Neurobiology of Mental Illness
Language: English
Pages: 1248
ISBN: B00O3F44YQ
Format: PDF / Kindle (mobi) / ePub
Our understanding of the neurobiological basis of psychiatric disease has accelerated in the past five years. The fourth edition of Neurobiology of Mental Illness has been completely revamped given these advances and discoveries on the neurobiologic foundations of psychiatry. Like its predecessors the book begins with an overview of the basic science. The emerging technologies in Section 2 have been extensively redone to match the progress in the field including new chapters on the applications of stem cells, optogenetics, and image guided stimulation to our understanding and treatment of psychiatric disorders. Sections' 3 through 8 pertain to the major psychiatric syndromes-the psychoses, mood disorders, anxiety disorders, substance use disorders, dementias, and disorders of childhood-onset. Each of these sections includes our knowledge of their etiology, pathophysiology, and treatment. The final section discusses special topic areas including the neurobiology of sleep, resilience, social attachment, aggression, personality disorders and eating disorders. In all, there are 32 new chapters in this volume including unique insights on DSM-5, the Research Domain Criteria (RDoC) from NIMH, and a perspective on the continuing challenges of diagnosis given what we know of the brain and the mechanisms pertaining to mental illness. This book provides information from numerous levels of analysis including molecular biology and genetics, cellular physiology, neuroanatomy, neuropharmacology, epidemiology, and behavior. In doing so it translates information from the basic laboratory to the clinical laboratory and finally to clinical treatment. No other book distills the basic science and underpinnings of mental disorders and explains the clinical significance to the scope and breadth of this classic text. The result is an excellent and cutting-edge resource for psychiatric residents, psychiatric researchers, doctoral students, and postdoctoral fellows the neurosciences.
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Processes as regional fate, cell type identity, neuronal maturation, and cell migration (Briscoe et al., 2000; Wilson and Rubenstein, 2000). Once neurons are generated, the next step in their differentiation is migration to the appropriate destination (Ayala et al., 2007). Each brain region has a specific migration program. In cortical structures (for example, cerebral cortex and superior colliculus), migrations are orchestrated to form layered or laminar structures. In most subcortical regions,.
Bilder, R.M., Goldman, R.S., Robinson, D., Reiter, G., Bell, L., Bates, J.A., Pappadopulos, E., Wilson, D.F., Alvir, J.M., Woerner, M.G., 11: NEUROCOGNITIVE ASSESSMENT Geisler, S., Kane, J.M., and Lieberman, J.A. (2000) Neuropsychology of first-episode schizophrenia: initial characterization and clinical correlates. Am. J. Psychiatry 157:549–559. Bowie, C.R., Reichenberg, A., Patterson, T.L., Heaton, R.K., and Harvey, P.D. (2006) Determinants of real-world functional performance in schizophrenia.
Network, from where it is ultimately packaged into vesicles. Because many neurotrophic factors lack a signal sequence, the idea that growth factors are secreted by the constitutive pathway occurred by default. However, specific antibodies used for immunohistochemical studies have revealed that BDNF is present in chromogranincontaining secretory granules and thus can secrete through the regulated pathway as well as the constitutive pathway. The pathway through which neurotrophic factors are.
Rectifying potassium current). cAMP: cyclic adenosine monophosphate; DAG: diacylglycerol; GABA: g -aminobutyric acid; 5HT: 5-hydroxytryptamine; IP3: intestinal peptide-3; VIP: vasoactive intestinal peptide. records from individual neurons and can examine how this neuron’s electrical activity is affected by different conditions. Yet here too, there can be logistical difficulties accounting for so many variables. Some investigators want to understand how one type of ion channel behaves under.
While mutations that hamper the GTPase activity of Ras are potently oncogenic. Second messengers themselves are rapidly degraded by specific enzymes. Phosphodiesterases transform cAMP and cGMP into inactive AMP and GMP, respectively (see Box 4.9). Inositol phosphates are dephosphorylated by specific phosphatases (see Box 4.12). Free cytosolic Ca2+ is buffered by binding proteins and rapidly eliminated by various pumps and exchangers either to the outside of the cell or into intracellular stores.