Medial prefrontal cortex in neurological diseases

The medial prefrontal cortex (mPFC) is a crucial cortical region that integrates information from numerous cortical and subcortical areas and converges updated information to output structures. It plays essential roles in the cognitive process, regulation of emotion, motivation, and sociability. Dysfunction of the mPFC has been found in various neurological and psychiatric disorders, such as depression, anxiety disorders, schizophrenia, autism spectrum disorders, Alzheimer’s disease, Parkinson’s disease, and addiction. In the present review, we summarize the preclinical and clinical studies to illustrate the role of the mPFC in these neurological diseases.

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An Update of Palmitoylethanolamide and Luteolin Effects in Preclinical and Clinical Studies of Neuroinflammatory Events

Antioxidants ◽

10.3390/antiox9030216 ◽

2020 ◽

Vol 9 (3) ◽

pp. 216 ◽

Cited By ~ 7

Author(s):

Marika Cordaro ◽

Salvatore Cuzzocrea ◽

Rosalia Crupi

Keyword(s):

Nervous System ◽

Neurological Diseases ◽

Autism Spectrum ◽

Monocytes And Macrophages ◽

Central Nervous Systems ◽

The Central Nervous System ◽

Spectrum Disorders ◽

Dynamic Series ◽

Preclinical And Clinical Studies

The inflammation process represents of a dynamic series of phenomena that manifest themselves with an intense vascular reaction. Neuroinflammation is a reply from the central nervous system (CNS) and the peripheral nervous system (PNS) to a changed homeostasis. There are two cell systems that mediate this process: the glia of the CNS and the lymphocites, monocytes, and macrophages of the hematopoietic system. In both the peripheral and central nervous systems, neuroinflammation plays an important role in the pathogenesis of neurodegenerative diseases, such as Parkinson’s and Alzheimer’s diseases, and in neuropsychiatric illnesses, such as depression and autism spectrum disorders. The resolution of neuroinflammation is a process that allows for inflamed tissues to return to homeostasis. In this process the important players are represented by lipid mediators. Among the naturally occurring lipid signaling molecules, a prominent role is played by the N-acylethanolamines, namely N-arachidonoylethanolamine and its congener N-palmitoylethanolamine, which is also named palmitoylethanolamide or PEA. PEA possesses a powerful neuroprotective and anti-inflammatory power but has no antioxidant effects per se. For this reason, its co-ultramicronization with the flavonoid luteolin is more efficacious than either molecule alone. Inhibiting or modulating the enzymatic breakdown of PEA represents a complementary therapeutic approach to treating neuroinflammation. The aim of this review is to discuss the role of ultramicronized PEA and co-ultramicronized PEA with luteolin in several neurological diseases using preclinical and clinical approaches.

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Neurobiological foundations of multisensory integration in people with autism spectrum disorders: the role of the medial prefrontal cortex

Frontiers in Human Neuroscience ◽

10.3389/fnhum.2014.00970 ◽

2014 ◽

Vol 8 ◽

Cited By ~ 6

Author(s):

Sonia MartÃnez-Sanchis

Keyword(s):

Autism Spectrum Disorders ◽

Prefrontal Cortex ◽

Medial Prefrontal Cortex ◽

Multisensory Integration ◽

Autism Spectrum ◽

Spectrum Disorders

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

Annual Review of Neuroscience ◽

10.1146/annurev-neuro-101420-011820 ◽

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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Haploinsufficiency of Tsc2 Leads to Hyperexcitability of Medial Prefrontal Cortex via Weakening of Tonic GABAB Receptor-mediated Inhibition

Cerebral Cortex ◽

10.1093/cercor/bhaa187 ◽

2020 ◽

Vol 30 (12) ◽

pp. 6313-6324

Author(s):

Davide Bassetti ◽

Aniello Lombardi ◽

Sergei Kirischuk ◽

Heiko J Luhmann

Keyword(s):

Prefrontal Cortex ◽

Medial Prefrontal Cortex ◽

Tumor Suppressor Genes ◽

Time Window ◽

Gabab Receptor ◽

Brain Slices ◽

Autism Spectrum ◽

Loss Of Function ◽

Electrophysiological Recordings ◽

Spectrum Disorders

Abstract Loss-of-function mutation in one of the tumor suppressor genes TSC1 or TSC2 is associated with several neurological and psychiatric diseases, including autism spectrum disorders (ASDs). As an imbalance between excitatory and inhibitory neurotransmission, E/I ratio is believed to contribute to the development of these disorders, we investigated synaptic transmission during the first postnatal month using the Tsc2+/− mouse model. Electrophysiological recordings were performed in acute brain slices of medial prefrontal cortex. E/I ratio at postnatal day (P) 15–19 is increased in Tsc2+/− mice as compared with wildtype (WT). At P25–30, facilitated GABAergic transmission reduces E/I ratio to the WT level, but weakening of tonic GABAB receptor (GABABR)-mediated inhibition in Tsc2+/− mice leads to hyperexcitability both at single cell and neuronal network level. Short (1 h) preincubation of P25–30 Tsc2+/− slices with baclofen restores the GABABR-mediated inhibition and reduces network excitability. Interestingly, the same treatment at P15–19 leads to weakening of GABABR-mediated inhibition. We hypothesize that a dysfunction of tonic GABABR-mediated inhibition might contribute to the development of ASD symptoms and suggest that GABABR activation within an appropriate time window may be considered as a therapeutic target in ASD.

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