Phenolic Acids as Antidepressant Agents.

Depression is a psychiatric disorder affecting the lives of patients and their families worldwide. It is an important pathophysiology; however, the molecular pathways involved are not well understood. Pharmacological treatment may promote side effects or be ineffective. Consequently, efforts have been made to understand the molecular pathways in depressive patients and prevent their symptoms. In this context, animal models have suggested phytochemicals from medicinal plants, especially phenolic acids, as alternative treatments. These bioactive molecules are known for their antioxidant and antiinflammatory activities. They occur in some fruits, vegetables, and herbal plants. This review focused on phenolic acids and extracts from medicinal plants and their effects on depressive symptoms, as well as the molecular interactions and pathways implicated in these effects. Results from preclinical trials indicate the potential of phenolic acids to reduce depressive-like behaviour by regulating factors associated with oxidative stress, neuroinflammation, autophagy, and deregulation of the hypothalamic-pituitary-adrenal axis, stimulating monoaminergic neurotransmission and neurogenesis, and modulating intestinal microbiota.

Carrion decomposition and assemblage of necrophagous dipterans associated with Terbufos (Organophosphate) intoxicated rat carcasses.

Organophosphate use represents one of the main causes of intentional and accidental poisoning in Brazil. Because they induce alteration in carcass decomposition and succession of necrophagous Diptera, they are important investigative tool in forensic entomology for determining the postmortem interval (PMI) and cause of death. Thus, this work aimed to evaluate the influence of Terbufos, the most commonly used organophosphate for suicides in Rio Grande do Norte, Brazil, in the decomposition process and necrophagous fly assemblies in intoxicated rat carcasses. For this, 150g female Wistar rats received, by gavage, 200µL of Terbufos (5mg/kg or 10mg/kg) or distilled water (control). Approximately 30 minutes after administration, animals were euthanized and distributed in suspended traps to decompose under environmental conditions. Decomposition was monitored daily, with photographic record and collection of the visiting dipterofauna until the dry phase. Data show that the higher dose of Terbufos i) accelerates carcass decomposition in 24h; ii) decreases the species richness and abundance of scavengers flies when compared to the control; iii) changes the succession pattern, delaying the arrival of important species for the PMI estimate and iv) causes 8% mortality of the visiting dipterofauna. This work provides relevant information about dipteran assemblages and changes in the cadaver decomposition process associated with Terbufos intoxication, which may assist in future investigative processes with suspected organophosphate poisoning.

The blockade of transient receptor potential ankirin 1 (TRPA1) signalling mediates antidepressant- and anxiolytic-like actions in mice.

BACKGROUND AND PURPOSE: Transient receptor potential vanilloid 1 (TRPV1) and TRP ankyrin 1 (TRPA1) are involved in many biological processes, including nociception and hyperalgesia. Whereas the involvement of TRPV1 in psychiatric disorders such as anxiety and depression has been reported, little is known regarding the role of TRPA1 in these conditions. EXPERIMENTAL APPROACH: We investigated the role of TRPA1 in mice models of depression [forced swimming test (FST)] and anxiety [elevated plus maze (EPM) test]. KEY RESULTS: Administration of the TRPA1 antagonist (HC030031, 30 nmol in 2 µL, i.c.v.) reduced immobility time in the FST. Similar results were obtained after oral administration of HC030031 (30-300 mg·kg(-1) ). The reduction in immobility time in FST induced by HC030031 (100 mg·kg(-1) ) was completely prevented by pretreatment with TRPA1 agonist, cinnamaldehyde (50 mg·kg(-1) , p.o.), which per se was inactive. In the EPM test, pretreatment with cinnamaldehyde (50 mg·kg(-1) , p.o.), which per se did not affect behaviour response, prevented the anxiolytic-like effect (increased open arm exploration) evoked by TRPA1 blockade (HC030031, 100 mg·kg(-1) , p.o.). Treatment with either cinnamaldehyde or HC030031 did not affect spontaneous ambulation. Furthermore, TRPA1-deficient mice showed anxiolytic- and antidepressant-like phenotypes in the FST and EPM test respectively. CONCLUSION AND IMPLICATIONS: The present findings indicate that genetic deletion or pharmacological blockade of TRPA1 produces inhibitory activity in mouse models of anxiety and depression. These results imply that TRPA1 exerts tonic control, promoting anxiety and depression, and that TRPA1 antagonism has potential as an innovative strategy for the treatment of anxiety and mood disorders.