Cognitive science typically postulates unconscious mental phenomena, computational or otherwise, to explain cognitive capacities. The mental phenomena in question are supposed to be inaccessible in principle to consciousness. I try to show that this is a mistake, because all unconscious intentionality must be accessible in principle to consciousness; we have no notion of intrinsic intentionality except in terms of its accessibility to consciousness. I call this claim the “Connection Principle.” The argument for it proceeds in six steps. The essential point is that intrinsic intentionality has aspectual shape: Our mental representations represent the world under specific aspects, and these aspectual features are essential to a mental state's being the state that it is.

Once we recognize the Connection Principle, we see that it is necessary to perform an inversion on the explanatory models of cognitive science, an inversion analogous to the one evolutionary biology imposes on preDarwinian animistic modes of explanation. In place of the original intentionalistic explanations we have a combination of hardware and functional explanations. This radically alters the structure of explanation, because instead of a mental representation (such as a rule) causing the pattern of behavior it represents (such as rule-governed behavior), there is a neurophysiological cause of a pattern (such as a pattern of behavior), and the pattern plays a functional role in the life of the organism. What we mistakenly thought were descriptions of underlying mental principles in, for example, theories of vision and language were in fact descriptions of functional aspects of systems, which will have to be explained by underlying neurophysiological mechanisms. In such cases, what looks like mentalistic psychology is sometimes better construed as speculative neurophysiology. The moral is that the big mistake in cognitive science is not the overestimation of the computer metaphor (though that is indeed a mistake) but the neglect of consciousness.

It is traditionally believed that cerebral activation (the presence of low voltage fast electrical activity in the neocortex and rhythmical slow activity in the hippocampus) is correlated with arousal, while deactivation (the presence of large amplitude irregular slow waves or spindles in both the neocortex and the hippocampus) is correlated with sleep or coma. However, since there are many exceptions, these generalizations have only limited validity. Activated patterns occur in normal sleep (active or paradoxical sleep) and during states of anesthesia and coma. Deactivated patterns occur, at times, during normal waking, or during behavior in awake animals treated with atropinic drugs. Also, the fact that patterns characteristic of sleep, arousal, and waking behavior continue in decorticate animals indicates that reticulo-cortical mechanisms are not essential for these aspects of behavior.

These puzzles have been largely resolved by recent research indicating that there are two different kinds of input from the reticular activating system to the hippocampus and neocortex. One input is probably cholinergic; it may play a role in stimulus control of behavior. The second input is noncholinergic and appears to be related to motor activity; movement-related input to the neocortex may be dependent on a trace amine.

Reticulo-cortical systems are not related to arousal in the traditional sense, but may play a role in the control of adaptive behavior by influencing the activity of the cerebral cortex, which in turn exerts control over subcortical circuits that co-ordinate muscle activity to produce behavior.

The paradigmatic assumption that REM sleep is the physiological equivalent of dreaming is in need of fundamental revision. A mounting body of evidence suggests that dreaming and REM sleep are dissociable states, and that dreaming is controlled by forebrain mechanisms. Recent neuropsychological, radiological, and pharmacological findings suggest that the cholinergic brain stem mechanisms that control the REM state can only generate the psychological phenomena of dreaming through the mediation of a second, probably dopaminergic, forebrain mechanism. The latter mechanism (and thus dreaming itself) can also be activated by a variety of nonREM triggers. Dreaming can be manipulated by dopamine agonists and antagonists with no concomitant change in REM frequency, duration, and density. Dreaming can also be induced by focal forebrain stimulation and by complex partial (forebrain) seizures during nonREM sleep, when the involvement of brainstem REM mechanisms is precluded. Likewise, dreaming is obliterated by focal lesions along a specific (probably dopaminergic) forebrain pathway, and these lesions do not have any appreciable effects on REM frequency, duration, and density. These findings suggest that the forebrain mechanism in question is the final common path to dreaming and that the brainstem oscillator that controls the REM state is just one of the many arousal triggers that can activate this forebrain mechanism. The “REM-on” mechanism (like its various NREM equivalents) therefore stands outside the dream process itself, which is mediated by an independent, forebrain “dream-on” mechanism.

What makes humans moral beings? This question can be understood either as a proximate “how” question or as an ultimate “why” question. The “how” question is about the mental and social mechanisms that produce moral judgments and interactions, and has been investigated by psychologists and social scientists. The “why” question is about the fitness consequences that explain why humans have morality, and has been discussed by evolutionary biologists in the context of the evolution of cooperation. Our goal here is to contribute to a fruitful articulation of such proximate and ultimate explanations of human morality. We develop an approach to morality as an adaptation to an environment in which individuals were in competition to be chosen and recruited in mutually advantageous cooperative interactions. In this environment, the best strategy is to treat others with impartiality and to share the costs and benefits of cooperation equally. Those who offer less than others will be left out of cooperation; conversely, those who offer more will be exploited by their partners. In line with this mutualistic approach, the study of a range of economic games involving property rights, collective actions, mutual help and punishment shows that participants' distributions aim at sharing the costs and benefits of interactions in an impartial way. In particular, the distribution of resources is influenced by effort and talent, and the perception of each participant's rights on the resources to be distributed.

Given that natural selection is so powerful at optimizing complex adaptations, why does it seem unable to eliminate genes (susceptibility alleles) that predispose to common, harmful, heritable mental disorders, such as schizophrenia or bipolar disorder? We assess three leading explanations for this apparent paradox from evolutionary genetic theory: (1) ancestral neutrality (susceptibility alleles were not harmful among ancestors), (2) balancing selection (susceptibility alleles sometimes increased fitness), and (3) polygenic mutation-selection balance (mental disorders reflect the inevitable mutational load on the thousands of genes underlying human behavior). The first two explanations are commonly assumed in psychiatric genetics and Darwinian psychiatry, while mutation-selection has often been discounted. All three models can explain persistent genetic variance in some traits under some conditions, but the first two have serious problems in explaining human mental disorders. Ancestral neutrality fails to explain low mental disorder frequencies and requires implausibly small selection coefficients against mental disorders given the data on the reproductive costs and impairment of mental disorders. Balancing selection (including spatio-temporal variation in selection, heterozygote advantage, antagonistic pleiotropy, and frequency-dependent selection) tends to favor environmentally contingent adaptations (which would show no heritability) or high-frequency alleles (which psychiatric genetics would have already found). Only polygenic mutation-selection balance seems consistent with the data on mental disorder prevalence rates, fitness costs, the likely rarity of susceptibility alleles, and the increased risks of mental disorders with brain trauma, inbreeding, and paternal age. This evolutionary genetic framework for mental disorders has wide-ranging implications for psychology, psychiatry, behavior genetics, molecular genetics, and evolutionary approaches to studying human behavior.

Several theories claim that dreaming is a random by-product of REM sleep physiology and that it does not serve any natural function. Phenomenal dream content, however, is not as disorganized as such views imply. The form and content of dreams is not random but organized and selective: during dreaming, the brain constructs a complex model of the world in which certain types of elements, when compared to waking life, are underrepresented whereas others are over represented. Furthermore, dream content is consistently and powerfully modulated by certain types of waking experiences. On the basis of this evidence, I put forward the hypothesis that the biological function of dreaming is to simulate threatening events, and to rehearse threat perception and threat avoidance. To evaluate this hypothesis, we need to consider the original evolutionary context of dreaming and the possible traces it has left in the dream content of the present human population. In the ancestral environment human life was short and full of threats. Any behavioral advantage in dealing with highly dangerous events would have increased the probability of reproductive success. A dream-production mechanism that tends to select threatening waking events and simulate them over and over again in various combinations would have been valuable for the development and maintenance of threat-avoidance skills. Empirical evidence from normative dream content, children's dreams, recurrent dreams, nightmares, post traumatic dreams, and the dreams of hunter-gatherers indicates that our dream-production mechanisms are in fact specialized in the simulation of threatening events, and thus provides support to the threat simulation hypothesis of the function of dreaming.

Throughout the world people differ in the magnitude with which they value strong family ties or heightened religiosity. We propose that this cross-cultural variation is a result of a contingent psychological adaptation that facilitates in-group assortative sociality in the face of high levels of parasite-stress while devaluing in-group assortative sociality in areas with low levels of parasite-stress. This is because in-group assortative sociality is more important for the avoidance of infection from novel parasites and for the management of infection in regions with high levels of parasite-stress compared with regions of low infectious disease stress. We examined this hypothesis by testing the predictions that there would be a positive association between parasite-stress and strength of family ties or religiosity. We conducted this study by comparing among nations and among states in the United States of America. We found for both the international and the interstate analyses that in-group assortative sociality was positively associated with parasite-stress. This was true when controlling for potentially confounding factors such as human freedom and economic development. The findings support the parasite-stress theory of sociality, that is, the proposal that parasite-stress is central to the evolution of social life in humans and other animals.

Blindsight is the term commonly used to describe visually guided behaviour elicited by a stimulus falling within the scotoma (blind area) caused by a lesion of the striate cortex. Such “vision” is normally held to be unconscious and to be mediated by subcortical pathways involving the superior colliculus. Blindsight is of considerable theoretical importance since it suggests that destriate man is more like destriate monkey than had been previously believed and also because it supports the classical notion of two visual systems. It is also of potential clinical importance, since it has been claimed recently that systematic practice in blindsight can lead to the recovery of normal visual function in patients with cortical lesions. From a review of the literature it is concluded that all of the phenomena of blindsight can be attributed either to light scatter into unimpaired parts of the visual field or to residual vision resulting from spared striate cortex. The possible contribution f other factors is also considered. It is concluded that blindsight studies have generally failed to control for such nonblindsight interpretations partly because of poor methodology and partly because of difficulties in defining the term “blindsight.”

Experiments were carried out to investigate the extent to which subjects can exhibit performance similar to blindsight when they are using scattered light as a cue. This was done both with hemianopic subjects (by manipulating the amount of scattered and direct light coming from a stimulus) and with normal subjects (by presenting targets within their blind spots). Good blindsight performance was observed when only scattered light was available as a cue to the subjects. It is therefore concluded that an adequate case for blindsight has not been made. It is probably impossible to demonstrate the existence of blindsight on purely behavioural grounds. What is required is the establishment of relationships between visual function and independent anatomical evidence.

The implicit-explicit distinction is applied to knowledge representations. Knowledge is taken to be an attitude towards a proposition which is true. The proposition itself predicates a property to some entity. A number of ways in which knowledge can be implicit or explicit emerge. If a higher aspect is known explicitly then each lower one must also be known explicitly. This partial hierarchy reduces the number of ways in which knowledge can be explicit. In the most important type of implicit knowledge, representations merely reflect the property of objects or events without predicating them of any particular entity. The clearest cases of explicit knowledge of a fact are representations of one's own attitude of knowing that fact. These distinctions are discussed in their relationship to similar distinctions such as procedural-declarative, conscious-unconscious, verbalizable-nonverbalizable, direct-indirect tests, and automatic-voluntary control. This is followed by an outline of how these distinctions can be used to integrate and relate the often divergent uses of the implicit-explicit distinction in different research areas. We illustrate this for visual perception, memory, cognitive development, and artificial grammar learning.

In this paper, we consider human handedness and cerebral lateralization in a general biological context, and attempt to arrive at some conclusions common to the growth of human laterality and of other structural asymmetries. We suggest that many asymmetries appear to be under the influence of a left-right maturational gradient, which often seems to favor earlier or more rapid development on the left than on the right. If the leading side is damaged or restricted, this gradient may be reversed so that growth occurs with the opposite polarity. A mechanism of this sort appears to underlie the phenomenon of situs inversus viscerum et cordis, and the same principle may help explain the equipotentiality of the two sides of the human brain with respect to the representation of language in the early years of life. However we must also suppose that the leading side normally exerts an inhibitory influence on the lagging side, for otherwise one would expect language ultimately to develop in both halves of the brain. Examples of an inhibitory influence of this kind can also be found in other biological asymmetries; for instance, in the crab Alpheus heterochelis, one claw is normally greatly enlarged relative to the other, but if the larger claw is removed the smaller one is apparently released from its inhibitory influence and grows larger.

This last example is particularly interesting because it suggests a mechanism comparable to that proposed by Annett to account for the distribution of handedness in the human population. She argued, in effect, that there is a “right shift” factor among the majority of the population, but that among a minority who lack this factor handedness is determined at random. If it is supposed that cerebral lateralization is also determined at random among this recessive minority, the model can be extended to provide a reasonable fit to the data on the correlation between handedness and cerebral lateralization. However this genetic model (or any other) still fails to account for the near-binomial distribution of handedness among twins and among nontwin siblings. We suggest that right-handedness and leftcerebral dominance for language are manifestations of an underlying gradient which is probably coded in the cytoplasm rather than in the genes. We must leave open the question as to whether departures from this pattern are due to a recessive gene which effectively cancels the asymmetry to environmental influences, or to both genetic and cytoplasmic factors.

A preliminary attempt is made to analyze the intraspecific aggressive behavior of mammals in terms of specific neural circuitry. The results of stimulation, lesion, and recording studies of aggressive behavior in cats and rats are reviewed and analyzed in terms of three hypothetical motivational systems: offense, defense, and submission. A critical distinction, derived from ethological theory, is made between motivating stimuli that simultaneously activate functional groupings of motor patterning mechanisms, and releasing and directing stimuli that are necessary for the activation of discrete motor patterning mechanisms. It is suggested that motivating stimuli activate pathways that converge upon sets of homogeneous neurons, called motivational mechanisms, whose activity determines the motivational state of the animal.

A defense motivational mechanism is hypothesized to be located in the midbrain central gray. In addition to tactile, auditory, and visual inputs from the paleospinothalamic tract, lateral lemniscus, and (perhaps) from the pretectum, it may receive inputs from a major forebrain pathway whose functional significance is not yet understood.

A submission motivational mechanism is also thought to be located in the central gray. In addition to inputs for defense, it is thought to receive a necessary input from a “consociate (social familiarity cue) modulator” located in the ventromedial hypothalamus, which can switch behavior from defense to submission. The location of the hypothetical offense motivational mechanism is not known, although the pathways by which it is activated are traced in some detail.

Brain mechanisms of aggression in primitive mammals and in primates are apparently similar to those in rats and cats.

Human agents draw a variety of inferences effortlessly, spontaneously, and with remarkable efficiency – as though these inferences were a reflexive response of their cognitive apparatus. Furthermore, these inferences are drawn with reference to a large body of background knowledge. This remarkable human ability seems paradoxical given the complexity of reasoning reported by researchers in artificial intelligence. It also poses a challenge for cognitive science and computational neuroscience: How can a system of simple and slow neuronlike elements represent a large body of systemic knowledge and perform a range of inferences with such speed? We describe a computational model that takes a step toward addressing the cognitive science challenge and resolving the artificial intelligence paradox. We show how a connectionist network can encode millions of facts and rules involving n-ary predicates and variables and perform a class of inferences in a few hundred milliseconds. Efficient reasoning requires the rapid representation and propagation of dynamic bindings. Our model (which we refer to as SHRUTI) achieves this by representing (1) dynamic bindings as the synchronous firing of appropriate nodes, (2) rules as interconnection patterns that direct the propagation of rhythmic activity, and (3) long-term facts as temporal pattern-matching subnetworks. The model is consistent with recent neurophysiological evidence that synchronous activity occurs in the brain and may play a representational role in neural information processing. The model also makes specific psychologically significant predictions about the nature of reflexive reasoning. It identifies constraints on the form of rules that may participate in such reasoning and relates the capacity of the working memory underlying reflexive reasoning to biological parameters such as the lowest frequency at which nodes can sustain synchronous oscillations and the coarseness of synchronization.

A general conceptual framework for large-scale neocortical dynamics based on data from many laboratories is applied to a variety of experimental designs, spatial scales, and brain states. Partly distinct, but interacting local processes (e.g., neural networks) arise from functional segregation. Global processes arise from functional integration and can facilitate (top down) synchronous activity in remote cell groups that function simultaneously at several different spatial scales. Simultaneous local processes may help drive (bottom up) macroscopic global dynamics observed with electroencephalography (EEG) or magnetoencephalography (MEG).

A local/global dynamic theory that is consistent with EEG data and the proposed conceptual framework is outlined. This theory is neutral about properties of neural networks embedded in macroscopic fields, but its global component makes several qualitative and semiquantitative predictions about EEG measures of traveling and standing wave phenomena. A more general “metatheory” suggests what large-scale quantitative theories of neocortical dynamics may be like when more accurate treatment of local and nonlinear effects is achieved.

The theory describes the dynamics of excitatory and inhibitory synaptic action fields. EEG and MEG provide large-scale estimates of modulation of these synaptic fields around background levels. Brain states are determined by neuromodulatory control parameters. Purely local states are dominated by local feedback gains and rise and decay times of postsynaptic potentials. Dominant local frequencies vary with brain region. Other states are purely global, with moderate to high coherence over large distances. Multiple global mode frequencies arise from a combination of delays in corticocortical axons and neocortical boundary conditions. Global frequencies are identical in all cortical regions, but most states involve dynamic interactions between local networks and the global system. EEG frequencies may involve a “matching” of local resonant frequencies with one or more of the many, closely spaced global frequencies.

This article argues that mirror neurons originate in sensorimotor associative learning and therefore a new approach is needed to investigate their functions. Mirror neurons were discovered about 20 years ago in the monkey brain, and there is now evidence that they are also present in the human brain. The intriguing feature of many mirror neurons is that they fire not only when the animal is performing an action, such as grasping an object using a power grip, but also when the animal passively observes a similar action performed by another agent. It is widely believed that mirror neurons are a genetic adaptation for action understanding; that they were designed by evolution to fulfill a specific socio-cognitive function. In contrast, we argue that mirror neurons are forged by domain-general processes of associative learning in the course of individual development, and, although they may have psychological functions, they do not necessarily have a specific evolutionary purpose or adaptive function. The evidence supporting this view shows that (1) mirror neurons do not consistently encode action “goals”; (2) the contingency- and context-sensitive nature of associative learning explains the full range of mirror neuron properties; (3) human infants receive enough sensorimotor experience to support associative learning of mirror neurons (“wealth of the stimulus”); and (4) mirror neurons can be changed in radical ways by sensorimotor training. The associative account implies that reliable information about the function of mirror neurons can be obtained only by research based on developmental history, system-level theory, and careful experimentation.

The well-replicated observation that many people maintain mental health despite exposure to severe psychological or physical adversity has ignited interest in the mechanisms that protect against stress-related mental illness. Focusing on resilience rather than pathophysiology in many ways represents a paradigm shift in clinical-psychological and psychiatric research that has great potential for the development of new prevention and treatment strategies. More recently, research into resilience also arrived in the neurobiological community, posing nontrivial questions about ecological validity and translatability. Drawing on concepts and findings from transdiagnostic psychiatry, emotion research, and behavioral and cognitive neuroscience, we propose a unified theoretical framework for the neuroscientific study of general resilience mechanisms. The framework is applicable to both animal and human research and supports the design and interpretation of translational studies. The theory emphasizes the causal role of stimulus appraisal (evaluation) processes in the generation of emotional responses, including responses to potential stressors. On this basis, it posits that a positive (non-negative) appraisal style is the key mechanism that protects against the detrimental effects of stress and mediates the effects of other known resilience factors. Appraisal style is shaped by three classes of cognitive processes – positive situation classification, reappraisal, and interference inhibition – that can be investigated at the neural level. Prospects for the future development of resilience research are discussed.

As many as two million people in the United Kingdom repeatedly see people, animals, and objects that have no objective reality. Hallucinations on the border of sleep, dementing illnesses, delirium, eye disease, and schizophrenia account for 90% of these. The remainder have rarer disorders. We review existing models of recurrent complex visual hallucinations (RCVH) in the awake person, including cortical irritation, cortical hyperexcitability and cortical release, top-down activation, misperception, dream intrusion, and interactive models. We provide evidence that these can neither fully account for the phenomenology of RCVH, nor for variations in the frequency of RCVH in different disorders. We propose a novel Perception and Attention Deficit (PAD) model for RCVH. A combination of impaired attentional binding and poor sensory activation of a correct proto-object, in conjunction with a relatively intact scene representation, bias perception to allow the intrusion of a hallucinatory proto-object into a scene perception. Incorporation of this image into a context-specific hallucinatory scene representation accounts for repetitive hallucinations. We suggest that these impairments are underpinned by disturbances in a lateral frontal cortex–ventral visual stream system. We show how the frequency of RCVH in different diseases is related to the coexistence of attentional and visual perceptual impairments; how attentional and perceptual processes can account for their phenomenology; and that diseases and other states with high rates of RCVH have cholinergic dysfunction in both frontal cortex and the ventral visual stream. Several tests of the model are indicated, together with a number of treatment options that it generates.

Emotional arousal enhances perception and memory of high-priority information but impairs processing of other information. Here, we propose that, under arousal, local glutamate levels signal the current strength of a representation and interact with norepinephrine (NE) to enhance high priority representations and out-compete or suppress lower priority representations. In our "glutamate amplifies noradrenergic effects" (GANE) model, high glutamate at the site of prioritized representations increases local NE release from the locus coeruleus (LC) to generate “NE hotspots.” At these NE hotspots, local glutamate and NE release are mutually enhancing and amplify activation of prioritized representations. In contrast, arousal-induced LC activity inhibits less active representations via two mechanisms: 1) Where there are hotspots, lateral inhibition is amplified; 2) Where no hotspots emerge, NE levels are only high enough to activate low-threshold inhibitory adrenoreceptors. Thus, LC activation promotes a few hotspots of excitation in the context of widespread suppression, enhancing high priority representations while suppressing the rest. Hotspots also help synchronize oscillations across neural ensembles transmitting high-priority information. Furthermore, brain structures that detect stimulus priority interact with phasic NE release to preferentially route such information through large-scale functional brain networks. A surge of NE before, during, or after encoding enhances synaptic plasticity at NE hotspots, triggering local protein synthesis processes that enhance selective memory consolidation. Together, these noradrenergic mechanisms promote selective attention and memory under arousal. GANE not only reconciles apparently contradictory findings in the emotion-cognition literature but also extends previous influential theories of LC neuromodulation by proposing specific mechanisms for how LC-NE activity increases neural gain.

Human cooperation is highly unusual. We live in large groups composed mostly of non-relatives. Evolutionists have proposed a number of explanations for this pattern, including cultural group selection and extensions of more general processes such as reciprocity, kin selection, and multi-level selection acting on genes. Evolutionary processes are consilient; they affect several different empirical domains, such as patterns of behavior and the proximal drivers of that behavior. In this target article, we sketch the evidence from five domains that bear on the explanatory adequacy of cultural group selection and competing hypotheses to explain human cooperation. Does cultural transmission constitute an inheritance system that can evolve in a Darwinian fashion? Are the norms that underpin institutions among the cultural traits so transmitted? Do we observe sufficient variation at the level of groups of considerable size for group selection to be a plausible process? Do human groups compete, and do success and failure in competition depend upon cultural variation? Do we observe adaptations for cooperation in humans that most plausibly arose by cultural group selection? If the answer to one of these questions is “no,” then we must look to other hypotheses. We present evidence, including quantitative evidence, that the answer to all of the questions is “yes” and argue that we must take the cultural group selection hypothesis seriously. If culturally transmitted systems of rules (institutions) that limit individual deviance organize cooperation in human societies, then it is not clear that any extant alternative to cultural group selection can be a complete explanation.

This paper examines research on three hypnotic phenomena: suggested amnesia, suggested analgesia, and “trance logic.” For each case a social-psychological interpretation of hypnotic behavior as a voluntary response strategy is compared with the traditional special-process view that “good” hypnotic subjects have lost conscious control over suggestion-induced behavior. I conclude that it is inaccurate to describe hypnotically amnesic subjects as unable to recall the material they have been instructed to forget. Although amnesics present themselves as unable to remember, they in fact retain control over retrieval processes and accommodate their recall (or lack of it) to the social demands of the test situation. Hypnotic suggestions of analgesia do not produce a dissociation of pain from phenomenal awareness. Nonhypnotic suggestions of analgesia and distractor tasks that deflect attention from the'noxious stimuli are as effective as hypnotic suggestions in producing reductions in reported pain. Moreover, when appropriately motivated, subjects low in hypnotic suggestibility report pain reductions as large as those reported by highly suggestible hypnotically analgesic subjects. Finally, the data fail to support the view that a tolerance for logical incongruity (i.e., trance logic) uniquely characterizes hypnotic responding. So-called trance-logic-governed responding appears to reflect the attempts of “good” subjects to meet implicit demands to report accurately what they experience.

The understanding of decision-making systems has come together in recent years to form a unified theory of decision-making in the mammalian brain as arising from multiple, interacting systems (a planning system, a habit system, and a situation-recognition system). This unified decision-making system has multiple potential access points through which it can be driven to make maladaptive choices, particularly choices that entail seeking of certain drugs or behaviors. We identify 10 key vulnerabilities in the system: (1) moving away from homeostasis, (2) changing allostatic set points, (3) euphorigenic “reward-like” signals, (4) overvaluation in the planning system, (5) incorrect search of situation-action-outcome relationships, (6) misclassification of situations, (7) overvaluation in the habit system, (8) a mismatch in the balance of the two decision systems, (9) over-fast discounting processes, and (10) changed learning rates. These vulnerabilities provide a taxonomy of potential problems with decision-making systems. Although each vulnerability can drive an agent to return to the addictive choice, each vulnerability also implies a characteristic symptomology. Different drugs, different behaviors, and different individuals are likely to access different vulnerabilities. This has implications for an individual's susceptibility to addiction and the transition to addiction, for the potential for relapse, and for the potential for treatment.