The molecular mechanisms, which are responsible for the functional differences between the various types of neuronal synapses, have become one of the central themes of modern neurobiology. It is becoming increasingly clear that a misregulation of synaptogenesis and synaptic remodeling and dysfunctional neuronal synapses are at the heart of several human diseases, both neurological disorders and psychiatric conditions. As synapses present specialized cellular junctions between neurons and their target cells, it may not come as a surprise that neural cell adhesion molecules (CAMs) are of special importance for the genesis and the maintenance of synaptic connections. Genes encoding adhesive molecules make up a significant portion of the human genome, and neural CAMs even have been postulated to be a major factor in the evolution of the human brain. These are just some of the many reasons why we thought a book on neural CAMs and their role in establishing and maintaining neuronal synapses would be highly appropriate for summarizing our current state of knowledge. Without question, over the near future, additional adhesive proteins will join the ranks of synaptic CAMs and our knowledge, and how these molecules enable neurons and their targets to communicate effectively will grow.

Conn’s Translational Neuroscience provides a comprehensive overview reflecting the depth and breadth of the field of translational neuroscience, with input from a distinguished panel of basic and clinical investigators. Progress has continued in understanding the brain at the molecular, anatomic, and physiological levels in the years following the 'Decade of the Brain,' with the results providing insight into the underlying basis of many neurological disease processes. This book alternates scientific and clinical chapters that explain the basic science underlying neurological processes and then relates that science to the understanding of neurological disorders and their treatment. Chapters cover disorders of the spinal cord, neuronal migration, the autonomic nervous system, the limbic system, ocular motility, and the basal ganglia, as well as demyelinating disorders, stroke, dementia and abnormalities of cognition, congenital chromosomal and genetic abnormalities, Parkinson's disease, nerve trauma, peripheral neuropathy, aphasias, sleep disorders, and myasthenia gravis. In addition to concise summaries of the most recent biochemical, physiological, anatomical, and behavioral advances, the chapters summarize current findings on neuronal gene expression and protein synthesis at the molecular level. Authoritative and comprehensive, Conn’s Translational Neuroscience provides a fully up-to-date and readily accessible guide to brain functions at the cellular and molecular level, as well as a clear demonstration of their emerging diagnostic and therapeutic importance. Provides a fully up-to-date and readily accessible guide to brain functions at the cellular and molecular level, while also clearly demonstrating their emerging diagnostic and therapeutic importance Features contributions from leading global basic and clinical investigators in the field Provides a great resource for researchers and practitioners interested in the basic science underlying neurological processes Relates and translates the current science to the understanding of neurological disorders and their treatment

Development of the brain and the emergence of the mind constitute some of the most important concerns of contemporary biology. Disturbances during fetal life may have profound implications for a child's future neurological and psychological development, which can in turn impact society. The new edition of this highly respected work presents a comprehensive review of the basic mechanisms of brain development and the pathophysiology of disorders of the infant brain, written by a team of distinguished neuroscientists, neonatologists, and neuropediatricians. The book follows the main milestones of brain development, from formation of the neural tube and wiring of the neurons in the brain. Neurotrophic factors, neurotransmitters, glial cell biology, cerebral circulation development of sensory functions are all described in detail. Furthermore, there are more philosophical chapters on the evolution of the brain and the emergence of consciousness. Clinical considerations are highlighted where relevant.

Written by an award-winning developmental neuroscientist, this is a comprehensive and cutting-edge account of the latest research on the adolescent brain.

GABA is the principal inhibitory neurotransmitter in the CNS and acts via GABAA and GABAB receptors. Recently, a novel form of GABAA receptor-mediated inhibition, termed “tonic” inhibition, has been described. Whereas synaptic GABAA receptors underlie classical “phasic” GABAA receptor-mediated inhibition (inhibitory postsynaptic currents), tonic GABAA receptor-mediated inhibition results from the activation of extrasynaptic receptors by low concentrations of ambient GABA. Extrasynaptic GABAA receptors are composed of receptor subunits that convey biophysical properties ideally suited to the generation of persistent inhibition and are pharmacologically and functionally distinct from their synaptic counterparts. This book highlights ongoing work examining the properties of recombinant and native extrasynaptic GABAA receptors and their preferential targeting by endogenous and clinically relevant agents. In addition, it emphasizes the important role of extrasynaptic GABAA receptors in GABAergic inhibition throughout the CNS and identifies them as a major player in both physiological and pathophysiological processes.

Neurofibrillary tangles (NFTs) composed of intracellular aggregates of tau protein are a key neuropathological feature of Alzheimer’s Disease (AD) and other neurodegenerative diseases, collectively termed tauopathies. The abundance of NFTs has been reported to correlate positively with the severity of cognitive impairment in AD. However, accumulating evidences derived from studies of experimental models have identified that NFTs themselves may not be neurotoxic. Now, many of tau researchers are seeking a “toxic” form of tau protein. Moreover, it was suggested that a “toxic” tau was capable to seed aggregation of native tau protein and to propagate in a prion-like manner. However, the exact neurotoxic tau species remain unclear. Because mature tangles seem to be non-toxic component, “tau oligomers” as the candidate of “toxic” tau have been investigated for more than one decade. In this topic, we will discuss our consensus of “tau oligomers” because the term of “tau oligomers” [e.g. dimer (disulfide bond-dependent or independent), multimer (more than dimer), granular (definition by EM or AFM) and maybe small filamentous aggregates] has been used by each researchers definition. From a biochemical point of view, tau protein has several unique characteristics such as natively unfolded conformation, thermo-stability, acid-stability, and capability of post-translational modifications. Although tau protein research has been continued for a long time, we are still missing the mechanisms of NFT formation. It is unclear how the conversion is occurred from natively unfolded protein to abnormally mis-folded protein. It remains unknown how tau protein can be formed filaments [e.g. paired helical filament (PHF), straight filament and twisted filament] in cells albeit in vitro studies confirmed tau self-assembly by several inducing factors. Researchers are still debating whether tau oligomerization is primary event rather than tau phosphorylation in the tau pathogenesis. Inhibition of either tau phosphorylation or aggregation has been investigated for the prevention of tauopathies, however, it will make an irrelevant result if we don’t know an exact target of neurotoxicity. It is a time to have a consensus of definition, terminology and methodology for the identification of “tau oligomers”.