Comparative analysis of the fatty acid and sterol profiles of widely consumed Mediterranean crustacean species

Comparative analysis of FA, NL and sterol profiles in the Nephrops norvegicus (langoustine), Palinurus vulgaris (lobster) and Penaeus kerathurus (shrimp) muscle and cephalothorax showed that C16:0, C16:1ω-7, C18:0, C18:1ω-9, C20:4ω-6, EPA and DHA were found to be their major FA. Highest EPA occurred in langoustine muscle TL, DHA in both shrimp tissues TL while C20:4ω-6 in lobster muscle and cephalothorax TL. Muscle and cephalothorax NL consisted mainly of sterols (42.5-54.4% and 13.7-43.1%) and triacylglycerols (35.4-45.8% and 44.6-59.4%). Cholesterol was the major sterol (70.90-98.58% and 97.10-98.31% of total sterols in muscle and cephalothorax respectively) followed by avenasterol (0.18-20.32% and 0.07-0.70%) and β-sitosterol (0.29-7.30% and 0.23-0.75%). Lower concentrations of brassicasterol, stigmasterol, Δ7-stigmasterol, campesterol and campestanol were also found. The examined crustaceans muscle (edible part) was found to be a good ω-3 PUFA source for the consumers, while the cephalothorax (which is usually discarded) could be used effectively as a source for ω-3 PUFA production. © 2010 Elsevier Ltd. All rights reserved

Genetic Inactivation of Cholinergic C Bouton Output Improves Motor Performance but not Survival in a Mouse Model of Amyotrophic Lateral Sclerosis

Amyotrophic Lateral Sclerosis (ALS) is a neurodegenerative disease that affects upper and lower motor neurons and leads to death a few years after symptom onset. Despite its high morbidity and mortality, its underlying pathogenic mechanisms still remain poorly understood. Although there is increasing evidence for significant changes in the structure and function of synapses on motor neurons, there is a need for a systematic investigation of the role of each synapse subtype in the course of the disease. Here, we focus on large cholinergic synapses on motor neurons, known as C boutons, and investigate their role during ALS progression. We implement a genetic strategy for inactivation of the cholinergic output of C boutons in the SOD1G93A transgenic mouse model of ALS. We demonstrate that although C bouton cholinergic inactivation does not alter mouse survival, it exerts a beneficial effect on motor performance in the rotarod motor task, as evidenced by an increased latency to fall in SOD1G93A mice lacking C bouton cholinergic output. Our results suggest that C bouton cholinergic transmission exerts a negative effect on motor neuron function in ALS, possibly via aberrant excitation, and render C boutons a potential target for future pharmacological intervention. © 2020 IBR