Does the Farming Method Influence the Porcine Vomeronasal Organ Condition? A Histological Study.

The vomeronasal organ (VNO) plays a key role in mammals, since it detects pheromones thus enabling social interactions between congeners. VNO inflammatory changes have been shown to severely impact animal life, leading to impaired social interactions in groups, such as in pigs. Environmental air is known to be strongly modified in farms, and it is suspected to be one of the causes of this alteration. This study aimed to compare via histology the VNOs of pigs housed in intensive conditions (n = 38) to those of pigs housed in free-range farming conditions (n = 35). VNO sections were stained in hematoxylin and eosin to assess the presence of nonsensory and sensory epithelium alterations and collagenolysis. The nonsensory epithelium was significantly more inflamed in animals in free-range farming conditions than those in intensive conditions (p < 0.0001) and was more strongly affected by signs of collagenolysis (p < 0.0001). The sensory epithelium seemed to be less altered by the different environmental conditions (p = 0.7267). These results suggest that species-typical pig behaviors, such as digging and rooting for food, could facilitate the presence of microparticles in the oral cavity and their entrance into the vomeronasal canals, leading to changes to the VNO.

Does the Environmental Air Impact the Condition of the Vomeronasal Organ? A Mouse Model for Intensive Farming.

Chemical communication in mammals is ensured by exchanging chemical signals through the vomeronasal organ (VNO) and its ability to detect pheromones. The alteration of this organ has been proven to impact animal life, participating in the onset of aggressive behaviors in social groups. To date, few studies have highlighted the possible causes leading to these alterations, and the farming environment has not been investigated, even though irritant substances such as ammonia are known to induce serious damage in the respiratory tract. The goal of this study was to investigate the environmental impact on the VNO structure. Thirty mice were split into three groups, one housed in normal laboratory conditions and the other two in confined environments, with or without the release of litter ammonia. VNOs were analyzed using histology and immunohistochemistry to evaluate the effect of different environments on their condition. Both restricted conditions induced VNO alterations (p = 0.0311), soft-tissue alteration (p = 0.0480), and nonsensory epithelium inflammation (p = 0.0024). There was glycogen accumulation (p < 0.0001), the olfactory marker protein was underexpressed (p < 0.0001), and Gαi2 positivity remained unchanged while Gαo expression was upregulated in confined conditions. VNO conditions seemed to worsen with ammonia, even if not always significantly. These murine model results suggest that the housing environment can strongly impact VNO conditions, providing novel insights for improving indoor farming systems.

Alteration of the Neuromuscular Junction and Modifications of Muscle Metabolism in Response to Neuron-Restricted Expression of the CHMP2Bintron5 Mutant in a Mouse Model of ALS-FTD Syndrome.

CHMP2B is a protein that coordinates membrane scission events as a core component of the ESCRT machinery. Mutations in CHMP2B are an uncommon cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), two neurodegenerative diseases with clinical, genetic, and pathological overlap. Different mutations have now been identified across the ALS-FTD spectrum. Disruption of the neuromuscular junction is an early pathogenic event in ALS. Currently, the links between neuromuscular junction functionality and ALS-associated genes, such as CHMP2B, remain poorly understood. We have previously shown that CHMP2B transgenic mice expressing the CHMP2Bintron5 mutant specifically in neurons develop a progressive motor phenotype reminiscent of ALS. In this study, we used complementary approaches (behavior, histology, electroneuromyography, and biochemistry) to determine the extent to which neuron-specific expression of CHMP2Bintron5 could impact the skeletal muscle characteristics. We show that neuronal expression of the CHMP2Bintron5 mutant is sufficient to trigger progressive gait impairment associated with structural and functional changes in the neuromuscular junction. Indeed, CHMP2Bintron5 alters the pre-synaptic terminal organization and the synaptic transmission that ultimately lead to a switch of fast-twitch glycolytic muscle fibers to more oxidative slow-twitch muscle fibers. Taken together these data indicate that neuronal expression of CHMP2Bintron5 is sufficient to induce a synaptopathy with molecular and functional changes in the motor unit reminiscent of those found in ALS patients.