Larry R. Squire
Format: PDF / Kindle (mobi) / ePub
Fundamental Neuroscience, 3rd Edition introduces graduate and upper-level undergraduate students to the full range of contemporary neuroscience. Addressing instructor and student feedback on the previous edition, all of the chapters are rewritten to make this book more concise and student-friendly than ever before. Each chapter is once again heavily illustrated and provides clinical boxes describing experiments, disorders, and methodological approaches and concepts. A companion web site contains test questions, and an imagebank of the figures for ready use in presentations, slides, and handouts.
Capturing the promise and excitement of this fast-moving field, Fundamental Neuroscience, 3rd Edition is the text that students will be able to reference throughout their neuroscience careers!
New to this edition:
* 30% new material including new chapters on Dendritic Development and Spine Morphogenesis, Chemical Senses, Cerebellum, Eye Movements, Circadian Timing, Sleep and Dreaming, and Consciousness
* Companion website with figures, web links to additional material, and test questions
* Additional text boxes describing key experiments, disorders, methods, and concepts
* Multiple model system coverage beyond rats, mice, and monkeys
* Extensively expanded index for easier referencing
electron micrographs, the active zone is likely to be a highly structured specialization of the membrane and cytoskeleton (Fig. 7.1; also, see discussion later). Action potentials release transmitter by triggering the exocytosis of vesicles (Fig. 7.1B and 7.1C) and the release of their contents into the narrow synaptic cleft (about 100 nm wide) separating the presynaptic terminal from high concentrations of receptors on the postsynaptic membrane. At neuromuscular junctions, one of the best
accessory protein(s), leading to a greater postsynaptic response (Lisman, Schulman, & Cline, 2002; Opazo et al., 2010). The autophosphorylated kinase also serves as a scaffold to recruit the ubiquitin proteasome to synaptic sites that enable dynamic changes at the synapse. Protein Kinase C PKC can also be converted into a form that is independent, or autonomous, of its second messenger and can be described as a cognitive kinase. During the persistent phase of long-term potentiation, some
studies in laboratory animals, tracer amounts of radioactive 2-DG are injected intravenously; the animal is subjected to the behavioral paradigms of interest and sacrificed at the end of the experiment. Serial thin sections of the brain are prepared and processed for autoradiography. This autoradiographic method provides, after appropriate corrections, an accurate measurement of LCMRglu with a spatial resolution of a few millimeters. Using this method, researchers have determined LCMRglu in
cells emerge from the neural tube, they first enter a cell-free space in which they are easily identifiable (Fig. 15.1). Subsequently, they invade other tissues in which they are difficult to distinguish. Therefore, it is necessary to mark neural crest cells in order to study their migratory patterns and derivatives. A variety of techniques have emerged for this purpose, ranging from transplantation of tissue containing premigratory neural crest cells to lineage tracers and molecular markers.
form the enteric nervous system, which also receives a contribution from the lumbosacral neural crest. Within the gut, the earliest generated crest cells move as a wave from anterior to posterior to populate the bowel, which they appear to populate in sequence such that the anterior portions are populated by neural crest cells first and the cells move to progressively more posterior sites. Mice bearing a “lethal spotted” mutation lack neural crest cells in a portion of their bowel. This leads to