scholarly journals Dopaminergic modulation of appetitive trace conditioning: the role of D1 receptors in medial prefrontal cortex

2015 ◽  
Vol 232 (15) ◽  
pp. 2669-2680 ◽  
Author(s):  
M. A. Pezze ◽  
H. J. Marshall ◽  
H. J. Cassaday
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Trace Conditioning ◽  
D1 Receptors ◽  
Dopaminergic Modulation

scholarly journals Dopamine modulates adaptive forgetting in medial prefrontal cortex

2021 ◽  
Author(s):  
Francisco Tomas Gallo ◽  
Maria Belen Zanoni-Saad ◽  
Juan Facundo Morici ◽  
Magdalena Miranda ◽  
Michael C Anderson ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Familiar Object ◽  
D1 Receptors ◽  
Long Term Memory ◽  
Dopamine Signaling ◽  
Induced Forgetting ◽  
Adaptive Forgetting

Active forgetting occurs in many species, but how the mechanisms that control behavior contribute to determining which memories are forgotten is still unknown. We previously found that when rats need to retrieve particular memories to guide exploration, it reduces later retention of other memories encoded in that environment. As with humans, this retrieval-induced forgetting relies on prefrontal control processes. The dopaminergic input to the prefrontal cortex is important for executive functions and cognitive flexibility. We found that, in a similar way, prefrontal dopamine signaling through D1 receptors is required for retrieval-induced forgetting in rats. Blockade of medial prefrontal cortex D1 receptors as animals encountered a familiar object impaired forgetting of the memory of a competing object in a subsequent long-term memory test. Inactivation of the ventral tegmental area produced the same pattern of behavior, a pattern that could be reversed by concomitant activation of prefrontal D1 receptors. We observed a bidirectional modulation of retrieval-induced forgetting by agonists and antagonists of D1 receptors in the medial prefrontal cortex. These findings establish the essential role of prefrontal dopamine in the active forgetting of competing memories, contributing to the shaping of retention in response to an organism behavioral goals.

scholarly journals Scopolamine Impairs Appetitive But Not Aversive Trace Conditioning: Role of the Medial Prefrontal Cortex

2017 ◽  
Vol 37 (26) ◽  
pp. 6289-6298 ◽  
Author(s):  
Marie-Astrid Pezze ◽  
Hayley J. Marshall ◽  
Helen J. Cassaday
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Trace Conditioning

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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