Elements of Molecular Neurobiology
C. U. M. Smith
Format: PDF / Kindle (mobi) / ePub
This edition of the popular text incorporates recent advances in neurobiology enabled by modern molecular biology techniques. Understanding how the brain works from a molecular level allows research to better understand behaviours, cognition, and neuropathologies. Since the appearance six years ago of the second edition, much more has been learned about the molecular biology of development and its relations with early evolution. This "evodevo" (as it has come to be known) framework also has a great deal of bearing on our understanding of neuropathologies as dysfunction of early onset genes can cause neurodegeneration in later life. Advances in our understanding of the genomes and proteomes of a number of organisms also greatly influence our understanding of neurobiology.
* Well known and widely used as a text throughout the UK, good reviews from students and lecturers.
* Good complement to Fundementals of Psychopharmacology by Brian Leonard.
This book will be of particular interest to biomedical undergraduates undertaking a neuroscience unit, neuroscience postgraduates, physiologists, pharmacologists.
It is also a useful basic reference for university libraries.
Maurice Elphick, Queen Mary, University of London
"I do like this book and it is the recommended textbook for my course in Molecular Neuroscience. The major strength of the book is the overall simplicity of the format both in terms of layout and diagrams."
372 372 374 376 380 382 383 385 389 18 . . . . . 390 . . . . . . . . . . . . . . . . . . . . 392 393 395 396 . . . . . 397 . . . . . 399 . . . . . 400 The Postsynaptic Cell . . . . . . . . . . . . . . 17.1 Synaptosomes . . . . . . . . . . . . . . . . . 17.2 The Postsynaptic Density . . . . . . . . . 17.3 Electrophysiology of the Postsynaptic Membrane. . . . . . . . . . . . . . . . . . . . 17.3.1 The Excitatory Synapse . . . . . . . BOX 17.1: Cajal, Sherrington and the beginnings of
formation of an aminoacyl–tRNA complex. First, an ATP molecule ﬁnds its way to the adenine site on the synthetase molecule and an amino acid with a side chain which ﬁts the amino acid site occupies the amino acid site. Next, the synthetase molecule catalyses the formation of aminoacyl-AMP, using the energy of one of ATP’s energy-rich bonds, and releasing pyrophosphate. The amino acid is said to be ‘activated’. Lastly, the aminoacyl-AMP reacts with tRNA to form an aminoacyl–tRNA complex, releasing
growth and cell division. They are called proto-oncogenes. When a protooncogene mutates it may result in an oncogene which programs unregulated cell division, i.e. cell division without regard to the needs of the rest of the organism. Oncogenes thus lead to cancerous growths. The study of proto-oncogenes and oncogenes has been of great importance in cancer research. It has been known for some ninety years that some viruses can cause cancer. It was shown by Rous in 1911 that a virus could cause
evolutionary time. The proto-oncogene has subsequently mutated or its expression otherwise altered so that when reincorporated into the eukaryotic genome and transcribed it acts as a cancer-forming oncogene. Biologists preﬁx the viral oncogene with ‘v’ and its eukaryotic homologue with ‘c’. How is it that mutation of a proto-oncogene can have such catastrophic eﬀects on the host cell and its neighbours? The answer to this question lies in the processes which proto-oncogenes control. These include
cases (e.g. sea-urchin oocyte) it can be shown that although all the necessary mRNA is present in the cytoplasm very little, if any, translation, occurs until the egg is fertilised. Presumably some triggering factor is released by sperm entry. In other cases the stability of the mRNA strand may be affected so that it persists for a longer or shorter time in the cytoplasm and hence programs the synthesis of more or less polypeptide. In yet other cases it has INFORMATION PROCESSING IN CELLS 75