Biological basis of substance abuse
This volume describes our current understanding of the biological mechanisms in the central nervous system of nicotine, alcohol, cocaine, heroin, marijuana, and other drugs of abuse. Organized to focus on the similarities rather than the differences between drug actions, the processes undergo examination by level of cellular organization rather than by substance. The book proceeds from characterization of drug effects in relation to neurotransmitters and their receptors, through localization of drug effects in the brain in relation to specific anatomic structures. The impact of local stimulation or lesions on animal behaviors with respect to reward, reinforcement, desensitization and sensitization receive attention. Human genetic studies and therapeutic trials of addiction management complete the presentations.
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Diversity Among the Opioid Receptors
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acetylcholine actions activity acute addiction adenylate cyclase agonist alcohol AMPH amphetamine animals antagonist behavioral sensitization binding Biochem brain regions Brain Res buprenorphine calcium cannabinoid receptor carbamazepine caudate cells cellular chronic cocaine clinical cloned cocaine cocaine abuse cocaine administration cocaine self-administration cortex decrease dopaminergic doses drug abuse drugs of abuse effects of cocaine electrophysiological endogenous opioid enhanced ethanol extracellular function G-proteins GABA Gawin gene hippocampal increase inhibition inhibitory injections interactions intravenous Koob lesions levels ligands locus coeruleus mechanisms mediated membrane mg/kg molecular monkeys morphine mRNA naltrexone Nestler neurochemical neurons Neurosci neurotransmitter nicotine NMDA receptor nucleus accumbens opiate receptor opioid peptides opioid receptors pathways patients Pharmacol pharmacological phencyclidine postsynaptic potential pretreatment produced protein psychomotor stimulant rat brain regulation release response reward role self-stimulation sigma specific studies substance abuse subunit suggest synaptic tion treatment uptake ventral tegmental area vitro vivo withdrawal