Mouse Htt (Huntingtin) ELISA Kit

Serotonin (5-hydroxytryptamine, 5-HT) regulates diverse physiological and behavioural and processes, also acts as a developmental signal in early embryogenesis and in regulation of fetal development. A number of studies have implicated the prominent role of serotonin transporter (SERT or 5-HTT) and 5-HT receptor subtypes in placental development and function. Here, in this article we have provided a comprehensive review on the important role of 5-HT homeostasis in pregnancy outcomes. More specifically, we have summarised the findings from experimental and clinical studies, the influence of maternal and placental inflammation associated with the gestational diabetes and obesity on placental serotonin synthesis, expression of SERT and 5-HT receptors and their activity. Understanding the molecular regulation of placental SERT and 5-HT receptors using selective pharmacological agonists or antagonists may identify the therapeutic potential of serotonin pathway to improve long-term health outcomes of mothers and her infants exposed to GDM and obesity.

Huntington's disease (HD) is a disorder characterized by chronic involuntary movements, dementia, and psychiatric symptoms. It is caused by a mutation in the gene that encodes for huntingtin protein (HTT), leading to the formation of mutant proteins expressed in various tissues. Although brain pathology has become the hallmark for HD, recent studies suggest that damage of peripheral structures also contributes to HD progression. We previously identified severe alterations in the motor units that innervate cervical muscles in 12-month-old BACHD (Bacterial Artificial Chromosome Huntington's Disease) mice, a well-established mouse model for HD. Here, we studied lumbar motoneurons and their projections onto hind limb fast-twitch skeletal muscles (tibialis anterior), which control balance and gait in HD patients. We found that lumbar motoneurons were altered in the HD mouse model; the number and size of lumbar motoneurons were reduced in BACHD. Structural alterations were also present in the sciatic nerve and neuromuscular junctions. Acetylcholine receptors were organized in several small patches (acetylcholine receptor fragmentation), many of which were partially innervated. In BACHD mice, we observed atrophy of tibialis anterior muscles, decreased expression of glycolytic fast Type IIB fibers, and at the ultrastructural level, alterations of sarcomeres and mitochondria. Corroborating all these findings, BACHD animals performed worse on motor behavior tests. Our results provide additional evidences that nerve-muscle communication is impaired in HD and that motoneurons from distinct spinal cord locations are similarly affected in the disease.