Effects of TRPV1 Activation by Capsaicin and Endogenous N-Arachidonoyl Taurine on Synaptic Transmission in the Prefrontal Cortex

Zhang, Mingyue; Ruwe, David; Saffari, Roja; Kravchenko, Mykola; Zhang, Weiqi

doi:10.3389/fnins.2020.00091

Cited by 19 publications

(11 citation statements)

References 36 publications

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“…Recently, the presence of TRPV1 in the soma of pyramidal neurons of the prelimbic cortex of the prefrontal cortex (PFC) has been reported [85]. This finding is interesting since the activation of TRPV1 produces an increase in the frequency of spontaneous excitatory postsynaptic currents (sEPSC) in the substantia gelatinosa of the rat spinal cord and in the substantia nigra [86,87].…”

Section: N-acyl Amino Acids/neurotransmittersmentioning

confidence: 94%

TRPV1: Structure, Endogenous Agonists, and Mechanisms

Benítez-Angeles

Morales‐Lázaro

Juárez-González

et al. 2020

IJMS

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The Transient Receptor Potential Vanilloid 1 (TRPV1) channel is a polymodal protein with functions widely linked to the generation of pain. Several agonists of exogenous and endogenous nature have been described for this ion channel. Nonetheless, detailed mechanisms and description of binding sites have been resolved only for a few endogenous agonists. This review focuses on summarizing discoveries made in this particular field of study and highlighting the fact that studying the molecular details of activation of the channel by different agonists can shed light on biophysical traits that had not been previously demonstrated.

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Section: N-acyl Amino Acids/neurotransmittersmentioning

confidence: 94%

TRPV1: Structure, Endogenous Agonists, and Mechanisms

Benítez-Angeles

Morales‐Lázaro

Juárez-González

et al. 2020

IJMS

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“…However, it is known that AEA is a partial agonist for CB 1 R [ 120 ] and it has been widely demonstrated that activation of CB 1 R reduces rather than facilitates GABAergic synaptic activity [ 98 , 99 ]. Similarly, AEA can activate transient receptor potential vanilloid type 1 (TRPV1) receptors [ 121 , 122 , 123 ], that also have been shown to decrease GABAergic neurotransmission in the mPFC of mice [ 124 ]. Noteworthy, as demonstrated in the present study, structurally related lipids to AEA, including PEA, OEA, and NAGly, which do not activate cannabinoid receptors, are often altered in parallel with changes in AEA [ 125 , 126 , 127 , 128 ].…”

Section: Discussionmentioning

confidence: 99%

Inhibitory Neurotransmission Is Sex-Dependently Affected by Tat Expression in Transgenic Mice and Suppressed by the Fatty Acid Amide Hydrolase Enzyme Inhibitor PF3845 via Cannabinoid Type-1 Receptor Mechanisms

Yadav-Samudrala

Nath

et al. 2022

Cells

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(1) Background. The endocannabinoid (eCB) system, which regulates physiological and cognitive processes, presents a promising therapeutic target for treating HIV-associated neurocognitive disorders (HAND). Here we examine whether upregulating eCB tone has potential protective effects against HIV-1 Tat (a key HIV transactivator of transcription) protein-induced alterations in synaptic activity. (2) Methods. Whole-cell patch-clamp recordings were performed to assess inhibitory GABAergic neurotransmission in prefrontal cortex slices of Tat transgenic male and female mice, in the presence and absence of the fatty acid amide hydrolase (FAAH) enzyme inhibitor PF3845. Western blot and mass spectrometry analyses assessed alterations of cannabinoid receptor and enzyme protein expression as well as endogenous ligands, respectively, to determine the impact of Tat exposure on the eCB system. (3) Results. GABAergic activity was significantly altered upon Tat exposure based on sex, whereas the effectiveness of PF3845 to suppress GABAergic activity in Tat transgenic mice was not altered by Tat or sex and involved CB1R-related mechanisms that depended on calcium signaling. Additionally, our data indicated sex-dependent changes for AEA and related non-eCB lipids based on Tat induction. (4) Conclusion. Results highlight sex- and/or Tat-dependent alterations of GABAergic activity and eCB signaling in the prefrontal cortex of Tat transgenic mice and further increase our understanding about the role of FAAH inhibition in neuroHIV.

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“…NAT reduces ACSL4, LPCAT3 and PLTP, which are all essential for AA incorporation into the plasma membrane [40,41]. Of note, NAT activates transient receptor potential vanilloid 1 (TRPV1) channel and Ca 2+ [47]; however, whether NAT suppresses the three enzymes via one common mechanism, such as TRPV1 and Ca 2+ , is unclear and worth investigating in the future.…”

Section: Discussionmentioning

confidence: 99%

The Essential Roles of Exosome and CircRNA_101093 to Desensitize Lung Adenocarcinoma to Ferroptosis

Zhang¹,

Xu²,

Ma³

et al. 2021

Preprint

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BackgroundResistance to ferroptosis, a regulated cell death caused by iron-dependent excessive accumulation of lipid peroxides has recently been linked to lung adenocarcinoma (LUAD), the most prevalent lung cancer subtype. Despite intracellular antioxidant system is required for protection against ferroptosis, whether and how extracellular system desensitizes LUAD cells to ferroptosis is incompletely known. MethodsImmunohistochemistry (IHC) and immunoblotting (IB) were used to analyze protein expression, and quantitative RT-PCR (qPCR) was used to analyze mRNA level. Cell viability, cell death and the lipid reactive oxygen species (ROS) generation were measured to evaluate the responses to ferroptosis induction. Metabolites were measured using appropriate kits. Exosomes were observed using transmission electron microscope (TEM). The localization of arachidonic acid (AA) was detected using click chemistry labeling followed by confocal microscope observation. Interaction between RNA and protein were detected using RNA-pulldown, RNA immunoprecipitation (RIP) and photoactivatable ribonucleoside-enhanced crosslinking and immunoprecipitation (PAR-CLIP). Proteomic analysis was used to investigate circRNA_101093 (cir93) regulated protein and metabolomic analysis was used to analyze metabolites that changed among LUAD tissues expressing low and high Fatty acid-binding protein 3 (FABP3) levels. Cell-derived xenograft (CDX), patient-derived xenograft (PDX) and cell-implanted intrapulmonary LUAD mouse models and plasma/tissue specimens from LUAD patients were used to validate the mechanism that exosome and cir93 desensitized ferroptosis in LUAD. ResultsHere, the roles of exosome and circular RNA (circRNA) to desensitize LUAD cells to ferroptosis were investigated. Plasma exosome from LUAD patients exclusively reduced lipid peroxidation and desensitized ferroptosis. This might because exosomal-cir93 sustained an elevation of intracellular-cir93 in LUAD to modulate AA, a poly-unsaturated fatty acid that is critical for ferroptosis-associated over peroxidation in the plasma membrane. Mechanistically, cir93 interacted and lifted FABP3, which transported and facilitated AA reaction with taurine. Thus, global-AA was reduced while N-Arachidonoyl taurine (NAT), the product of AA and taurine, was induced. Notably, a role of NAT to suppress AA incorporation into plasma membrane was also revealed. In pre-clinical in vivo models, reducing exosome exhibited an improvement of ferroptosis-based treatment. ConclusionExosome and cir93 are essential for desensitizing LUAD cells to ferroptosis, and blocking exosome will be helpful for future LUAD treatment.

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Effects of TRPV1 Activation by Capsaicin and Endogenous N-Arachidonoyl Taurine on Synaptic Transmission in the Prefrontal Cortex

Cited by 19 publications

References 36 publications

TRPV1: Structure, Endogenous Agonists, and Mechanisms

TRPV1: Structure, Endogenous Agonists, and Mechanisms

Inhibitory Neurotransmission Is Sex-Dependently Affected by Tat Expression in Transgenic Mice and Suppressed by the Fatty Acid Amide Hydrolase Enzyme Inhibitor PF3845 via Cannabinoid Type-1 Receptor Mechanisms

The Essential Roles of Exosome and CircRNA_101093 to Desensitize Lung Adenocarcinoma to Ferroptosis

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