scholarly journals The Role of the Medial Prefrontal Cortex in Regulating Social Familiarity-Induced Anxiolysis

2013 ◽  
Vol 39 (4) ◽  
pp. 1009-1019 ◽  
Author(s):  
Elizabeth A Lungwitz ◽  
Garret D Stuber ◽  
Philip L Johnson ◽  
Amy D Dietrich ◽  
Nicole Schartz ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Social Familiarity

scholarly journals Assessing the Role of Projections from the Ventral Hippocampus (vHIP) to the Medial Prefrontal Cortex (mPFC) in the Neural Circuitry of Social Familiarity-induced Anxiolysis (SoFiA) using Gi-DREADDs

2020 ◽  
Vol 3 ◽  
Author(s):  
M. Regina Barron ◽  
William Truitt
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Social Memory ◽  
Neural Circuitry ◽  
Ventral Hippocampus ◽  
Designer Drugs ◽  
Axon Terminals ◽  
Social Familiarity ◽  
Adenovirus Receptor

The social interaction habituation (SI-hab) protocol has been used to demonstrate that rats acquire Social Familiarity-induced Anxiolysis (SoFiA), a form of safety learning where rats display anxiolysis in the presence of a familiar conspecific. SoFiA acquisition and expression can be simplified into four different constructs: social memory, anxiety, safety learning and anxiolysis. The neural circuitry of SoFiA; however, has not been fully identified. As a step towards elucidating the SoFiA neural circuitry we are identifying the role of projections from the ventral hippocampus (vHIP) to the medial prefrontal cortex (mPFC) in SoFiA acquisition.   Prior work from our lab has shown that the mPFC is needed for acquisition and expression of SoFiA. The mPFC may be the location of convergence of anxiety and social memory processing, making it a loci for safety learning. The goal of the current work is to identify the inputs to the mPFC that are pivotal for SoFiA acquisition. vHIP has been implicated in social memory and projects to the mPFC leading to the hypothesis that SoFiA acquisition requires vHIP projections to mPFC.  This hypothesis will be tested via intersectional genetics where neural tracts are selectively targeted through viruses. One virus is introduced at the soma of the neuron, and another is introduced at the end of the axon. The first virus, adeno-associated virus 8 (AAV8) will contain Cre-dependent code for an inhibitory DREADD (designer receptors exclusively activated by designer drugs.) The second virus, canine adenovirus 2 (CAV2) is picked up by axon terminals and transported to the soma where it will express Cre. Unfortunately, the uptake and transport of these viruses require specific receptors and the vHIP-mPFC pathway has poor CAV2 uptake. CAV2 levels will be increased by the introduction of Coxsackievirus and Adenovirus receptor (CAR) via AAV8 two weeks prior to CAV2-Cre injection.  

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.

The Role of the Medial Prefrontal Cortex in Moderating Neural Representations of Self and Other in Primates

2021 ◽  
Vol 44 (1) ◽  
Author(s):  
Masaki Isoda
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Critical Role ◽  
Autism Spectrum ◽  
Annual Review ◽  
Publication Date ◽  
Self And Other ◽  
Neural Representations ◽  
The Social

As a frontal node in the primate social brain, the medial prefrontal cortex (MPFC) plays a critical role in coordinating one's own behavior with respect to that of others. Current literature demonstrates that single neurons in the MPFC encode behavior-related variables such as intentions, actions, and rewards, specifically for self and other, and that the MPFC comes into play when reflecting upon oneself and others. The social moderator account of MPFC function can explain maladaptive social cognition in people with autism spectrum disorder, which tips the balance in favor of self-centered perspectives rather than taking into consideration the perspective of others. Several strands of evidence suggest a hypothesis that the MPFC represents different other mental models, depending on the context at hand, to better predict others’ emotions and behaviors. This hypothesis also accounts for aberrant MPFC activity in autistic individuals while they are mentalizing others. Expected final online publication date for the Annual Review of Neuroscience, Volume 44 is July 2021. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.

scholarly journals Transcranial Magnetic Stimulation of the Medial Prefrontal Cortex Decreases Emotional Memory Schemas

2020 ◽  
Vol 30 (6) ◽  
pp. 3608-3616 ◽  
Author(s):  
Leonore Bovy ◽  
Ruud M W J Berkers ◽  
Julia C M Pottkämper ◽  
Rathiga Varatheeswaran ◽  
Guillén Fernández ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Transcranial Magnetic Stimulation ◽  
Medial Prefrontal Cortex ◽  
Magnetic Stimulation ◽  
Mood Induction ◽  
Recognition Performance ◽  
Memory Task ◽  
Emotional Memory ◽  
Memory Bias

Abstract Mood-congruent memory bias is a critical characteristic of depression, but the underlying neural mechanism is largely unknown. Negative memory schemas might enhance encoding and consolidation of negative experiences, thereby contributing to the genesis and perpetuation of depressive pathology. To investigate this relationship, we aimed to perturb medial prefrontal cortex (mPFC) processing, using neuronavigated transcranial magnetic stimulation (TMS) targeting the mPFC. Forty healthy volunteers first underwent a negative mood induction to activate negative schema processing after which they received either active inhibitory (N = 20) or control (N = 20) stimulation to the mPFC. Then, all participants performed the encoding of an emotional false memory task. Recall and recognition performance was tested the following morning. Polysomnographic data were recorded continuously during the night before and after encoding. We observed a significantly lower false recognition of negative critical lures following mPFC inhibition, but no differences in veridical memory. These findings were supported by reaction time data, showing a relative slower response to negative compared with positive critical lures. The current findings support previous causal evidence for a role of the mPFC in schema memory processing and further suggest a role of the mPFC in memory bias.

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