scholarly journals Bidirectional Control of Anxiety-Related Behaviors in Mice: Role of Inputs Arising from the Ventral Hippocampus to the Lateral Septum and Medial Prefrontal Cortex

2017 ◽  
Vol 42 (8) ◽  
pp. 1715-1728 ◽  
Author(s):  
Gustavo Morrone Parfitt ◽  
Robin Nguyen ◽  
Jee Yoon Bang ◽  
Afif J Aqrabawi ◽  
Matthew M Tran ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Ventral Hippocampus ◽  
Lateral Septum

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.  

scholarly journals Transient Inactivation of the Medial Prefrontal Cortex and Ventral Hippocampus Impairs Active Place Avoidance Retrieval on a Rotating Arena

2021 ◽  
Vol 15 ◽  
Author(s):  
Daniela Cernotova ◽  
Ales Stuchlik ◽  
Jan Svoboda
Keyword(s):  
Prefrontal Cortex ◽  
Spatial Memory ◽  
Medial Prefrontal Cortex ◽  
Ventral Hippocampus ◽  
Avoidance Task ◽  
Exact Role ◽  
Spatial Coordination ◽  
Place Avoidance ◽  
Long Evans

It is well known that communication between the medial prefrontal cortex (mPFC) and the ventral hippocampus (vHPC) is critical for various cognitive and behavioral functions. However, the exact role of these structures in spatial coordination remains to be clarified. Here we sought to determine the involvement of the mPFC and the vHPC in the spatial retrieval of a previously learned active place avoidance task in adult male Long-Evans rats, using a combination of unilateral and bilateral local muscimol inactivations. Moreover, we tested the role of the vHPC-mPFC pathway by performing combined ipsilateral and contralateral inactivations. Our results showed not only bilateral inactivations of either structure, but also the combined inactivations impaired the retrieval of spatial memory, whereas unilateral one-structure inactivations did not yield any effect. Remarkably, muscimol injections in combined groups exerted similar deficits, regardless of whether the inactivations were contralateral or ipsilateral. These findings confirm the importance of these structures in spatial cognition and emphasize the importance of the intact functioning of the vHPC-mPFC pathway.

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.

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