T

acth

'adrenal cortex

Fig. 3.9. Diagram showing the primary stress circuits. Note the bimodal modulatory effects of cortisol on the amygdala and hippocampus. In the amygdala, cortisol stimulates the transmission of signals to the hypothalamus that cause it to release corticotropin-releasing factor (CRF), whereas, in the hippocampus, cortisol exercises an inhibitory influence over the secretion of CRF. In sum, these influences regulate (augment or restrain) the activation of the physiological response to stress via CRF-mediated adrenocorticotrophic hormone (ACTH) release by the pituitary gland. After LeDoux, (1996).

tations of the aversive CS (Richardson et al., 1988). Riccio and Spear suggest that the hormonal enhancement of extinction is attributable to the reenactment of a more complete internal representation of the original fear occurring when the aversive CS is presented without the US:

Further investigation is needed, but this finding is provocative in suggesting that, in addition to cognitive information about contingencies, elicitation of an affective response may contribute importantly to the elimination of fear-motivated behavior. (1991:232)

An opposite effect on learning appears to occur in the presence of endogenous opioids and narcotics (McGaugh, 1990). Opiates exert a strong inhibitory influence over noradrenergic neurons—an effect that is blocked by the administration of opioid antagonists (e.g., naloxone). NE-producing neurons projecting to the amygdala appear to play an important role in the retention of aversive associative learning. When narcotics are administered after aversive training, they interfere with the retention of fear conditioning. Also, increased opioid activity in the amygdala reverses the facilitatory effect of ep-inephrine on memory.

The memory-enhancing effect of epineph-rine is dose dependent, with high doses stimulating the memory-blocking activity of the opioid system. These observations suggest that the brain may actually have a built-in memory modulating or "erasing" mechanism associated with particularly aversive traumatic events. During times of intense sympathetic arousal when large amounts of epinephrine are secreted, stressful memories may be disrupted or prevented from forming. These findings are highly suggestive with regard to the persistence of some conditioned stimuli to extinction. Fanselow (1991) notes that aversive conditioning results in conditioned stimuli capable of evoking endogenous opi-oid production. Consequently, the presentation of the aversive CS in the absence of the US may impede extinction of the CS by eliciting the simultaneous release of beta-endor-phins, thereby physiologically obstructing the reenactment or representation of the original fear-conditioning situation.

In general, though, emotionally significant events are better remembered than nonemotional ones. An interesting implication of these findings is the possible beneficial effects of blocking adrenergic activity shortly after the occurrence of traumatic events. LeDoux (1996) has suggested that the administration of an epinephrine-blocking agent may serve as a prophylaxis against the development of lasting fears, negative memories, and the elaboration of emotional disorders following a traumatic experience. Since, as already noted, the brain opioid system appears to interfere with memory formation and retention, it may not be such a bad idea after all to take a good stiff drink following a particularly traumatic event. A potential implication of these findings for dogs is that increased opioid activity might reduce learned social fears following agonistic encounters, perhaps facilitating subsequent reconciliation between combatants, as well. Evidence from rodent studies suggests that strong opioid activity does occur following defeat. Miczek (1983) found that mice confronted with inescapable defeat experience a "large, lasting pain suppression" that appears to be mediated by endogenous opioid activity. Endorphins have also been shown to reduce affective aggression. If a similar phenomenon is present in dogs, this may have potential value in understanding some important aspects of dog social behavior. The emotions associated with submission are clearly of a different origin and quality than those associated with fear and avoidance, the former of which may include some element of fear but, in addition, is well buffered with very strong affiliative overtones. Submissive dogs do not avoid dominant opponents but accept defeat and adopt a subordinate role without an appearance of lasting fear. The possible facilitatory social function of opioids following defeat is consistent with the proposed general role of endogenous opioids in the formation and maintenance of social attachment and bonding among dogs (Panksepp, 1988; Hoffman, 1996).

Stress-related Influences on Cortical Functions

The disruptive influences of stress extend beyond the limbic feedback loops and the HPA system. In addition to the impact of stress on subcortical and physiological mechanisms, acute and persistent stress can generate pronounced dysregulatory effects over higher cortical activities as well. As already discussed, the prefrontal area serves many vital integrative and executive functions, which include impulse control and the coordinated regulation of behavioral systems needed to meet the various internal and external demands placed on the animal to adjust. The provision of a flexible adaptational interface between the organism and the environment appears to be a prominent function of the prefrontal cortex. This prefrontal function is mediated by learning and the exertion of inhibitory and modulatory influences over subcortical processes. Under the adverse conditions of excessive stress, however, subcortical activities are amplified while, at the same time, corresponding cortical regulatory functions may be temporarily disrupted. In particular, acute stress has a robust excitatory effect on the amygdala, which, in turn, coordinates the expression of numerous preparatory systems that mobilize an organism for impending emergency action. During such stressful activation, increased levels of NE and dopamine are released in the pre-frontal cortex. Although increased cate-cholamine activity appears to have a facilita-tory effect on subcortical processes, the release of these neurotransmitters in the pre-frontal area has an opposite effect, causing it temporarily to suspend its efficient functioning. Instead of enhancing prefrontal functions, as it does in the amygdala, increased dopamine (especially involving D1 receptors) tends to suspend or disrupt cortical restraint over subcortical activity (Arnsten, 1998). As a result, the benefits of previous learning, impulse control, and social inhibition may be momentarily compromised or turned off, with control taken over by species-typical offensive and defensive action patterns. Under the influence of stress, the behavioral thresholds for these innate patterns are lowered while, simultaneously, their expression is amplified by limbic pathways enhanced by increased catecholamine and CRF activity.

These changes point to several significant effects of stress on the behavior of dogs. Foremost is the possibility that stress-mediated activation of the nervous system may disrupt normal cortical control over the expression of undesirable behavior associated with fear and anger. The foregoing findings underscore the importance of canine husbandry and management efforts that strive to reduce stressful influences in a dog's environment. Unfortunately, stress is a fairly ubiquitous phenomenon in the life of most dogs. Among the most common sources of adverse stress are excessive confinement, insufficient exercise and attention, sensory distress (e.g., exposure to loud noises), separation distress, poorly predicted and uncontrollable training events (especially excessive punishment), and frustration. The loss of predictability and control over significant aversive and appetitive events results in increased anxious arousal and frus-trative persistence—both sources of stress associated with the development of many behavior problems. Although the connection between anxiety and the physiological mobilization of stress is well known and recognized, frustration is also an important source of stress (Coover et al., 1971). The combined influence of such behavioral sources of stress on the elaboration of behavioral dysfunction and disorganization are discussed at length in Chapter 9, which is dedicated to the influence of adverse learning conditions on behavior.

Exercise and the Neuroeconomy of Stress

Counteracting the effects of stress depends on a twofold process of altering the environment and providing training and socialization activities that are both highly predictable and controllable. Another common recommendation used to counteract the adverse effects of stress is exercise. The experimental study of exercise indicates that it exerts a considerable, and potentially therapeutic, influence on the physiology of dogs. For example, Radosevich and colleagues (1989) demonstrated that moderate exercise produces pervasive modu-latory effects on both peripheral and central endocrine activity in dogs. In addition to the release of various HPA system hormones (beta-endorphins, ACTH, and cortisol), exercise also increases the production of NE. Surprisingly, under conditions of low-intensity exercise (running a treadmill at 4.2 miles/hour on a 6% incline for 90 minutes), a coordinated and commensurate increase of beta-endorphins and ACTH was observed; whereas, in the case of high-intensity exercise (4.2 miles/hour on a 20% incline for 90 minutes), the expected trajectory of increased production of these substances did not proceed linearly—that is, the release of beta-en-dorphins and ACTH is dose dependent on the amount of exercise received. Also, the cerebrospinal fluid (CSF) of exercised dogs contains greater amounts of NE.

Many studies with animals (especially rodents) have shown that neurotransmitter activity is influenced by exercise (Meeusen and DeMeirleir, 1995). Although acute and forced treadmill exercise appears to deplete NE stores in the brain (as observed in learned helplessness) and is physiologically stressful for animals, chronic exercise appears to enhance noradrenergic activity and increases the amount of NE stored in several parts of the brain. Besides enhancing noradrenergic activity, exercise was also found to increase serotonin levels in the central amygdala (Chaouloff, 1997). These combined influences are believed to be responsible for some of the beneficial mood effects associated with exercise.

The finding that exercise enhances sero-tonergic activity is of considerable importance with respect to the use of exercise for the management of stress-related behavior problems. Within the brain's neuroeconomy, serotonin plays an important modulatory role over stress and the control of undesirable impulsive behavior. Promising evidence in support of a functional link between serotonin production and exercise has been reported by Dey and his associates (1992), who demonstrated a significant alteration of central sero-tonergic activity in rats exposed to chronic exercise. Daily exercise was found to generate pronounced and sustained enhancement of serotonin metabolism in various areas of the brain, including the cerebral cortex. The au thors suggest that the cortex is the most likely neural site mediating the beneficial effects of exercise over depression. They refer to other research with rodents that has shown that experimentally induced depression produces a decreased level of serotonin in the frontal area. Signs of depression in these animals were reversed by administering microinjections of serotonin into the frontal cortex, whereas similar microinjections of NE, dopamine, and gamma-aminobutyric acid failed to alleviate depression similarly. Interestingly, Dey (1994) found that long-term exercise (4 weeks) had a pronounced immunizing effect on rats exposed to stress-induced depression. Chronic exercise prevented the signs of behavioral depression and generated a "remarkable enhancement" of 5-HT2 receptor subtype responsiveness. In general, the response of serotonin receptor subtypes to exercise was very similar to the effects produced by tricyclic antidepressants. A similar effect has been reported by Chaouloff (1997) with respect to NE. He found that exposure to chronic and free-choice wheel running has an immunizing effect against NE depletion resulting from uncontrollable and inescapable foot shock.

The aforementioned studies support the hypothesis that exercise, especially daily and long-term exercise, has potentially beneficial effects on the neuroeconomy of the dog. Many dog-behavior consultants and trainers have long recommended exercise for the amelioration of a wide variety of behavior problems. Although the research is far from conclusive, the beneficial influence of exercise in combination with appropriate behavioral (e.g., basic training and behavior modification) and environmental interventions is a sensible approach to the management of stress-related behavior problems.

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Dog Owners Handbook

Dog Owners Handbook

There are over a hundred registered breeds of dogs. Recognizing the type of the dog is basically associated with its breed. A purebred animal belongs to a documented and acknowledged group of unmixed lineage. Before a breed of dog is recognized, it must be proven that mating two adult dogs of the sametype would have passed on their exact characteristics, both appearance and behavior, to their offspring.

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