Isolation and Characterization of Two Novel, Cytoplasmically Polyadenylated, Oocyte-Specific, Mouse Maternal RNAs

AbstractDuring early development in mouse andXenopus,translational activation of stored maternal mRNAs by cytoplasmic polyadenylation requires both the nuclear polyadenylation signal AAUAAA and U-richcis-acting adenylation control elements (ACEs), also termed cytoplasmic polyadenylation elements, located in the 3′ UTR. Using an ACE-based PCR strategy (Salléset al.,1992) we have isolated two novel cDNAs from mouse oocytes: OM2a and OM2b (for Oocyte Maturation). Each message contains an ACE consensus sequence upstream of AAUAAA, is specifically transcribed in the growing oocyte, and is cytoplasmically polyadenylated upon oocyte maturation. Comparison of the mouse and rat homologs reveals considerable nucleotide sequence homology and conservation of overall gene organization. However, the predicted open reading frames are far less conserved, suggesting that these genes may not be functioning as proteins. The tissue specificity and tight temporal regulation of the RNAs suggest a role for these genes during early development

First diclofenac intoxication in a wild avian scavenger in Europe

Diclofenac is a non-steroidal anti-inflammatory drug (NSAID) with a well-known toxicity for old world vultures that ingest the carrion of domestic animals treated with it. Diclofenac intoxication was directly related to the dramatic declines in the populations of three native South Asian Gyps vulture species two decades ago. In 2013, this NSAID was authorised for veterinary use in Spain, which has the largest vulture populations in Europe. One of these species is the cinereous vulture (Aegypius monachus), which is classified as “near threatened” by the International Union for Conservation of Nature (IUCN). This species has been reintroduced and monitored in Catalonia (NE Spain) since 2007, and in 2020 its current population consisted of 15 breeding pairs and a total number of 61 individuals. In September 2020, one fledgling was found dead in the nest. Post-mortem examination revealed severe generalised visceral and articular gout, which was confirmed histologically. Diclofenac was detected at average concentrations of 26.5 ng/g in the liver and 51.4 ng/g in kidney replicates (n = 3), respectively. These findings support a diagnosis of fatal gout caused by diclofenac intoxication. This is the first case of diclofenac poisoning in Spain (and in Europe), in addition to being the first report of diclofenac poisoning in cinereous vultures. This case report, therefore, supports the need to closely monitor vulture populations and carry out strict regulatory measures with which to prevent these poisonings.The programme to reintroduce the cinereous vulture into the Catalan pre-Pyrenees has been funded by “Obra Social la Caixa” (through a contract with the “Generalitat de Catalunya”), the “Red Eléctrica de España” and the “Fundación Biodiversidad” from the Spanish Ministry of Ecological Transition and Demographic Challenge (MITECO).Peer reviewe

Intermittent ethanol exposure during adolescence impairs cannabinoid type 1 receptor-dependent long-term depression and recognition memory in adult mice.

Binge drinking is a significant problem in adolescent populations, and because of the reciprocal interactions between ethanol (EtOH) consumption and the endocannabinoid (eCB) system, we sought to determine if adolescent EtOH intake altered the localization and function of the cannabinoid 1 (CB1) receptors in the adult brain. Adolescent mice were exposed to a 4-day-per week drinking in the dark (DID) procedure for a total of 4 weeks and then tested after a 2-week withdrawal period. Field excitatory postsynaptic potentials (fEPSPs), evoked by medial perforant path (MPP) stimulation in the dentate gyrus molecular layer (DGML), were significantly smaller. Furthermore, unlike control animals, CB1 receptor activation did not depress fEPSPs in the EtOH-exposed animals. We also examined a form of excitatory long-term depression that is dependent on CB1 receptors (eCB-eLTD) and found that it was completely lacking in the animals that consumed EtOH during adolescence. Histological analyses indicated that adolescent EtOH intake significantly reduced the CB1 receptor distribution and proportion of immunopositive excitatory synaptic terminals in the medial DGML. Furthermore, there was decreased binding of [35S]guanosine-5*-O-(3-thiotriphosphate) ([35S] GTPγS) and the guanine nucleotide-binding (G) protein Gαi2 subunit in the EtOH-exposed animals. Associated with this, there was a significant increase in monoacylglycerol lipase (MAGL) mRNA and protein in the hippocampus of EtOH-exposed animals. Conversely, deficits in eCB-eLTD and recognition memory could be rescued by inhibiting MAGL with JZL184. These findings indicate that repeated exposure to EtOH during adolescence leads to long-term deficits in CB1 receptor expression, eCB-eLTD, and reduced recognition memory, but that these functional deficits can be restored by treatments that increase endogenous 2-arachidonoylglycerol