The hypothesis that dopamine is important for reward has been proposed in a number of forms, each of which has been challenged. Normally, rewarding stimuli such as food, water, lateral hypothalamic brain stimulation and several drugs of abuse become ineffective as rewards in animals given performance-sparing doses of dopamine antagonists. Dopamine release in the nucleus accumbens has been linked to the efficacy of these unconditioned rewards, but dopamine release in a broader range of structures is implicated in the 'stamping-in' of memory that attaches motivational importance to otherwise neutral environmental stimuli.

Dopamine, learning and motivation

The theory is advanced that the common denominator of a wide range of addictive substances is their ability to cause psychomotor activation. This view is related to the theory that all positive reinforcers activate a common biological mechanism associated with approach behaviors and that this mechanism has as one of its components dopaminergic fibers that project up the medial forebrain bundle from the midbrain to limbic and cortical regions. Evidence is reviewed that links both the reinforcing and locomotor-stimulating effects of both the psychomotor stimulants and the opiates to this brain mechanism. It is suggested that nicotine, caffeine, barbiturates, alcohol, benzodiazepines, cannabis, and phencyclidine----each ofwhich also has psychomotor stimulant actions--may activate the docaminergic fibers or their output circuitry. The role of physical dependence in addiction is suggested to vary from drug to drug and to be of secondary importance in the understanding of compulsive drug self-administration. Attempts at a general theory of addiction are attempts to isr late--from a variety of irrelevant actionsmthose drug actions that are responsible for habitual, compulsive, nonmedical drug self-administration. The common assumption of addiction theorists is that general principles of addiction can be learned from the study of one drug and that these principles will have heuristic value for the study of other drugs. Thus far, attempts at a general theory of addiction have failed to isolate common actions that can account for addiction across the range of major drug classes. A major stumbling block has been the psychomotor stimulants--amph etamine and cocainemwhich do not readily fit models traditionally based on depressant drug classes. The present article offers a new attempt at a general theory of addiction. It differs from earlier theories (e.g., Collier, 1968; Himmelsbach, 1943; Jaffe & Sharpless, 1968; Jellinek, 1960; Kalant, 1977; Lindsmith, 1947; Solomon & Corbit, 1974) in that it is based on the common denominator of the psychomotor stimulants---amphetamine, cocaine, and related drugs---rather than on the common denominator of the socalled depressant drugs~opiates, barbiturates, alcohol, and others. We take up two topics before presenting the new theory. First, we briefly discuss the heuristic value of a biological approach and suggest that the biologist's distinction between homology and analogy offers a useful insight. Next we discuss the shortcomings of earlier theories--variants of dependence theory. Then we outline the new theory and review the relevant evidence for its three major assertions: (a) that all addictive drugs have psychomotor stimulant actions, (b) that the stimulant actions of these different drugs have a shared biological mechanism, and (c) that the biological mechanism of these stimulant

A psychomotor stimulant theory of addiction

There is an important gap between the implications of clinical research evidence and the routine clinical practice of healthcare professionals. Because individual decisions are often central to adoption of a clinical-related behaviour, more information about the cognitive mechanisms underlying behaviours is needed to improve behaviour change interventions targeting healthcare professionals. The aim of this study was to systematically review the published scientific literature about factors influencing health professionals' behaviours based on social cognitive theories. These theories refer to theories where individual cognitions/thoughts are viewed as processes intervening between observable stimuli and responses in real world situations. We searched psycINFO, MEDLINE, EMBASE, CIHNAL, Index to theses, PROQUEST dissertations and theses and Current Contents for articles published in English only. We included studies that aimed to predict healthcare professionals' intentions and behaviours with a clear specification of relying on a social cognitive theory. Information on percent of explained variance (R2) was used to compute the overall frequency-weighted mean R2 to evaluate the efficacy of prediction in several contexts and according to different methodological aspects. The cognitive factors most consistently associated with prediction of healthcare professionals' intention and behaviours were documented. Seventy eight studies met the inclusion criteria. Among these studies, 72 provided information on the determinants of intention and 16 prospective studies provided information on the determinants of behaviour. The theory most often used as reference was the Theory of Reasoned Action (TRA) or its extension the Theory of Planned Behaviour (TPB). An overall frequency-weighted mean R2 of 0.31 was observed for the prediction of behaviour; 0.59 for the prediction of intention. A number of moderators influenced the efficacy of prediction; frequency-weighted mean R2 varied from 0.001 to 0.58 for behaviour and 0.19 to 0.81 for intention. Our results suggest that the TPB appears to be an appropriate theory to predict behaviour whereas other theories better capture the dynamic underlying intention. In addition, given the variations in efficacy of prediction, special care should be given to methodological issues, especially to better define the context of behaviour performance.

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Healthcare professionals' intentions and behaviours: A systematic review of studies based on social cognitive theories

Nucleus accumbens shell and core dopamine: differential role in behavior and addiction

Behavioral models of impulsivity in relation to ADHD: Translation between clinical and preclinical studies

1 * Schedule-Controlled Behavior and the Effects of Drugs.- 1. Introduction.- 2. Schedule-Controlled Behavior.- 2.1. Processes of Reinforcement and Punishment.- 2.2. Schedules and Other Determinants of Reinforcement and Punishment.- 2.3. Control of Behavior by Noxious Stimuli.- 2.4. Nature and Significance of Schedule-Controlled Behavior.- 3. Effects of Drugs on Schedule-Controlled Behavior.- 3.1. Response Rate as a Determinant of the Behavioral Effects of Drugs.- 3.2. Effects of Drugs on Behaviors Maintained by Different Events.- 3.3. Effects of Drugs on Punished Responding.- 4. Summary and Conclusions.- 5. References.- 2 * The Effects of Drugs on Behavior Controlled by Aversive Stimul.- 1. Introduction.- 1.1. Methodological Issues Surrounding the Use of Electric Shock.- 1.2. Problems Associated with Operant Schedules That Utilize Electric Shock.- 2. Drug-Behavior Interactions in Conflict-Punishment Procedures.- 2.1. Geller Conflict Schedule.- 2.2. Effects of Drugs on Other Punishment Schedules and Species.- 2.3. Review of Drug Effects upon a Standard Conflict-Punishment Paradigm.- 2.4. Analysis of the Mechanisms by Which Drugs May Affect Punished Responding.- 2.5. Effects of Drugs That Alter Synaptic Activity upon Punished Behavior.- 2.6. Summary.- 3. Continuous Avoidance Procedures.- 3.1. Methodological Problems Associated with Continuous Avoidance Procedures.- 3.2. Analysis of Continuous Avoidance Behavior in Terms of Motivational Processes.- 3.3. Review of the Drug Literature.- 3.4. Classification of Drugs by Bovet-Gatti Profiles.- 3.5. Effects of Drugs That Alter Synaptic Activity on Continuous Avoidance Behavior.- 3.6. Conclusions Concerning the Effects of Drugs upon Continuous Avoidance Behavior.- 4. The Conditioned Emotional Response.- 4.1. Methodological Problems Associated with the CER Technique.- 4.2. Review of Drug Effects upon the CER.- 4.3. Conclusions Concerning the Effects of Drugs upon the CER.- 4.4. Continuous Avoidance and the CER.- 5. General Summary and Conclusions.- 6. References.- 3 * Stimulus Control and Drug Effects.- 1. Introduction.- 2. Multiple Schedules and Related Procedures.- 2.1. SD-S? Multiple Schedules.- 2.2. SD-SDMultiple Schedules.- 2.3. SD-SD Two-Key Procedures.- 3. Chained Schedules and Related Procedures.- 3.1. Chained Schedules.- 3.2. Signaled Fixed Consecutive Number.- 3.3. Matching to Sample.- 3.4. Repeated Acquisition of Behavioral Chains.- 4. Summary and Conclusions.- 5. References.- 4 * Drug-Induced Stimulus Control.- 1. Introduction.- 1.1. Scope.- 1.2. Terminology.- 2. Methods for the Demonstration of Drug-Induced Stimulus Control.- 2.1. Introduction.- 2.2. Response Choice.- 2.3. Response Emission.- 2.4. Comment.- 3. Interpretations of Drug-Induced Stimulus Control.- 3.1. Dimensions.- 3.2. Analysis of Data.- 3.3. Origin and Nature of Drug-Induced Stimuli.- 4. Epilogue.- 5. References.- 5 * The Effects of Drugs on Adjunctive Behavior.- 1. Operant and Adjunctive Behavior.- 1.1. Introduction.- 1.2. Examples of Adjunctive Behavior.- 1.3. Interpretations of Schedule-Induced Behavior.- 1.4. Importance of Adjunctive Behavior in Behavioral Pharmacology.- 2. Drugs and Adjunctive Behavior.- 2.1. Effects of Amphetamines.- 2.2. Effects of Anxiolytics.- 2.3. Effects of Anticholinergic Drugs and the Central Control of Adjunctive Behavior.- 2.4. Effects of Other Drugs.- 3. Conclusions.- 4. References.- 6 * Schedule-Induced Self-Administration of Drugs.- 1. Introduction.- 2. Schedule-Induced Ethanol Consumption.- 2.1. Lester's Original Observations.- 2.2. Differences between Schedule-Induced Ethanol Polydipsia and Schedule-Induced Water Polydipsia.- 2.3. Schedule Induction as a Means of Generating Excessive Ethanol Consumption.- 3. Determinants of Schedule-Induced Ethanol Polydipsia.- 3.1. Ethanol's Calorific Value.- 3.2. Ethanol's Pharmacological Effect.- 3.3. Taste.- 3.4. Polydipsia under Conditions of Choice.- 3.5. Loss of Control by the Inducing Schedule.- 4. Schedule-Induced Consumption of Drugs Other Than Ethanol.- 5. An Animal Model of Human Alcoholism.- 5.1. Forced Consumption of Ethanol.- 5.2. Intravenous and Intragastric Self-Administration.- 5.3. Schedule-Induced Ethanol Consumption.- 6. Summary.- 7. References.- 7 * Drugs as Reinforcers.- 1. Introduction.- 2. Establishment of Drugs as Reinforcers.- 2.1. Fixed-Ratio Schedules.- 2.2. Fixed-Interval Schedules.- 2.3. Complex Schedules.- 3. Type of Drug.- 4. Magnitude of Reinforcement.- 5. Satiation and Deprivation.- 6. Conditioned Drug Effects.- 7. Drugs as Negative Reinforcers.- 8. Punishment.- 9. An Application of Drug Self-Administration Techniques: The Preclinical Assessment of the Abuse Liability of New Compounds.- 10. Human Self-Administration Studies.- 11. Summary.- 12. References.- 8 * Behavioral Tolerance.- 1. Introduction.- 2. Behavioral Tolerance in Perspective.- 2.1. Behavioral Tolerance.- 2.2. Metabolic Tolerance.- 2.3. Learned Tolerance.- 2.4. Acute Tolerance.- 2.5. Cross Tolerance.- 2.6. Sensitization (Reverse Tolerance).- 3. Pharmacological and Organismic Factors.- 3.1. Dose Level.- 3.2. Dose Frequency.- 3.3. Response Topography.- 4. Environmental Factors: The Reinforcement Density Hypothesis.- 4.1. Data Consistent with the Hypothesis.- 4.2. Direct Support from Differential Tolerance.- 4.3. Exceptions.- 4.4. Assessment of the Density Hypothesis.- 5. Tolerance to Stimulus Properties of Drugs.- 6. Conclusions.- 7. References.- 9 * Behavioral Toxicology.- 1. Introduction.- 1.1. What Is Toxicology?.- 1.2. Origins of Behavioral Toxicology.- 2. Distinguishing Features of Behavioral Toxicology.- 2.1. Qualitative Evaluation of Effects.- 2.2. Role of Threshold Estimates.- 2.3. Chronicity Factor.- 2.4. Complications Associated with Chronic Studies.- 2.5. Multidisciplinary Features.- 3. Behavioral Toxicology in the Soviet Union.- 4. Substances of Current Interest.- 4.1. Mercury.- 4.2. Lead.- 4.3. Carbon Monoxide.- 4.4. Pesticides.- 4.5. Volatile Anesthetics and Solvents.- 5. Factors That Modulate the Behavioral Effects of Toxins.- 5.1. Diurnal Rhythms.- 5.2. Degree of Schedule Control.- 5.3. Discriminative Stimuli.- 5.4. Stimulus Complexity.- 6. Future Developments.- 6.1. Food Additives.- 6.2. Behavioral Teratology.- 6.3. Evaluations in the Natural Environment.- 6.4. Premarket Screening.- 7. Summary.- 8. References.- Author Index.

Contemporary Research in Behavioral Pharmacology

Part 1 Chronobiology - ethological and behavioural perspectives: circadian temporal orientation, B.J. Aschoff temporal regulation of behaviour in humans - a developmental approach, B.V. Pouthas timing - differences in continuity or generality beyond differences?, B.H. Lejeune. Part 2 Behaviour analysis and the emergence of rational thinking: equivalence relations - where do they come from?, B.M. Sidman naming and stimulus equivalence, B.N. Dugdale and C.F. Lowe development of thinking in mentally retarded children - has behaviourism something to offer?, B.J.L. Lambert reasoning and associative learning, B.G. Hall. Part 3 Behaviour analysis and language: some determinants of the production of temporal markers, B.J.P. Bronckart language and theory of mind - Vygotsky, Skinner and beyond, B.A. Riviere properties of rule-governed behaviour and their implications - behavioural medicine, A.C. Catania, et al behavioural and visceral functions, B.G. Adam, et al contribution of behavioural medicine to the research and prevention of AIDS, B.R. Bayes MammaCare - a case history in behavioural medicine, H.S. Pennypaker and M.M. Iwata. Part 5 Conclusion: behaviour, past and future, M. Richelle.

Behaviour analysis in theory and practice : contributions and controversies

The approach to psychology advocated by the radical behaviourists was often misunderstood and frequently gave rise to controversy. Originally published in 1974, this book introduced current research in operant conditioning and explains the attempt to understand behaviour inherent in such experiments at the time. After considering the philosophical context in which behaviouristic psychology developed, the author outlines the basic characteristics of operant research by reviewing single experiments on the effects of reinforcement on behaviour. Chapters on schedules of intermittent reinforcement extend this approach to more complex situations and emphasize that behaviour can be maintained and controlled in many different ways by environmental events.
The author then discusses recent work on conditional reinforcement and on the discriminative control of behaviour and shows how operant research has changed our understanding of these important concepts in psychology. Subsequent chapters review research within the operant paradigm on the effects on behaviour of punishment, anxiety, aversive stimuli and drugs, again by emphasising the special contribution to these topics made by operant conditioning techniques and methodology. The final chapters consider the general implications of operant research for educational practice and for clinical psychology, and place this approach within the context of psychology as a whole. Dr Blackman argues that it should be recognized as one important attempt to further the scientific analysis of behaviour.
This book, filled a long recognized need for an undergraduate text in this area at the time, and helped students form their own evaluation. Now it should be read in its historical context.

Derek E. Blackman

Papers

Contemporary Research in Behavioral Pharmacology

Behaviour analysis in theory and practice : contributions and controversies

Operant Conditioning: An Experimental Analysis of Behaviour

Behaviour Analysis and Contemporary Psychology

Experimental and Applied Analysis of Human Behavior