scholarly journals Impairment of the context preexposure facilitation effect in juvenile rats by neonatal alcohol exposure is associated with decreased Egr-1 mRNA expression in the prefrontal cortex.

2018 ◽  
Vol 132 (6) ◽  
pp. 497-511 ◽  
Author(s):  
Sarah A. Jablonski ◽  
Patrese A. Robinson-Drummer ◽  
William B. Schreiber ◽  
Arun Asok ◽  
Jeffrey B. Rosen ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Mrna Expression ◽  
Alcohol Exposure ◽  
Facilitation Effect ◽  
Juvenile Rats ◽  
Neonatal Alcohol Exposure

CB1R Promotes Chronic Alcohol-Induced Neuronal Necroptosis in Mice Prefrontal Cortex

2020 ◽  
Author(s):  
Lin Ye ◽  
Shuhao Li ◽  
Xiaochen Liu ◽  
Dingang Zhang ◽  
Liliang Li ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Protein Level ◽  
Cannabinoid Receptors ◽  
Alcohol Exposure ◽  
Global Burden ◽  
Dependent Manner ◽  
Chronic Alcohol ◽  
Inverse Agonists ◽  
Alcohol Vapor ◽  
Chronic Alcohol Exposure

Abstract Aims Alcohol abuse induces multiple neuropathology and causes global burden to human health. Prefrontal cortex (PFC) is one of the most susceptible regions to alcohol-induced neuropathology. However, precise mechanisms underlying these effects on PFC remain to be elucidated. Herein, we investigated whether RIP1/RIP3/MLKL-mediated necroptosis was involved in the alcohol-induced PFC injury, and explored the effect that cannabinoid receptors (CBRs) exerted on the neurotoxicity of alcohol. Methods In this study, dynamic development of neuronal necroptosis in the PFC region was monitored after 95% (v/v) alcohol vapor administration for 15 and 30 days, respectively. Selective CBRs agonists or inverse agonists were pretreated according to the experimental design. All the PFC tissues were isolated and further examined by biochemical and histopathological analyses. Results It was found that chronic alcohol exposure increased the protein level of MLKL and also the phosphorylated levels of RIP1, RIP3 and MLKL in a time-dependent manner, all of which indicated the activation of necroptosis signaling. Particularly, compared to astrocytes, neurons from the PFC showed more prototypical necrotic morphology in response to alcohol insults. In parallel, an increased protein level of CB1R was also found after 15 and 30 days alcohol exposure. Administration of specific inverse agonists of CB1R (AM251 and AM281), but not its agonists or CB2R modulators, significantly alleviated the RIP1/RIP3/MLKL-mediated neuronal necroptosis. Conclusion We reported the involvement of RIP1/RIP3/MLKL-mediated necroptosis in alcohol-induced PFC neurotoxicity, and identified CB1R as a critical regulator of neuronal necroptosis that enhanced our understanding of alcohol-induced neuropathology in the PFC.

scholarly journals Effects of neonatal alcohol exposure on vasoactive intestinal polypeptide neurons in the rat suprachiasmatic nucleus

Alcohol ◽  
2009 ◽  
Vol 43 (5) ◽  
pp. 387-396 ◽  
Author(s):  
Yuhua Z. Farnell ◽  
Gregg C. Allen ◽  
Nichole Neuendorff ◽  
James R. West ◽  
A. Chen Wei-Jung ◽  
...  
Keyword(s):  
Suprachiasmatic Nucleus ◽  
Vasoactive Intestinal Polypeptide ◽  
Alcohol Exposure ◽  
Neonatal Alcohol Exposure ◽  
Intestinal Polypeptide

scholarly journals Abnormal protein and mRNA expression of inflammatory cytokines in the prefrontal cortex of depressed individuals who died by suicide

2018 ◽  
Vol 43 (6) ◽  
pp. 376-385 ◽  
Author(s):  
Ghanshyam N. Pandey ◽  
Hooriyah S. Rizavi ◽  
Hui Zhang ◽  
Runa Bhaumik ◽  
Xinguo Ren
Keyword(s):  
Prefrontal Cortex ◽  
Mrna Expression ◽  
Inflammatory Cytokines ◽  
Abnormal Protein

Lower antioxidant capacity in the prefrontal cortex of individuals with schizophrenia

2017 ◽  
Vol 52 (7) ◽  
pp. 690-698 ◽  
Author(s):  
Yiru Zhang ◽  
Vibeke Sørensen Catts ◽  
Cynthia Shannon Weickert
Keyword(s):  
Prefrontal Cortex ◽  
Antioxidant Capacity ◽  
Mrna Expression ◽  
Antioxidant System ◽  
Messenger Rna ◽  
Total Glutathione ◽  
Protein Levels ◽  
Significant Difference ◽  
Dorsolateral Prefrontal ◽  
And Control

Objective: The glutathione (GSH) pathway is the main antioxidant system to protect against oxidative stress in the human brain. In this study, we tested whether molecular components of the GSH antioxidant system are changed in dorsolateral prefrontal cortex tissue from people with schizophrenia compared to controls. Method: The levels of total glutathione and reduced GSH were determined by fluorometric assay via quantifying thiols in extracts from frontal cortex of 68 people. Immunoblotting was used to measure levels of enzymes responsible for maintaining GSH, the glutamyl-cysteine ligase (GCL) catalytic subunit (GCLC) and the GSH peroxidase (GPx)-like protein ( n = 74). Quantitative reverse transcription polymerase chain reaction (RT-PCR) was used to measure GCLC messenger RNA (mRNA) expression. Results: Both total glutathione ( t(66) = 2.467, p = 0.016) and reduced GSH ( t(66) = 3.001, p = 0.004) levels were significantly less in people with schizophrenia than in controls. However, there were no significant differences in either GCLC-like protein ( t(72) = −1.077, p = 0.285) or GCLC mRNA expression ( t(71) = −0.376, p = 0.708) between people with schizophrenia and control subjects. There was also no significant difference of GPx-like protein levels between schizophrenia and controls ( t(72) = −0.060, p = 0.952). Moreover, no significant correlations of putative confounding factors with GSH changes were detected. Discussion: These results suggest that people with schizophrenia have impaired GSH antioxidant capacity, alongside normal levels of key regulatory proteins.

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