the NMDA receptor glycine-binding site has not been examined. To examine the effects on CTA of the glycinergic NMDA receptor agonist D-cycloserine, rats received D-cycloserine (15 mg/kg, i.p.) or vehicle 15 min before 10-min access to 0.125% saccharin, followed by a low dose of LiCl (19 mg/kg, i.p.). CTA was measured with 24-h, 2-bottle preference tests between water and saccharin. Vehicle-treated rats formed a mild CTA that rapidly extinguished, while D-cycloserine-treated rats formed a stronger CTA that extinguished slowly. The effect of D-cycloserine was specific to the NMDA receptor glycine-binding site, because pretreatment with HA-966 (6 mg/kg), a partial glycinergic agonist, blocked enhancement by Dcycloserine. Three follow-up experiments suggest that the enhancement of CTA was not due to an aversive effect of D-cycloserine. First, saccharin paired with D-cycloserine (15 mg/kg) alone did not induce a CTA, although a higher dose (30 mg/kg) did significantly lower saccharin preference. Second, pretreatment with D-cycloserine did not increase the duration of "lying-on-belly" behavior induced by LiCl. Third, pretreatment with D-cycloserine did not increase c-Fos induction by either LiCl or vehicle injection in central visceral relays (the nucleus of the solitary tract, the parabrachial nucleus, the central nucleus of the amygdala, the supraoptic nucleus, and the paraventricular nucleus). These results confirm the participation of NMDA receptor, and specifically the glycine-binding site of NMDA receptor, in CTA learning.

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“…Furthermore, BLA lesions may impair taste neophobia [150] and arousal-induced taste neophobia, as well as passive avoidance [149]. Pharmacological BLA manipulations suggest a modulatory role in CTA after novel taste presentation, during visceral malaise and its association with the taste [193][194][195][196][197].…”

Section: The Role Of the Amygdala In Taste Functionmentioning

confidence: 99%