TLR4 receptor expression and function in F11 dorsal root ganglion × neuroblastoma hybrid cells

TLR4 respond to bacterial LPS to produce inflammatory cytokines. TLR4 are expressed in dorsal root ganglia and play a role in pain. F11 dorsal root ganglia × mouse neuroblastoma cells possess many of the properties seen in nociceptive dorsal root ganglia neuronal cells. Here, we investigated the effect of 2 h and 6 h treatment with LPS upon the expression of inflammatory proteins in undifferentiated and differentiated F11 cells. The cells expressed mRNA for TRL4 (mouse, not rat) and proteins involved in TLR4 signaling. TLR4 expression was confirmed using immunohistochemistry. LPS produced modest increases in mouse and rat IL-6 and in mouse cyclooxygenase-2 levels in undifferentiated cells, but did not significantly affect mouse TNF-α expression. This contrasts with the robust effects of LPS upon cyclooxygenase-2 expression in cultured dorsal root ganglia neurons. F11 cells expressed the endocannabinoid metabolizing enzymes fatty acid amide hydrolase and N-acylethanolamine acid amidase (both murine), which were functionally active. These data suggest that F11 cells are not a useful model for the study of LPS-mediated effects but may be useful for the study of endocannabinoid catabolism.

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Distribution of 5-HT1B, 5-HT1D and 5-HT1F receptor expression in rat trigeminal and dorsal root ganglia neurons: Relevance to the selective anti-migraine effect of triptans

Brain Research ◽

10.1016/j.brainres.2010.09.004 ◽

2010 ◽

Vol 1361 ◽

pp. 76-85 ◽

Cited By ~ 37

Author(s):

J.D. Classey ◽

T. Bartsch ◽

P.J. Goadsby

Keyword(s):

Dorsal Root Ganglia ◽

Dorsal Root ◽

Receptor Expression ◽

Dorsal Root Ganglia Neurons

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Expression and Function of the Endocannabinoid Modulating Enzymes Fatty Acid Amide Hydrolase and N-Acylphosphatidylethanolamine-Specific Phospholipase D in Endometrial Carcinoma

Frontiers in Oncology ◽

10.3389/fonc.2019.01363 ◽

2019 ◽

Vol 9 ◽

Cited By ~ 1

Author(s):

Thangesweran Ayakannu ◽

Anthony H. Taylor ◽

Monica Bari ◽

Nicoletta Mastrangelo ◽

Mauro Maccarrone ◽

...

Keyword(s):

Fatty Acid ◽

Endometrial Carcinoma ◽

Phospholipase D ◽

Fatty Acid Amide Hydrolase ◽

Acid Amide ◽

Amide Hydrolase ◽

And Function ◽

Fatty Acid Amide

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Individual differences in frontolimbic circuitry and anxiety emerge with adolescent changes in endocannabinoid signaling across species

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1600013113 ◽

2016 ◽

Vol 113 (16) ◽

pp. 4500-4505 ◽

Cited By ~ 27

Author(s):

Dylan G. Gee ◽

Robert N. Fetcho ◽

Deqiang Jing ◽

Anfei Li ◽

Charles E. Glatt ◽

...

Keyword(s):

Gene Expression ◽

Anxiety Disorders ◽

Neural Circuit ◽

Fatty Acid Amide Hydrolase ◽

Acid Amide ◽

Genetic Alterations ◽

Phenotypic Differences ◽

Brain Circuitry ◽

Amide Hydrolase ◽

And Function

Anxiety disorders peak in incidence during adolescence, a developmental window that is marked by dynamic changes in gene expression, endocannabinoid signaling, and frontolimbic circuitry. We tested whether genetic alterations in endocannabinoid signaling related to a common polymorphism in fatty acid amide hydrolase (FAAH), which alters endocannabinoid anandamide (AEA) levels, would impact the development of frontolimbic circuitry implicated in anxiety disorders. In a pediatric imaging sample of over 1,000 3- to 21-y-olds, we show effects of the FAAH genotype specific to frontolimbic connectivity that emerge by ∼12 y of age and are paralleled by changes in anxiety-related behavior. Using a knock-in mouse model of the FAAH polymorphism that controls for genetic and environmental backgrounds, we confirm phenotypic differences in frontoamygdala circuitry and anxiety-related behavior by postnatal day 45 (P45), when AEA levels begin to decrease, and also, at P75 but not before. These results, which converge across species and level of analysis, highlight the importance of underlying developmental neurobiology in the emergence of genetic effects on brain circuitry and function. Moreover, the results have important implications for the identification of risk for disease and precise targeting of treatments to the biological state of the developing brain as a function of developmental changes in gene expression and neural circuit maturation.

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