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Competing Conceptualizations of Anxiety

Competing Conceptualizations of Anxiety

In a number of papers published in the 1970s, Gray proposed a ‘‘neuropsychological theory of anxiety’’ that draws on the motivational constructs described before. This early work can best be viewed as an attempt to understand, in terms of the constructs of learning theory, the common behavioral effects of those pharmacological agents that clinically reduce anxiety. Among these are alcohol, barbiturates, and minor tranquilizers.

Gray  reviewed the extensive literature on the behavioral effects of antianxiety drugs, and he  summarized the conclusions from that review. The studies reviewed pointed to reduced effectiveness of the BIS in inhibiting behavior in response to PUN-CSs and nonREW-CSs. With respect to the paradigms described before, the antianxiety drugs disinhibit behavior in the passiveavoidance situation, and they increase resistance to extinction following continuous reinforcement. Rates of response are also reliably increased under fixed-interval, fixed-ratio, and differential reinforcement of low-rate (DRL) schedules. The common feature of these three schedules is that an event signals that the animal’s responses will not be rewarded for a period of time, thereby serving as a nonREW-CS. On the other hand, the antianxiety drugs do not affect responses that are viewed as primarily mediated by the BAS (e.g., simple reward learning and one-way active avoidance) or the fight/flight system. This specific effect of antianxiety drugs on the BIS, combined with the aversive quality of the stimuli that activate the BIS (i.e., cues for punishment and frustrative nonreward) make a strong case for Gray’s conclusion that the BIS represents an anxiety system.

Thus, Gray’s work provides a behavioral construct (the BIS) that is centrally involved in anxiety and that provides a link to biological treatments. In recent years, however, a burgeoning literature has emphasized the importance of the amygdala for developing conditioned fear. More specifically, the lateral nucleus of the amygdala receives input (CSs from fear conditioning), and the central nucleus of the amygdala generates output for the fear response (e.g., freezing, autonomic nervous system responses, stress hormone release, etc.). The work of Davis on the ability of CSs from fear conditioning to potentiate the startle response inspired Lang and his colleagues to develop the fear-potentiated startle paradigm with human subjects. This paradigm stimulated hundreds of studies and underscored the importance of the amygdala in fear and anxiety. Noting the popularity of this work on the amygdala and the view of many that the amygdala rather than the SHS is centrally involved in anxiety, Gray and McNaughton attributed the differences between the SHS/BIS theory and the amygdala/ startle theory to different starting points. Gray begins with the assumption that anxiolytic drugs affect anxiety and this path leads to the SHS. LeDoux and Davis begin with the assumption that responses to the CS in a classical aversive conditioning paradigm define anxiety and follow a path to the amygdala. In a summary and revision of Gray’s theory, McNaughton and Gray include the amygdala in an expanded and somewhat more complex BIS that provides, to some degree, an integration of the two approaches to understanding anxiety. McNaughton and Gray employ Blanchard’s distinction between fear-related versus anxiety-related behaviors. Fear-related behaviors are those associated with the fight/flight response when a predator or an impending punishment is present. In contrast, anxiety-related behaviors are associated with exploration or approach in an approach–avoidance conflict, when a predator/punishment may or may not be present, that is, fear involves simple avoidance without conflict, whereas anxiety involves approach and goal conflict. In this view, the SHS codes anxiety, whereas the amygdala mediates the fear that underlies both active and passive avoidance tendencies, controls behavioral avoidance consequent on anxiety, and increases arousal and autonomic responding. The SHS and its control of theta in the hippocampus is still the most important neural component of the BIS/anxiety system, and the amygdala is more obviously related to fear and fight/flight. However, the two structures are viewed as interacting in many situations as part of the BIS, and the amygdala contributes especially to passive avoidance in response to output from the SHS. To summarize, the different perspectives offered by the septohippocampal and the amygdala literatures have not been fully reconciled, but some suggestions can be made. First, the cornerstone of Gray’s theory of anxiety is the effects of anxiolytic drugs, whereas the amygdala/startle literature is tied strongly to immediate fear stimuli such as the CS in classical conditioning paradigms. Second, in the revised theory, the BIS is tied to approach–avoidance (goal) conflict. Anxiety derived from activity of the BIS involves approach to a source of danger, whereas the fight/ f light system and fear involve avoidance of a source of danger. The amygdala is centrally involved in fear and fight/flight. Third, activity in the central nucleus of the amygdala produces an increase in autonomic and central nervous system arousal, whereas activity in the SHS involves more information processing and is more cognitive.

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