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- BookEric J. Nestler, MD, PhD, Nash Family Professor and Chair of Neuroscience, Director, ... Show More Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, New York, Steven E. Hyman, MD, Harvard University Distinguished Service Professor, Professor of Stem Cell and Regenerative Biology, Director, Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, Massachusetts, David M. Holtzman, MD, Andrew B. and Gretchen P. Jones Professor, Chair, Department of Neurology, Washington University School of Medicine, St. Louis, Missouri, Robert C. Malenka, MD, PhD, Pritzker Professor of Psychiatry, Deputy Director, Stanford Neurosciences Institute, Stanford University, Palo Alto, California.Summary: Reviews the fundamental biochemistry of the functioning nervous system and then describes how nerve cells communicate with one another through numerous types of neurotransmitters involving amino acids, monoamines, neuropeptides, and neurotrophic factors, among several others.
Contents:
Basic principles of neuropharmacology
Cellular basis of communication
Synaptic transmission
Signal transduction in the brain
Excitatory and inhibitory amino acids
Widely projecting systems: monoamines, acetylcholine, and orexin
Neuropeptides
Atypical neurotransmitters
Autonomic nervous system
Neural and neuroendocrine control of the internal milieu
Pain
Neuroinflammation
Sleep and arousal
Higher cognitive function and behavioral control
Mood and emotion
Reinforcement and addictive disorders
Schizophrenia and bipolar disorder
Neurodegeneration
Seizure disorders
Stroke and migraine.Digital Access AccessNeurology 2015 - ArticleSteinmuller DR, Stilmant MM, Idelson BA, Monaco AP, Sahyoun AI, Lewis EJ, Davis RC, Couser WG.Clin Nephrol. 1978 May;9(5):210-8.Glomerulonephritis in transplant recipients often reflects recurrence of the immunopathogenetic mechanism causing the original renal disease. Membranous nephropathy (MN), a progressive immune complex mediated glomerular disease and the commonest cause of idiopathic nephrotic syndrome in adults, has been virtually unreported in transplant recipients. Two cases are reported here of typical MN (by clinical, light, immunofluorescent and electron microscopic criteria) developing de novo in the transplants of patients whose original diseases were anti-GBM nephritis and focal glomerular sclerosis. NM developed following episodes of viral hepatitis and renal infarction respectively. Possible mechanisms by which this lesion might develop in these patients are investigated and discussed. Chronic immune complex nephropathy (MN) can develop de novo in immunosuppressed transplant recipients apparently initiated by events in the post-transplant period.