scholarly journals Insula to mPFC reciprocal connectivity differentially underlies novel taste neophobic response and learning

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Haneen Kayyal ◽  
Sailendrakumar Kolatt Chandran ◽  
Adonis Yiannakas ◽  
Nathaniel Gould ◽  
Mohammad Khamaisy ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Sensory Information ◽  
Insular Cortex ◽  
Memory Formation ◽  
Intrinsic Properties ◽  
Insight Into ◽  
Taste Experience ◽  
Neophobic Response

To survive in an ever-changing environment, animals must detect and learn salient information. The anterior insular cortex (aIC) and medial prefrontal cortex (mPFC) are heavily implicated in salience and novelty processing, and specifically, the processing of taste sensory information. Here, we examined the role of aIC-mPFC reciprocal connectivity in novel taste neophobia and memory formation, in mice. Using pERK and neuronal intrinsic properties as markers for neuronal activation, and retrograde AAV (rAAV) constructs for connectivity, we demonstrate a correlation between aIC-mPFC activity and novel taste experience. Furthermore, by expressing inhibitory chemogenetic receptors in these projections, we show that aIC-to-mPFC activity is necessary for both taste neophobia and its attenuation. However, activity within mPFC-to-aIC projections is essential only for the neophobic reaction but not for the learning process. These results provide an insight into the cortical circuitry needed to detect, react to- and learn salient stimuli, a process critically involved in psychiatric disorders.

scholarly journals Insula to mPFC reciprocal connectivity differentially underlies novel taste neophobic response and learning

2021 ◽  
Author(s):  
Haneen Kayyal ◽  
Sailendrakumar Kolatt Chandran ◽  
Adonis Yiannakas ◽  
Nathaniel Gould ◽  
Mohammad Khamaisy ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Sensory Information ◽  
Insular Cortex ◽  
Memory Formation ◽  
Intrinsic Properties ◽  
Insight Into ◽  
Taste Experience ◽  
Neophobic Response

To survive in an ever-changing environment, animals must detect and learn salient information. The anterior insular cortex (aIC) and medial prefrontal cortex (mPFC) are heavily implicated in salience and novelty processing, and specifically, the processing of taste sensory information. Here, we examined the role of aIC-mPFC reciprocal connectivity in novel taste neophobia and memory formation, in mice. Using pERK and neuronal intrinsic properties as markers for neuronal activation, and retrograde AAV (rAAV) constructs for connectivity, we demonstrate a correlation between aIC-mPFC activity and novel taste experience. Furthermore, by expressing inhibitory chemogenetic receptors in these projections, we show that aIC-to-mPFC activity is necessary for both taste neophobia and its attenuation. However, activity within mPFC-to-aIC projections is essential only for the neophobic reaction but not for the learning process. These results provide an insight into the cortical circuitry needed to detect, react to- and learn salient stimuli, a process critically involved in psychiatric disorders.

scholarly journals The Medial Prefrontal Cortex and Fear Memory: Dynamics, Connectivity, and Engrams

2021 ◽  
Vol 22 (22) ◽  
pp. 12113
Author(s):  
Lucie Dixsaut ◽  
Johannes Gräff
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Memory Formation ◽  
Memory Storage ◽  
Long Term Memory ◽  
Brain Areas ◽  
Long Term Storage ◽  
And Storage

It is becoming increasingly apparent that long-term memory formation relies on a distributed network of brain areas. While the hippocampus has been at the center of attention for decades, it is now clear that other regions, in particular the medial prefrontal cortex (mPFC), are taking an active part as well. Recent evidence suggests that the mPFC—traditionally implicated in the long-term storage of memories—is already critical for the early phases of memory formation such as encoding. In this review, we summarize these findings, relate them to the functional importance of the mPFC connectivity, and discuss the role of the mPFC during memory consolidation with respect to the different theories of memory storage. Owing to its high functional connectivity to other brain areas subserving memory formation and storage, the mPFC emerges as a central hub across the lifetime of a memory, although much still remains to be discovered.

scholarly journals Modulation of Memory Formation by Stimulus Content: Specific Role of the Medial Prefrontal Cortex in the Successful Encoding of Social Pictures

2007 ◽  
Vol 19 (2) ◽  
pp. 351-362 ◽  
Author(s):  
Philippe-Olivier Harvey ◽  
Philippe Fossati ◽  
Martin Lepage
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Brain Activity ◽  
Imaging Study ◽  
Memory Formation ◽  
Analytical Strategy ◽  
Stimulus Content ◽  
Variable Contribution ◽  
The Brain

It is unclear whether the involvement of the medial prefrontal cortex (mPFC) during encoding is restricted to the evaluative processing of to-be-encoded stimuli or if it is instead actively engaged during memory formation. The difficulty of assessing the contribution of the mPFC to encoding based on previous neuroimaging studies partly arises from the use of several types of stimuli, such as emotional or social ones. These different types of stimulus content could differently modulate mPFC activity during memory formation and thus partly explain the variable contribution of this region to encoding. Using emotional/neutral and social/nonsocial pictures, we conducted an event-related functional magnetic resonance imaging study using a subsequent memory paradigm as the main analytical strategy. We observed that the brain activity in the dorsal and orbital mPFC is significantly and specifically predictive of the successful encoding of social compared with nonsocial pictures. In contrast, the activity in the amygdala specifically predicts the successful encoding of emotional compared with neutral pictures. The modulation of the mPFC by social information in a memory encoding context could be associated with the initiation of self-referential processes whose contribution is to enhance memory formation.

Amyloid-β Protein Precursor Deficiency Changes Neuronal Electrical Activity and Levels of Mitochondrial Proteins in the Medial Prefrontal Cortex

2021 ◽  
pp. 1-14
Author(s):  
Qingwei Huo ◽  
Sidra Tabassum ◽  
Ming Chen ◽  
Mengyao Sun ◽  
Yueming Deng ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Amyloid Β ◽  
Neuronal Firing ◽  
Mitochondrial Proteins ◽  
Amyloid Β Protein ◽  
Protein Precursor ◽  
Β Protein ◽  
Neuronal Electrical Activity

Background: Neuropathological features of Alzheimer’s disease are characterized by the deposition of amyloid-β (Aβ) plaques and impairments in synaptic activity and memory. However, we know little about the physiological role of amyloid-β protein precursor (AβPP) from which Aβ derives. Objective: Evaluate APP deficiency induced alterations in neuronal electrical activity and mitochondrial protein expression. Methods: Utilizing electrophysiological, biochemical, pharmacological, and behavioral tests, we revealed aberrant local field potential (LFP), extracellular neuronal firing and levels of mitochondrial proteins. Result: We show that APP knockout (APP -/- ) leads to increased gamma oscillations in the medial prefrontal cortex (mPFC) at 1-2 months old, which can be restored by baclofen (Bac), a γ-aminobutyric acid type B receptor (GABABR) agonist. A higher dose and longer exposure time is required for Bac to suppress neuronal firing in APP -/-  mice than in wild type animals, indicating enhanced GABABR mediated activity in the mPFC of APP -/-  mice. In line with increased GABABR function, the glutamine synthetase inhibitor, L-methionine sulfonate, significantly increases GABABR levels in the mPFC of APP -/-  mice and this is associated with a significantly lower incidence of death. The results suggest that APP -/-  mice developed stronger GABABR mediated inhibition. Using HEK 293 as an expression system, we uncover that AβPP functions to suppress GABABR expression. Furthermore, APP -/-  mice show abnormal expression of several mitochondrial proteins. Conclusion: APP deficiency leads to both abnormal network activity involving defected GABABR and mitochondrial dysfunction, suggesting critical role of AβPP in synaptic and network function.

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