Animal Models in Clinical Psychology Research Paper

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Over the years, considerable debate has surrounded the question of whether psychopathology and its treatment can be studied meaningfully in animals. One side has argued that psychopathological syndromes such as anxiety and depression are uniquely human and cannot be experienced in animals. Another side argues that there are both naturally occurring and experimentally induced psychopathological states in animals that closely parallel those seen in humans. This side also argues that there is so much to be learned from the systematic study in controlled settings of emotional or otherwise disturbed behavior in animals that this more than offsets any problems created by potential species differences. Proponents of this position bring animals into laboratory settings and study them under controlled experimental conditions to help us better understand various aspects of human disorders. The goal in these attempts is to develop an animal model of a disorder or its treatment.

1. Historical Background

Although the study of emotions such as fear and sadness in animals dates back at least to Darwin (1872), the experimental study in animals of the neurotic extremes of emotional states and other aspects of psychopathology did not begin until some years later (e.g., Pavlov 1927). Shortly after that time in the United States, where the methods of Pavlov and Thorndike to study learning were enthusiastically embraced, interest in Pavlov’s so-called ‘neuroses of the experiment’ spread during the 1930s and 1940s. Indeed, a number of well-known laboratories were established to study what came to be called experimental neurosis (e.g., Liddell, Gantt, Masserman, and N. R. F. Maier). At the time, this work was reasonably influential, partly because other extant models of what causes psychopathology were generally very primitive. By contrast, ideas for studying human psychopathologies through developing animal models seemed remarkably advanced. Indeed, the success of various experimental manipulations in producing disordered behavior and emotions in several different species, was clearly influential in establishing the foundations of behavioral approaches to the etiology and treatment of anxious and depressive disorders.

Unfortunately, this early work on experimental neurosis was fairly unsystematic. Investigators explored the effects of experimental variants on traditional learning paradigms (often discovered accidentally) that seemed to produce disturbed behavior in their animals. However, the next steps were not taken. One would have been to manipulate systematically various aspects of the procedures to determine what the critical (causal) features were. Investigators also needed to demonstrate (but did not) compelling phenotypic (symptomatic) and/or functional similarities between the ‘neurotic symptoms’ seen in animals and human patients. Instead, somewhat superficial, and often anthropomorphic, assertions of similarity were made. As a consequence of these failures, the study of animal models for psychopathological dis-orders fell into relative obscurity for several decades (see Mineka and Kihlstrom 1978).

2. Contemporary Use Of Animal Models

A resurgence of interest started about 1970, when a number of investigators began to make persuasive arguments that animal models of some disorders could be very useful if certain criteria are adhered to in developing the model. For example, Seligman (1975) and McKinney (1974) both argued that animal models can be useful if one attempts to document similarities and parallels in the symptoms, etiology, therapy, and prevention of the animal and human syndromes. Obviously, at the outset not all of the parallels will be possible to detail because little may be known about some of these factors (e.g., prevention) for either the animal or the human disorder. Nevertheless, herein lies one of the special advantages of developing an animal model. Initially some compelling similarities must be drawn between the human disorder and the animal model. Then, however, the animal model can be used to test hypotheses about other possible parallels (e.g., prevention) that often cannot easily be tested experimentally with humans. Some of the work developing such full-fledged animal models has been quite successful, as discussed below.

Alternatively, others have argued that requiring adherence to all these criteria may be unnecessarily restrictive, given that for most disorders no such complete models have yet been discovered. This is partly because of significant limitations on the range of human symptoms that can be modeled in animals— especially if expression of that symptom is mediated by higher cortical structures in the brain not shared by most species. There are, however, many very interesting and important ‘mini-models’ which help illuminate different aspects of the symptomatology, or etiology, or prevention, or treatment of these dis-orders. Mini-models are emotional, behavioral, cognitive, and/or physiological phenomena studied in animals (or humans) that may clarify some of the most prominent features of the origins or treatment of a disorder. The behaviors and emotional responses are manipulated experimentally through either behavioral or physiological experimental manipulations. Al-though any given mini-model may illuminate only a subset of prominent features of a disorder, in nature such factors would operate in interaction with other factors in the etiology or treatment of a human disorder.

3. Animal Models In Psychopharmacology And Behavioral Pharmacology

Nowhere has the use of animal models been more prominent than in the fields of psychopharmacology and behavioral pharmacology, where researchers develop new medications to treat mental disorders and try to understand how the medications work to ameliorate symptoms. Nearly all medications are initially tested on animals before being approved for use by humans—to determine both their effectiveness and their safety. However, before this can be done, researchers must first develop and validate an animal model of the human disorder (or often just a subset of symptoms of a disorder) before they can test their medications. For example, determining if a new medication serves as an anxiolytic (anxiety-reducing) medication, requires knowing how to produce strong symptoms of anxiety in animals (as well as knowing that the measure of anxiety is functionally if not phenotypically, related to human anxiety). The same, of course, applies to treatments of other disorders.

Staying with the anxiety example, at least 30 different animal models have been used to test the effectiveness of anxiolytic drugs. One of the most common uses a conflict punishment procedure. Rats are first trained to press a bar to obtain food reinforcement on an occasional basis. Later they can still obtain food on some trials but now they also receive an unpleasant electric shock following the food. Not surprisingly, this punishment procedure puts hungry rats in a state of conflict: anxiety about punishment now conflicts with hunger. Typically, rates of responding for the food are diminished substantially unless an effective anxiolytic medication is given (e.g., diazepam from the benzodiazepine category). Having been validated as a model in numerous studies with medications known to reduce anxiety in humans, the model is then used to test potential new anxiolytic compounds.

Researchers must beware, however, that this method produces both false positives and false negatives. Sometimes a medication that seems to work in the animal model, is later shown not to work in humans. Alternatively, a medication that does not seem effective with animal models may nonetheless be effective in humans. In such cases further work is needed to determine the source of the discrepancy. To illustrate, a relatively new anxiolytic compound known as buspirone (not from the benzodiazepine category) did not initially seem effective using the conflict punishment procedure in rats. However, buspirone operates through different physiological mechanisms, and has a different time course of action, than do traditional benzodiazepine compounds. Animal models incorporating this knowledge do show buspirone to be effective. Thus researchers must beware, when an established animal model does not demonstrate effectiveness of a novel compound, that the new compound should not be dismissed without further work. Such work is needed to avoid the risk of prematurely screening out potentially effective novel medications (e.g., Rodgers 1997).

Another use of pharmacological models involves testing theories of the physiological underpinnings of different disorders, rather than their treatment. Here researchers use various pharmacological agents to induce physiological and behavioral states in animals that resemble those seen in a human disorder. Caution is also needed here. Observing that a drug induces a state in animals resembling that in humans neither justifies the conclusion that the same system is normally involved in the human case, nor speaks to the issue of whether there may be a number of alternative routes to the human disorder (e.g., Weiss and Uhde 1990).

4. Animal Models Of Anxiety And Anxiety Disorders

4.1 Specific And Social Phobias

Historically, research on animal models of anxiety— especially fears and phobias—began before models of other disorders. The role of classical conditioning in the etiology of specific phobias, first proposed by Watson and Rayner (1920) has been the subject of some controversy since about 1970. Some theorists ask how classical conditioning can play an important role both: (a) when some people recall no traumatic conditioning experiences; and (b) and when others who can recall traumatic experiences are not fearful phobic. They have also wondered why some objects and situations are much more likely to become the objects of fears and phobias than others (e.g., phobias for snakes, spiders, and heights are far more common than for cars, guns, or knives, which may also be associated with trauma).

However, contemporary research with animal models illustrates that Pavlov’s and Watson’s core ideas about the role of classical conditioning were sound, but need to be expanded to incorporate the broader knowledge now available about the complexities of conditioning. For example, a primate model showed that conditioning sometimes occurs observationally or vicariously—that is, watching someone behave fearfully with, for example, a snake, may be sufficient to induce a fear of snakes in the observer (without any direct trauma occurring). Moreover, the role of conditioning (vicarious or direct) must be considered in light of various vulnerability and invulnerability factors that influence the outcome of a traumatic conditioning experience (cf. Mineka and Zinbarg 1996). For example, animal research by Pavlov and others laid the foundation for showing how individual differences in personality temperament (such as levels of trait anxiety) affect conditioning and the likelihood of acquiring fears and phobias. Animal work also illustrates a wide range of experiential differences across individuals that strongly affect the outcome of direct or indirect conditioning experiences (and therefore why many without phobias will have such histories that involved putative conditioning events). For example, having extensive previous neutral or positive experiences with a potentially phobic object (e.g., a dog) can prevent the acquisition of dog phobia if the individual is later bitten by a dog. Moreover, a primate model showed that being reared with a strong sense of mastery and control over one’s environment makes one less susceptible to the effects of the stressors that later may be involved in conditioning incidents.

Finally, there are evolutionarily based predispositions to acquire fears and phobias of certain objects or situations (e.g., snakes, water) that once posed a threat to our early ancestors more readily than other objects and situations not present in our early evolutionary history (e.g., guns, knives). Thus animal models have shown us that personality, experiential, and evolutionary factors may serve as diatheses or vulnerability factors for the development of phobias in certain individuals, given appropriate experiential input (cf., Mineka and Zinbarg 1996).

In social phobias, people have strong and persistent fears of various types of social interaction where they fear they may be evaluated and judged unfavorably. Again, traumatic conditioning experiences (direct or vicarious) are thought to play an important role, but with the same caveat as for specific phobias. That is, animal models demonstrate that personality, experiential, and evolutionary variables determine a person’s level of vulnerability invulnerability to developing social phobias. Considerable knowledge in this area stems from animal models of social anxiety (such as occur following defeats in physical fighting, when the animal typically becomes afraid of all dominant conspecifics rather than simply the one involved in the defeat) (cf. Mineka and Zinbarg 1996).

4.2 Panic Disorder With Agoraphobia

Individuals with panic disorder have recurrent un-expected panic attacks, usually associated with persistent anxiety about having another attack (anticipatory anxiety). Many also develop some degree of agoraphobic avoidance, learning to avoid situations in which they fear panicking. A full-fledged animal model of panic disorder remains elusive, although some pharmacological agents that provoke panic attacks in humans with the disorder, do seem to produce a panic-like state in some primates. Nevertheless, animal mini-models of panic and anxiety together have proved important in the development of a new theory of the origins of panic disorder that is largely based on contemporary principles of learning studied in animals (Bouton et al. 2001). The essence of this complex theory is that the occurrence of panic attacks sets the stage for the conditioning of anxiety to both internal and external cues that preceded a panic attack, thus explaining the development of both anticipatory anxiety and anxiety leading to agoraphobic avoidance. In addition, internal cues associated with the be-ginning of an attack can become conditioned to elicit panic attacks themselves. For example, a few heart palpitations that often occur early during an attack could come to serve as conditional stimuli that trigger full-blown panic attacks.

4.3 Post-Traumatic Stress Disorder (PTSD)

This disorder develops in some individuals following exposure to a traumatic event in which the person experienced or witnessed events involving actual or threatened death to themselves or others. Symptoms include persistent re-experiencing of the event (e.g., through nightmares and flashbacks), persistent avoidance of stimuli associated with the trauma, and arousal symptoms such as difficulty concentrating and exaggerated startle responses. Recently, animal models of PTSD have been the focus of much research, providing useful insights into the nature of this disorder as well as its etiology and treatment. Animal models involve exposure to unpredictable and/or uncontrollable stress which initiates the emotional, behavioral, and physiological symptoms resembling those seen in human PTSD. The intense physical stressors used in animal studies resemble those in some forms of human traumatization associated with PTSD, including torture, abuse, and assault. This has in turn drawn attention to the role that perceptions of uncontrollability unpredictablity play in the development of human PTSD symptoms and has led to studies testing these ideas.

This animal model has also shown the powerful role that various vulnerability and invulnerability factors play in determining who is more or less likely to develop PTSD, given exposure to the same trauma. For example, the animal model has revealed that prior exposure to uncontrollable stressors prior to the relevant trauma sensitizes the animal (or human), making it more likely to develop PTSD-like symptoms than animals without prior exposure to the uncontrollable stressors. Conversely, prior exposure to controllable stressors before the relevant trauma leads to an immunization effect, making it less likely the animal will develop PTSD-like symptoms. These hypotheses are beginning to be corroborated in human research. Finally, the idea that perceptions of uncontrollability and unpredictability mediate many aspects of PTSD has led to the formulation of hypotheses about the importance of re-instilling a sense of control and predictability as part of treatment. Such hypotheses are currently being tested (see Mineka and Zinbarg 1996).

5. Animal Models Of Depression

Clinically significant depression is a surprisingly common condition. There are emotional, motivational, cognitive and somatic symptoms. Some of these can be modeled better in animals than others (the cognitive ones are especially difficult). Since the 1960s, various animal models of depression have produced useful insights into human depression, ranging from new ideas concerning etiology, prevention, and treatment. The models have differed in several ways, perhaps most notably in the methods used for causing ‘depression’ in the animals.

Some of the earliest and most striking work with primates used a social separation paradigm. Following on earlier work demonstrating that human infants undergoing prolonged separations from their mothers showed a biphasic response to the separation, Harlow and colleagues in the 1960s began to study this phenomenon in infant rhesus monkeys separated from their mothers. Both the monkey and human infants typically go through an initial state of intense agitation and distress (the protest phase—often seen as a prototype of anxiety), followed several days later (if the separation persists) by a phase of despair depression, characterized by social withdrawal and rejection. Although some have argued this is at best a model of infant depression, others have argued that infant depression is in fact a prototype for adult human depression, with most of the prominent symptoms being functionally quite similar (except the cognitive ones).

By studying social separation in monkeys one can manipulate experimentally numerous variables, both before and during the separation, to test hypotheses about factors promoting minimal versus exaggerated responses to separation—something that obviously cannot be done in human infants. Research using animal models made it clear, for example, that having a sibling or alternate caregiver present during the separation from mother can attenuate (but usually not eliminate) the response to separation. But similar research with different species of monkeys, in which separated infants automatically get adopted by ‘aunts,’ also showed that reducing behavioral signs of distress is not tantamount to reducing physiological signs of distress and arousal which can remain high (e.g., Coe et al. 1985). Another line of primate work showed the importance of preseparation experiences in determining the outcome of any given separation. For example, infant monkeys of one species (bonnet macaques) whose mothers are relatively permissive, allowing the infants considerable freedom to interact with other adults, cope reasonably well with separations. By contrast, infants of another species (pigtail macaques) whose mothers are quite possessive and restrictive of their infant’s freedom, do not cope as well with separations (e.g., Kaufman 1973). Observational follow-up work with human infants has often corroborated the hypotheses developed based on experimental animal models which are better able to pinpoint causal factors (see Mineka and Zinbarg 1991).

Another influential animal model of depression derives from the learned helplessness phenomenon and theory (e.g., Seligman 1975). In the late 1960s, Seligman and his colleagues Maier and Overmier noted that laboratory dogs initially exposed to un-controllable shocks later showed major deficits in learning to control shock in different situations; indeed, they mostly seemed to accept the shock passively rather than trying to escape it. Yet animals first exposed to equal amounts of controllable shock showed no such deficits. Learned helplessness theory proposed that exposure to uncontrollable events leads one to learn that responses are ineffective in bringing relief, i.e., one is helpless to control important out-comes. The expectation of helplessness leads to: (a) cognitive deficits (difficulty learning to control shock), (b) motivational deficits (reduced incentive to try responding in other situations because of a belief that responses will be ineffective); (c) emotional changes (e.g., feelings of sadness, depression, and anxiety); and (d) physiological changes that occur with uncontrollable but not controllable stress. Seligman (1975) later proposed that the primary symptoms of depression resembled these primary changes seen with learned helplessness quite strongly.

Seligman also proposed etiological similarities. A large percentage of humans experiencing clinical depression have had one or more significant life stressors in the recent past (such as a major loss or unemployment, etc.). His argument was that all such precipitants could be seen as inducing a sense of lack or loss of control over important aspects of one’s environment. Thus perceptions of helplessness may be the proximal cause of such cases of depression. Finally, Seligman also developed the corollary hypothesis that re-instilling a sense of control may be a core ingredient in the most effective treatments for depression (see Peterson et al. 1993).

This animal model of depression led to an enormous amount of animal and human research, much of it continuing today. Interestingly, although originally developed as a model of depression, its relevance has expanded to include a role in theories of several anxiety disorders (most notably PTSD, see above). For example, the initial emotional state during and following uncontrollable stress is one of intense and diffuse anxiety, which may lapse later into a depressive state. This idea is highly consistent with neurochemical results, indicating a shift from an intense aroused anxious state to a later depressed state, sometimes called conservation-withdrawal (e.g., Woodson et al. 1998). Interestingly, as noted above, anxious symptoms also precede depressive symptoms during primate and human infant separations, as well as following major losses in adults (Bowlby 1980). In addition, far more people who suffer depression at some point in their lives have suffered from an anxiety disorder first than the reverse (cf. Maser and Cloninger 1990). Thus both animal models of depression discussed here illustrate important features of the sequential relationship between anxious and depressed symptoms that also occurs in humans.

Other animal models of depression have also pro-vided somewhat different but also partially overlap-ping information about both the symptom picture, and etiological factors in depression. The learned helplessness model has also generated hypotheses about effective treatment and prevention. Pharmaceutical companies make ample use of the most practical animal models to test their antidepressant com-pounds. Although recent etiological theories of human depression have generally now come to incorporate features that cannot be modeled in animals (such as feelings of hopelessness about the future), many useful insights from the original models remain generally intact.

6. Other Animal Models

Animal models of numerous other disorders have also been studied, including psychopathy, schizophrenia, and addictions. For example, regarding psychopathy, Newman (1997) and his colleagues used the well-known animal syndrome that stems from dysfunction in septo-hippocampal areas of the brain to model various features of psychopathic behavior—most notably the failure to inhibit inappropriate behaviors and inability to delay gratification. Fowles and Missel (1994) also summarized an important series of findings using animal and human mini-models, indicating the centrality of deficits in passive avoidance learning (learning what not to do to avoid punishment) to many important features of psychopathy. Both lines of work have led to new insights on psychopathy.

In schizophrenia, one early example of the use of animal models came when researchers first attempted to discovered how traditional antipsychotic medications work to reduce schizophrenic symptoms in humans. Animal research helped to show the important role that the neurotransmitter dopamine plays in the effects of these medications, and also helped lead to the development of the dopamine hypothesis of schizophrenia (including its etiology). This very influential theory, now known to be overly simplistic, was developed and tested in good part with animal mini-models.

Finally, the use of animal models to study of addictions has proved very important for understanding how addictive substances induce brain and behavioral changes. Using alcohol as an example, initially this work necessitated developing methods through which animals became addicted to alcohol (or other drug of interest). Subsequently, animal research with alcohol has revealed the numerous different neurotransmitter pathways in the brain with which alcohol interacts, leading to numerous alterations in brain function and behavior. Animal research has also facilitated understanding of brain mechanisms involved in maintaining the motivation and desire to drink. In addition, animal research focusing on environ-mental determinants of alcohol use, such as availability of alternative reinforcers, stress, and ease of access, etc., has provided important information. Some of this work has also focussed on genetic determinants of alcohol preference and alcohol use, and on how genetic factors interact with environ-mental factors (National Institute on Alcohol Abuse and Alcoholism 1997).

7. Conclusions

As indicated by this necessarily selective review of historical and contemporary research on animal models, such research has made important contributions to our understanding of various forms of human psychopathology and its treatment. Some of this research has attempted to develop full-fledged models by uncovering parallels between symptoms, etiology, treatment, and prevention in the animal model and the human disorder (e.g., the learned helplessness model of depression). However, an even greater amount of work exemplifies the mini-model approach in which only a subset of cardinal features of a human disorder are studied. An important advantage of studying animal models is that through experimental manipulation one can better determine what the critical causal features are than is generally possible in human research. With this background of success, further research with animal models certainly will continue to provide important new insights and information about many areas of human psychopathology and its treatment.

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