Correlation Between Activation of the Prelimbic Cortex, Basolateral Amygdala, and Agranular Insular Cortex During Taste Memory Formation

Background It has been reported that bilateral lesions of the basolateral amygdala complex (BLA) blocked propofol-induced amnesia of inhibitory avoidance (IA) training. Based on these results, the authors hypothesized that the amnesia effect of propofol was partly due to its impairment of memory formation in the hippocampus through activating the BLA gamma-aminobutyric acid type A receptor function. The authors determined the changes in activity-regulated cytoskeleton-associated protein (Arc) expression to be an indicator of IA memory formation. Methods Male Sprague-Dawley rats received bilateral injection of bicuculline methiodide (10, 50, or 100 pmol/0.5 microl) or saline (0.5 microl) into the BLA. Fifteen minutes later, the rats were intraperitoneally injected with either propofol (25 mg/kg) or saline. After 5 min, the one-trial IA training was conducted. Rats intraperitoneally infused with saline served as controls and only received saline injections into the BLA. Twenty-four hours later, the IA retention latency was tested. Separate groups of rats treated the same way were killed either 30 min after IA training for hippocampal Arc mRNA measurement or after 45 min for protein level quantification. Results The largest dose of bicuculline methiodide (100 pmol) not only blocked the propofol-induced amnesia but also reversed the inhibition effect of propofol on Arc protein expression in the hippocampus (P < 0.05). However, the mRNA level of Arc showed no significant changes after propofol and bicuculline methiodide administration. Conclusions The amnesic effect of propofol seems to involve the modulation of Arc protein expression in the hippocampus, occurring through a network interaction with the BLA.

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Withdrawal from chronic ethanol exposure increases postsynaptic glutamate function of insular cortex projections to the rat basolateral amygdala

Neuropharmacology ◽

10.1016/j.neuropharm.2020.108129 ◽

2020 ◽

Vol 172 ◽

pp. 108129 ◽

Cited By ~ 4

Author(s):

Molly M. McGinnis ◽

Brian C. Parrish ◽

Brian A. McCool

Keyword(s):

Basolateral Amygdala ◽

Insular Cortex ◽

Ethanol Exposure ◽

Chronic Ethanol ◽

Chronic Ethanol Exposure

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Linking emotional valence and anxiety in a mouse insula-amygdala circuit

10.21203/rs.3.rs-964107/v1 ◽

2021 ◽

Author(s):

Céline Nicolas ◽

Anes Ju ◽

Yifan Wu ◽

Hazim Eldirdiri ◽

Sebastien Delcasso ◽

...

Keyword(s):

Basolateral Amygdala ◽

Ex Vivo ◽

Insular Cortex ◽

Emotional Valence ◽

Projection Neurons ◽

Negative Valence ◽

Glutamatergic Neurons ◽

Related Information ◽

Starting Point ◽

Positive And Negative Valence

Abstract The response of the insular cortex (IC) and amygdala to stimuli of positive and negative valence were found to be altered in patients with anxiety disorders. However, the coding properties of neurons controlling anxiety and valence remain unknown. Combining photometry recordings and chemogenetics in mice, we uncover the anxiogenic control of projection neurons in the anterior IC (aIC), independently of their projection target. Using viral tracing and ex vivo electrophysiology, we characterize the monosynaptic aIC to the basolateral amygdala (BLA) connection, and employed projection-specific optogenetics, to reveal anxiogenic properties of aIC-BLA neurons in anxiety-related behaviors. Finally, using photometry recordings, we identified that aIC-BLA neurons are active in anxiogenic spaces, and in response to aversive stimuli. Together, these findings show that negative valence, as well as anxiety-related information and behaviors, are encoded by aICBLA glutamatergic neurons, providing a starting point to understand how alterations of this pathway contribute to psychiatric disorders.

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Molecular Signals into the Insular Cortex and Amygdala During Aversive Gustatory Memory Formation

Cellular and Molecular Neurobiology ◽

10.1023/b:cemn.0000012722.45805.c8 ◽

2004 ◽

Vol 24 (1) ◽

pp. 25-36 ◽

Cited By ~ 44

Author(s):

Federico Bermúdez-Rattoni ◽

Leticia Ramírez-Lugo ◽

Ranier Gutiérrez ◽

María Isabel Miranda

Keyword(s):

Insular Cortex ◽

Memory Formation ◽

Molecular Signals

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Basolateral amygdala glutamatergic activation enhances taste aversion through NMDA receptor activation in the insular cortex

European Journal of Neuroscience ◽

10.1111/j.1460-9568.2005.04440.x ◽

2005 ◽

Vol 22 (10) ◽

pp. 2596-2604 ◽

Cited By ~ 46

Author(s):

G. Ferreira ◽

M.I. Miranda ◽

V. Cruz ◽

C.J. Rodríguez-Ortiz ◽

F. Bermúdez-Rattoni

Keyword(s):

Nmda Receptor ◽

Taste Aversion ◽

Basolateral Amygdala ◽

Insular Cortex ◽

Receptor Activation ◽

Nmda Receptor Activation

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The forgotten insular cortex: Its role on recognition memory formation

Neurobiology of Learning and Memory ◽

10.1016/j.nlm.2014.01.001 ◽

2014 ◽

Vol 109 ◽

pp. 207-216 ◽

Cited By ~ 71

Author(s):

Federico Bermudez-Rattoni

Keyword(s):

Recognition Memory ◽

Insular Cortex ◽

Memory Formation

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Glucocorticoid enhancement of recognition memory via basolateral amygdala-driven facilitation of prelimbic cortex interactions

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1901513116 ◽

2019 ◽

Vol 116 (14) ◽

pp. 7077-7082 ◽

Cited By ~ 9

Author(s):

Areg Barsegyan ◽

Gabriele Mirone ◽

Giacomo Ronzoni ◽

Chunan Guo ◽

Qi Song ◽

...

Keyword(s):

Object Recognition ◽

Recognition Memory ◽

Memory Consolidation ◽

Basolateral Amygdala ◽

Emotional Arousal ◽

Brain Regions ◽

Prelimbic Cortex ◽

Stress Hormone ◽

Functional Connections ◽

Functional Interactions

Extensive evidence indicates that the basolateral amygdala (BLA) interacts with other brain regions in mediating stress hormone and emotional arousal effects on memory consolidation. Brain activation studies have shown that arousing conditions lead to the activation of large-scale neural networks and several functional connections between brain regions beyond the BLA. Whether such distal interactions on memory consolidation also depend on BLA activity is not as yet known. We investigated, in male Sprague–Dawley rats, whether BLA activity enables prelimbic cortex (PrL) interactions with the anterior insular cortex (aIC) and dorsal hippocampus (dHPC) in regulating glucocorticoid effects on different components of object recognition memory. The glucocorticoid receptor (GR) agonist RU 28362 administered into the PrL, but not infralimbic cortex, immediately after object recognition training enhanced 24-hour memory of both the identity and location of the object via functional interactions with the aIC and dHPC, respectively. Importantly, posttraining inactivation of the BLA by the noradrenergic antagonist propranolol abolished the effect of GR agonist administration into the PrL on memory enhancement of both the identity and location of the object. BLA inactivation by propranolol also blocked the effect of GR agonist administration into the PrL on inducing changes in neuronal activity within the aIC and dHPC during the postlearning consolidation period as well as on structural changes in spine morphology assessed 24 hours later. These findings provide evidence that BLA noradrenergic activity enables functional interactions between the PrL and the aIC and dHPC in regulating stress hormone and emotional arousal effects on memory.

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