Physostigmine and norepinephrine: Effects of injection into the amygdala on taste associations

Ellis, Maureen E.; Kesner, Raymond P.

doi:10.1016/0031-9384(81)90258-4

Cited by 31 publications

(9 citation statements)

References 32 publications

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“…Our results indicate that blockade of cholinergic muscarinic receptors but not NMDA or AMPA receptors in the perirhinal cortex impaired taste recognition memory as well as conditioned taste aversion. It is well known that the amygdala is important for learned taste aversion, neophobia, and attenuation of neophobia (Ellis and Kesner 1981;Yasoshima et al 2000). Because the amygdala is anatomically close to perirhinal cortex (see Fig.…”

Section: Discussionmentioning

confidence: 99%

Perirhinal Cortex Muscarinic Receptor Blockade Impairs Taste Recognition Memory Formation

Gutiérrez¹,

Cruz²,

Rodriguez‐Ortiz³

et al. 2004

Learn. Mem.

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The relevance of perirhinal cortical cholinergic and glutamatergic neurotransmission for taste recognition memory and learned taste aversion was assessed by microinfusions of muscarinic (scopolamine), NMDA (AP-5), and AMPA (NBQX) receptor antagonists. Infusions of scopolamine, but not AP5 or NBQX, prevented the consolidation of taste recognition memory using attenuation of neophobia as an index. In addition, learned taste aversion in both shortand long-term memory tests was exclusively impaired by scopolamine. These data provide neurochemical support for the theory that cholinergic activity of the perirhinal cortex participates in the formation of the taste memory trace and that it is independent of the NMDA and AMPA receptor activity. These results support the idea that cholinergic neurotransmission in the perirhinal cortex is also essential for acquisition and consolidation of taste recognition memory.

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Section: Discussionmentioning

confidence: 99%

Perirhinal Cortex Muscarinic Receptor Blockade Impairs Taste Recognition Memory Formation

Gutiérrez¹,

Cruz²,

Rodriguez‐Ortiz³

et al. 2004

Learn. Mem.

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“…These results contrast with our failure to find effects on neophobia. A possible explanation is that taste neophobia would be mediated mainly by subcortical and limbic structures, whereas AN would require both subcortical (Kesner & Berman, 1977; Ellis & Kesner, 1981; Hernadi et al ., 1997) and cortical components (Buresova & Bures, 1980).…”

Section: Discussionmentioning

confidence: 99%

Blockade of cortical muscarinic but not NMDA receptors prevents a novel taste from becoming familiar

Gutiérrez

Téllez

Bermúdez‐Rattoni

2003

Eur J of Neuroscience

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Exposure to a novel taste solution in the rat is followed by a decrease in its intake known as neophobia. This effect gradually disappears, and consumption increases from the second presentation of the taste (attenuation of neophobia), reflecting that the animal learned that it is safe to drink it. Conversely, if gastric malaise is induced after first intake, the rat will develop a long-lasting aversion (conditioned taste aversion). Previous attempts to elucidate the physiological nature of taste memory trace stems only from procedures that require malaise to measure taste memory. Here we assess the relevance of both muscarinic and N-methyl-d-aspartate receptors, known to be involved in conditioned taste aversion, on taste memory using a nonaversive procedure (attenuation of neophobia learning). Attenuation of neophobia was impaired by the muscarinic receptor antagonist, scopolamine, microinjected 20 min before, immediately after or up to 2 h after the first taste experience, suggesting that muscarinic receptors are involved in the acquisition and consolidation of attenuation of neophobia learning. However, the N-methyl-d-aspartate receptor antagonist, d,l-2-amino-5-phosphonovaleric acid, did not affect attenuation of neophobia even when the same dose of the drug was able to disrupt conditioned taste aversion learning, which suggests that attenuation of neophobia learning would be independent of N-methyl-d-aspartate receptors activity in the insular cortex. The neophobic response induced by strong saccharin presentation was not affected by either of the treatments given, which rules out any impairment in taste perception. These results indicate that while cortical muscarinic receptors are important in the formation and consolidation of safe memory trace, N-methyl-d-aspartate receptor activity appears to be noncritical.

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“…Findings of experiments by Kesner (Kesner et al, 1983;Ellis et al, 1981) and Gallagher (Gallagher et al, 1981) were the first to suggest that the noradrenergic system of the amygdala is involved in influencing memory consolidation. A ß-adrenoceptor antagonist administered into the amygdala post-training was shown to impair memory, while concurrent infusion of norepinephrine blocked this memory impairment (Gallagher et al, 1981).…”

Section: Evidence For a Modulatory Role Of The Amygdala In Rodentsmentioning

confidence: 99%

How the amygdala affects emotional memory by altering brain network properties

Hermans

Battaglia

Atsak

et al. 2014

Neurobiology of Learning and Memory

136

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The amygdala has long been known to play a key role in supporting memory for emotionally arousing experiences. For example, classical fear conditioning depends on neural plasticity within this anterior medial temporal lobe region. Beneficial effects of emotional arousal on memory, however, are not restricted to simple associative learning. Our recollection of emotional experiences often includes rich representations of, e.g., spatiotemporal context, visceral states, and stimulus-response associations. Critically, such memory features are known to bear heavily on regions elsewhere in the brain. These observations led to the modulation account of amygdala function, which postulates that amygdala activation enhances memory consolidation by facilitating neural plasticity and information storage processes in its target regions. Rodent work in past decades has identified the most important brain regions and neurochemical processes involved in these modulatory actions, and neuropsychological and neuroimaging work in humans has produced a large body of convergent data. Importantly, recent methodological developments make it increasingly realistic to monitor neural interactions underlying such modulatory effects as they unfold. For instance, functional connectivity network modeling in humans has demonstrated how information exchanges between the amygdala and specific target regions occur within the context of large-scale neural network interactions. Furthermore, electrophysiological and optogenetic techniques in rodents are beginning to make it possible to quantify and even manipulate such interactions with millisecond precision. In this paper we will discuss that these developments will likely lead to an updated view of the amygdala as a critical nexus within large-scale networks supporting different aspects of memory processing for emotionally arousing experiences.

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Physostigmine and norepinephrine: Effects of injection into the amygdala on taste associations

Cited by 31 publications

References 32 publications

Perirhinal Cortex Muscarinic Receptor Blockade Impairs Taste Recognition Memory Formation

Perirhinal Cortex Muscarinic Receptor Blockade Impairs Taste Recognition Memory Formation

Blockade of cortical muscarinic but not NMDA receptors prevents a novel taste from becoming familiar

How the amygdala affects emotional memory by altering brain network properties

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