Mice use ultrasonic vocalizations (USVs) to communicate each other and to convey their emotional state. USVs have been greatly characterized in specific life phases and contexts, such as mother isolation-induced USVs for pups or female-induced USVs for male mice during courtship. USVs can be acquired by means of specific tools and later analyzed on the base of both quantitative and qualitative parameters. Indeed, different ultrasonic call categories exist and have already been defined. The understanding of different calls meaning is still missing, and it will represent an essential step forward in the field of USVs. They have long been studied in the ethological context, but recently they emerged as a precious instrument to study pathologies characterized by deficits in communication, in particular neurodevelopmental disorders (NDDs), such as autism spectrum disorders. This review covers the topics of USVs characteristics in mice, contexts for USVs emission and factors that modulate their expression. A particular focus will be devoted to mouse USVs in the context of NDDs. Indeed, several NDDs murine models exist and an intense study of USVs is currently in progress, with the aim of both performing an early diagnosis and to find a pharmacological/behavioral intervention to improve patients' quality of life.Protein phosphorylation and dephosphorylation are two essential and vital cellular mechanisms that regulate many receptors and enzymes through kinases and phosphatases. Ca2+- dependent kinases and phosphatases are responsible for controlling neuronal processing; balance is achieved through opposition. During molecular mechanisms of learning and memory, kinases generally modulate positively while phosphatases modulate negatively. This review outlines some of the critical physiological and structural aspects of kinases and phosphatases involved in maintaining postsynaptic structural plasticity. It also explores the link between neuronal disorders and the deregulation of phosphatases and kinases.Acute central nervous system injuries are among the most common causes of disability worldwide, with widespread social and economic implications. Motor tract injury accounts for the majority of this disability; therefore, there is impetus to understand mechanisms underlying the pathophysiology of injury and subsequent reorganization of the motor tract that may lead to recovery. After acute central nervous system injury, there are changes in the microenvironment and structure of the motor tract. For example, ischemic stroke involves decreased local blood flow and tissue death from lack of oxygen and nutrients. https://www.selleckchem.com/ Traumatic injury, in contrast, causes stretching and shearing injury to microstructures, including myelinated axons and their surrounding vessels. Both involve blood-brain barrier dysfunction, which is an important initial event. After acute central nervous system injury, motor tract reorganization occurs in the form of cortical remapping in the gray matter and axonal regeneration and rewiring in the whi, and the implementation of neurotechnologies, such as central nervous system stimulators and robotics. The translation of these advances depends on careful alignment of preclinical studies and human clinical trials. As experimental data mount, the future is one of optimism.The mammalian retina displays incomplete intrinsic regenerative capacities; therefore, retina degeneration is a major cause of irreversible blindness such as glaucoma, age-related macular degeneration and diabetic retinopathy. These diseases lead to the loss of retinal cells and serious vision loss in the late stage. Stem cell transplantation is a great promising novel treatment for these incurable retinal degenerative diseases and represents an exciting area of regenerative neurotherapy. Several suitable stem cell sources for transplantation including human embryonic stem cells, induced pluripotent stem cells and adult stem cells have been identified as promising target populations. However, the retina is an elegant neuronal complex composed of various types of cells with different functions. The replacement of these different types of cells by transplantation should be addressed separately. So far, retinal pigment epithelium transplantation has achieved the most advanced stage of clinical trials, while transplantation of retinal neurons such as retinal ganglion cells and photoreceptors has been mostly studied in pre-clinical animal models. In this review, we opine on the key problems that need to be addressed before stem cells transplantation, especially for replacing injured retinal ganglion cells, may be used practically for treatment. A key problem we have called the Switchboard Dilemma is a major block to have functional retinal ganglion cell replacement. We use the public switchboard telephone network as an example to illustrate different difficulties for replacing damaged components in the retina that allow for visual signaling. Retinal ganglion cell transplantation is confronted by significant hurdles, because retinal ganglion cells receive signals from different interneurons, integrate and send signals to the correct targets of the visual system, which functions similar to the switchboard in a telephone network - therefore the Switchboard Dilemma.Osteopontin is a broadly expressed pleiotropic protein, and is attracting increased attention because of its role in the pathophysiology of several inflammatory, degenerative, autoimmune, and oncologic diseases. In fact, in the last decade, several studies have shown that osteopontin contributes to tissue damage not only by recruiting harmful inflammatory cells to the site of lesion, but also increasing their survival. The detrimental role of osteopontin has been indeed well documented in the context of different neurological conditions (i.e., multiple sclerosis, Parkinson's, and Alzheimer's diseases). Intriguingly, recent findings show that osteopontin is involved not only in promoting tissue damage (the Yin), but also in repair/regenerative mechanisms (the Yang), mostly triggered by the inflammatory response. These two apparently discordant roles are partly related to the presence of different functional domains in the osteopontin molecule, which are exposed after thrombin or metalloproteases cleavages. Such functional domains may in turn activate intracellular signaling pathways and mediate cell-cell and cell-matrix interactions.