scholarly journals Disturbed Prefrontal Cortex Activity in the Absence of Schizophrenia-Like Behavioral Dysfunction in Arc/Arg3.1 Deficient Mice

2019 ◽  
Vol 39 (41) ◽  
pp. 8149-8163 ◽  
Author(s):  
Xiaoyan Gao ◽  
Jasper Grendel ◽  
Mary Muhia ◽  
Sergio Castro-Gomez ◽  
Ute Süsens ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Behavioral Dysfunction ◽  
Deficient Mice

scholarly journals Parvalbumin interneuron dysfunction in a thalamus - prefrontal cortex circuit in Disc1 deficiency mice

2016 ◽  
Author(s):  
Kristen Delevich ◽  
Hanna Jaaro-Peled ◽  
Mario Penzo ◽  
Akira Sawa ◽  
Bo Li
Keyword(s):  
Prefrontal Cortex ◽  
Mouse Models ◽  
Pyramidal Neurons ◽  
Neural Circuit ◽  
Gaba Release ◽  
Parvalbumin Interneurons ◽  
Parvalbumin Interneuron ◽  
Inhibitory Circuit ◽  
Circuit Function ◽  
Deficient Mice

AbstractTwo of the most consistent findings across disrupted-in-schizophrenia-1 (DISC1) mouse models are impaired working memory and reduced number or function of parvalbumin interneurons within the prefrontal cortex. While these findings suggest parvalbumin interneuron dysfunction in DISC1-related pathophysiology, to date, cortical inhibitory circuit function has not been investigated in depth in DISC1 deficiency mouse models. Here we assessed the function of a feedforward circuit between the mediodorsal thalamus (MD) and the medial prefrontal cortex (mPFC) in mice harboring a deletion in one allele of the Disc1 gene. We found that the inhibitory drive onto layer 3 pyramidal neurons in the mPFC was significantly reduced in the Disc1 deficient mice. This reduced inhibition was accompanied by decreased GABA release from local parvalbumin, but not somatostatin, inhibitory interneurons, and by impaired feedforward inhibition in the MD-mPFC circuit. Our results reveal a cellular mechanism by which deficiency in DISC1 causes neural circuit dysfunction frequently implicated in psychiatric disorders.

Paternal bisphenol a diet changes prefrontal cortex proteome and provokes behavioral dysfunction in male offspring

Chemosphere ◽  
2017 ◽  
Vol 184 ◽  
pp. 720-729 ◽  
Author(s):  
Guangying Luo ◽  
Ruifen Wei ◽  
Shaolin Wang ◽  
Jundong Wang
Keyword(s):  
Prefrontal Cortex ◽  
Bisphenol A ◽  
Male Offspring ◽  
Behavioral Dysfunction

scholarly journals Modulation of prefrontal cortex excitation/inhibition balance rescues social behavior inCNTNAP2-deficient mice

2017 ◽  
Vol 9 (401) ◽  
pp. eaah6733 ◽  
Author(s):  
Aslihan Selimbeyoglu ◽  
Christina K. Kim ◽  
Masatoshi Inoue ◽  
Soo Yeun Lee ◽  
Alice S. O. Hong ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Social Behavior ◽  
Deficient Mice

scholarly journals A two-hit adversity model in developing rats reveals sex-specific impacts on prefrontal cortex structure and behavior

2020 ◽  
Author(s):  
Kelsea R. Gildawie ◽  
Lilly M. Ryll ◽  
Jessica C. Hexter ◽  
Shayna Peterzell ◽  
Alissa A. Valentine ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Maternal Separation ◽  
Structural Integrity ◽  
Later Life ◽  
Female Rats ◽  
Critical Periods ◽  
Early Life Adversity ◽  
Behavioral Dysfunction ◽  
Male And Female Rats ◽  
Adverse Experiences

AbstractAdversity early in life substantially impacts prefrontal cortex (PFC) development and vulnerability to later-life psychopathology. Importantly, repeated adverse experiences throughout childhood increase the risk for PFC-mediated behavioral deficits more commonly in women. Evidence from animal models points to effects of adversity on later-life neural and behavioral dysfunction; however, few studies have investigated the neurobiological underpinnings of sex-specific, long term consequences of multiple developmental stressors. We modeled early life adversity in rats via maternal separation (postnatal day (P)2-20) and juvenile social isolation (P21-35). Adult (P85) male and female rats were assessed for differences in the presence and structural integrity of PFC perineuronal nets (PNNs) enwrapping parvalbumin (PV)-expressing interneurons. PNNs are extracellular matrix structures formed during critical periods in postnatal development that play a key role in the plasticity of PV cells. Females – but not males – exposed to multiple hits of adversity demonstrated a reduction in PFC PV cells in adulthood. We also observed a sex-specific, potentiated reduction in PV+ PNN structural integrity. Moreover, correlations between neural disruption and hyperactivity/risk-assessment behavior were altered by adversity differently in males and females. These findings suggest a sex-specific impact of repeated adversity on neurostructural development and implicate PNNs as a contributor to associated behavioral dysfunction.

The effect of 3-nitropropionic acid on behavioral dysfunction, neuron loss and gliosis in the brain of adult male rats: The case of prefrontal cortex, hippocampus and the cerebellum

Toxicon ◽  
2020 ◽  
Vol 183 ◽  
pp. 44-50 ◽  
Author(s):  
Abolfazl Torabi ◽  
Mohammadjavad Joneidi ◽  
Ibrahim Mohammadzadeh ◽  
Mohammad-amin Abdollahifar ◽  
Aysan Khatmi ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Adult Male ◽  
Male Rats ◽  
Neuron Loss ◽  
Nitropropionic Acid ◽  
Behavioral Dysfunction ◽  
The Brain ◽  
3 Nitropropionic Acid

scholarly journals EphB6 regulates social behavior through gut microbiota-mediated vitamin B6 metabolism and excitation/inhibition balance of medial prefrontal cortex in mice

2019 ◽  
Author(s):  
Ying Li ◽  
Zheng-Yi Luo ◽  
Yu-Ying Hu ◽  
Yue-Wei Bi ◽  
Jian-Ming Yang ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Social Behavior ◽  
Gut Microbiota ◽  
Medial Prefrontal Cortex ◽  
Vitamin B6 ◽  
Fecal Microbiota ◽  
Autism Spectrum ◽  
Dopamine Synthesis ◽  
New Strategy ◽  
Deficient Mice

AbstractAutism spectrum disorder (ASD) is a developmental disorder with no effective pharmacological treatments so far. Gut microbiota has been suggested to contribute to autistic symptoms. However, the key genes and the mechanisms linking gut microbiota and brain dysfunctions in ASD are still unclear. Here, we found deletion of EphB6, an ASD-associated candidate gene, induced dysregulated gut microbiota and autism-like behavior in mice. More importantly, transplanting fecal microbiota from EphB6-deficient mice resulted in disturbed gut microbiota and autism-like behavior in antibiotics-treated C57BL/6J mice. Meanwhile, transplanting fecal microbiota from wild-type mice ameliorated disturbed gut microbiota and autism-like behavior in mice with deletion of EphB6. At the metabolic levels, dysregulated gut microbiota led to vitamin B6 and dopamine defects in EphB6-deficient mice. At the cellular levels, excitation/inhibition (E/I) imbalance in medial prefrontal cortex was induced by gut microbiota-mediated defects of vitamin B6 metabolism in EphB6-deficient mice. Our study uncovers a key role for EphB6 in regulation of social behavior by gut microbiota-mediated vitamin B6 metabolism, dopamine synthesis and E/I balance, suggesting a new strategy for treatment of ASD patients.

scholarly journals Acute sleep fragmentation does not alter pro-inflammatory cytokine gene expression in brain or peripheral tissues of leptin-deficient mice

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e4423 ◽  
Author(s):  
Jennifer E. Dumaine ◽  
Noah T. Ashley
Keyword(s):  
Gene Expression ◽  
Prefrontal Cortex ◽  
Inflammatory Cytokine ◽  
Cytokine Gene Expression ◽  
Cytokine Gene ◽  
Wild Type ◽  
Peripheral Tissues ◽  
Tnf Α ◽  
Deficient Mice ◽  
Tgf Β1

Obesity and sleep fragmentation (SF) are often co-occurring pro-inflammatory conditions in patients with obstructive sleep apnea. Leptin is a peptide hormone produced by adipocytes that has anorexigenic effects upon appetite while regulating immunity. The role of leptin in mediating inflammatory responses to SF is incompletely understood. Male C57BL/6j (lean) and ob/ob mice (leptin-deficient mice exhibiting obese phenotype) were subjected to SF or control conditions for 24 h using an automated SF chamber. Trunk blood and tissue samples from the periphery (liver, spleen, fat, and heart) and brain (hypothalamus, prefrontal cortex, and hippocampus) were collected. Quantitative PCR was used to determine relative cytokine gene expression of pro-inflammatory (IL-1β, TNF-α) and anti-inflammatory (TGF-β1) cytokines. Enzyme-linked immunosorbent assay (ELISA) was used to determine serum corticosterone concentration. Ob/ob mice exhibited elevated cytokine gene expression in liver (TNF-α, TGF-β1), heart (TGF-β1), fat (TNF-α), and brain (hippocampus, hypothalamus, prefrontal cortex: IL-1β, TNF-α) compared with wild-type mice. Conversely, leptin deficiency decreased pro-inflammatory cytokine gene expression in heart (IL-1β, TNF-α). SF significantly increased IL-1β and TNF-α gene expression in fat and TGF-β1 expression in spleen relative to controls, but only in wild-type mice. SF increased basal serum corticosterone regardless of genotype. Taken together, these findings suggest that leptin deficiency affects cytokine gene expression differently in the brain compared to peripheral tissues with minimal interaction from acute SF.

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