A wealth of evidence indicates that the lateral wings subnucleus of the dorsal raphe nucleus (lwDR) is implicated in the processing of panic-associated stimuli. Escape expression in the elevated T-maze, considered a panic-related defensive behavior, markedly and selectively recruits non-serotonergic cells within this DR subregion and in the dorsal periaqueductal gray (dPAG), another key panic-associated area. However, whether anti-panic drugs may interfere with this pattern of neuronal activation is still unknown. In the present study, the effects of acute (10 mg/kg) or chronic fluoxetine (10 mg/kg/daily/21 days) treatment on the number of serotonergic and non-serotonergic cells induced by escape expression within the rat DR and PAG subnuclei were investigated by immunochemistry. The results showed that chronic, but not acute, treatment with fluoxetine impaired escape expression, indicating a panicolytic-like effect, and markedly decreased the number of non-serotonergic cells that were recruited in the lwDR and dPAG. The same treatment selectively increased the number of serotonergic neurons within the lwDR. Our immunochemistry analyses also revealed that the non-serotonergic cells recruited in the lwDR and dPAG by the escape expression were not nitrergic. Overall, our findings suggest that the anti-panic effect of chronic treatment with fluoxetine is mediated by stimulation of the lwDR-dPAG pathway that controls the expression of panic-associated escape behaviors.
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http://dx.doi.org/10.1007/s12035-019-1536-z | DOI Listing |
Int J Mol Sci
December 2024
Vascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.
One of the key factors that contribute to tumor progression and resistance is the immunosuppressive microenvironment of the tumor. CD200 is a recently identified cell surface glycoprotein recognized as an important molecule in breast cancer for its versatile modulation of the immune response via its receptor, CD200R. The interaction between CD200 and CD200R suppresses the immune activities against tumor cells and allows them to be undetected and, in doing so, to escape from the destructive capability of the immune cells.
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January 2025
Department of Hepatopancreatobiliary Surgery, Suzhou Ninth Hospital Affiliated to Soochow University; Department of Pharmacology, College of Pharmaceutical Sciences, Soochow University; Jiangsu, China. Electronic address:
Inactivation of p53 by mutations commonly occurs in human cancer. The mutated p53 proteins may escape proteolytic degradation and exhibit high expression in tumors, and acquire gain-of-function activity that promotes tumor progression and chemo-resistance. Therefore, selectively targeting of the gain-of-function p53 mutants may serve as a promising therapeutic strategy for cancer prevention and treatment.
View Article and Find Full Text PDFSci Adv
January 2025
Zhejiang Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Zhejiang Key Laboratory of Frontier Medical Research on Cancer Metabolism, Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, China.
The unfolded protein response (UPR) pathway is crucial for tumorigenesis, mainly by regulating cancer cell stress responses and survival. However, whether UPR factors facilitate cell-cell communication between cancer cells and immune cells to drive cancer progression remains unclear. We found that adenosine 3',5'-monophosphate response element-binding protein 3-like protein 2 (CREB3L2), a noncanonical UPR factor, is overexpressed and activated in triple-negative breast cancer, where its cleavage releases a C-terminal fragment that activates the Hedgehog pathway in neighboring CD8+ T cells.
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January 2025
Neuroscience Graduate Program, University of Michigan, Ann Arbor, MI, USA; Graduate Program in Cell and Molecular Biology, University of Michigan, Ann Arbor, MI, USA; Medical Scientist Training Program, University of Michigan, Ann Arbor, MI, USA; Department of Neurology, University of Michigan, Ann Arbor, MI, USA. Electronic address:
The nuclear RNA-binding protein TDP43 is integrally involved in the pathogenesis of amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). Previous studies uncovered N-terminal TDP43 isoforms that are predominantly cytosolic in localization, prone to aggregation, and enriched in susceptible spinal motor neurons. In healthy cells, however, these shortened (s)TDP43 isoforms are difficult to detect in comparison to full-length (fl)TDP43, raising questions regarding their origin and selective regulation.
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January 2025
State Key Laboratory of Virology, Institute of Medical Virology, Taikang Medical School (School of Basic Medical Sciences), Wuhan University, Wuhan, Hubei, China.
Hantaan virus (HTNV) infection causes severe hemorrhagic fever with renal syndrome (HFRS) in humans and the infectious process can be regulated by autophagy. The phosphatase and tensin homolog (PTEN) protein has antiviral effects and plays a critical role in the autophagy pathway. However, the relationship between PTEN and HTNV infection is not clear and whether PTEN-regulated autophagy involves in HTNV replication is unknown.
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