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The results of the study showed that D-Amphetamine had a significant effect on the acquisition of the active avoidance conditioning (CAR).

No description available.

For over half of a century, social and behavioral scientists have been investigating the construct of psychopathy. Even so, psychopathy is still a highly misunderstood personality construct. Even though it has been estimated that psychopaths make up only about 1% of the general population, they are believed to consist of 15-25% of the prison population (Hare, 1996). However, not all psychopaths are in prison. Psychopaths can also be found in such fields as the legal profession, the business world and in politics (Babiak, 1995). In terms of criminal behaviors, psychopaths are arrested at earlier ages, have a higher rate of offending, commit a wider array of offenses, are more likely to have used weapons and threatened violence, and are more likely to have used violence (Hart and Hare, 1997; Hare and McPherson, 1984; Serin, 1991; Wong, 1985). Also, once released from an institution, rates of recidivism for psychopaths are found to be higher than those for other criminals regarding both violent and FTSnon-violent criminal acts (Hemphill, Hare & Wong, 1998). Therefore, the societal importance of the psychopathy construct demanded that more research be conducted to better understand its underlying etiology, potential variants in typology, clinical course and potential treatment. Prior theories have proposed subtypes of psychopathy based on cognitive variables (passive avoidance errors) and on physiological variables (BIS/BAS) and on environmental variables (supportive upbringing or not). This study utilized self-report measures to assess the presence of psychopathy and to test the validity of the cognitive and physiological explanations for subtypes of psychopathy. A cognitive dissonance task tested the validity of the physiological theory and an alteration of a punishment task which increases the degree and strength of punishment tested the cognitive theory. Further, for the first time the construct of optimism was tested to determine it's role in parsing out two types of psychopathy.

Project success rate declined from 62% in 2012 to 60% in 2015 despite advances in methods and tools. Project managers need emotional intelligence and leadership style to reduce the risk of project failure. Successful projects are assets to the organization and to the whole community. The purpose of this correlational study was to examine the relationship between transformational leadership, transactional leadership, passive avoidance leadership, emotional intelligence, and project manager performance. Project managers from different industries in the states of Virginia and Maryland, and the District of Columbia were administered the Multifactor Leadership Questionnaire, Self-Report of Emotional Intelligence, and Behaviorally Anchored Rating Scales questionnaires. The results of the multiple linear regression analysis indicated the full model (nine predictors) significantly predict project manager performance, F(9, 92) = 8.330, p = .002, R2 = .449. The R2 value (.449) indicated approximately 45% of the variance in project manager performance was accounted for by the linear combination of the predictor variables. Inspirational motivation was the only significant contributor to the model (t = 3.213, Ã? = 3.959, p = .002). The result indicated that project manager performance tends to increase as inspirational motivation increases. The results of this study may have implications for positive social change include the potential for business leaders to enhance project manager performance through employing inspirational, motivational, and charismatic leadership techniques. Business leaders who improve project managers' performance increase the propensity of organizational success. Successful organizations are sources of economic growth which reduces poverty and improves the quality of life.

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No description available.

Posttraumatic stress disorder is a debilitating anxiety disorder that can develop in the aftermath of a traumatic or life–threatening event involving extreme horror, intense fear or bodily harm. The disorder is typified by a symptom triad consisting of re–experiencing, hyperarousal and avoidance symptoms. Approximately 15–25% of trauma–exposed individuals go on to develop PTSD, depending on the nature and severity of the trauma. Although dysfunctional adaptive responses exist in multiple neurobiological pathways in the disorder, e.g. glutamate, GABA, glucocortocoids and serotonin, the noradrenergic system is particularly prominent and represents an important pharmacological target in attempts at preventing the development of PTSD posttrauma. However, current literature shows opposing and conflicting results regarding the effect of selective noradrenergic agents in memory processing, and the effect of modulation of selective noradrenergic receptors are spread over diverse protocols and paradigms of learning and fear also employing different strains of animals. Fear conditioning is a behavioural paradigm that uses associative learning to study the neural mechanisms underlying learning, memory and fear. It is useful in investigating the underpinnings of disorders associated with maladaptive fear responses. Performing fear conditioning experiments with the aim of applying it to an animal model of PTSD, and relating these behavioural responses to a defined neural mechanism, will assist both in the elucidation of the underlying pathology of the disease, as well as the development of more effective treatment. This project has set about to re–examine the diverse and complex role of noradrenergic receptors in the conditioned fear response with relevance to PTSD. To the best of my knowledge, this study represents the first attempt at studying a range of noradrenergic compounds with diverse actions and their ability to modify conditioned fear in a single animal model. This work thus introduces greater consistency and comparative relevance not currently available in the literature, and will also provide much needed pre–clinical evidence in support of treatment strategies targeting the noradrenergic system in the prevention of PTSD posttrauma. The first objective of this study was to set up and validate a passive avoidance fear conditioning protocol under our laboratory conditions using the Gemini Avoidance System. The noradrenergic system plays a prominent role in memory consolidation and fear conditioning, while administration of –adrenergic blockers, such as propranolol, have been shown to abolish learning and fear conditioning in both humans and animals. Propranolol has also demonstrated clinical value in preventing the progression of acute traumatic stress syndrome immediately posttrauma to full–blown PTSD. To confer predictive validity to our model, the centrally active –adrenergic antagonist, propranolol, and the non–centrally acting –adrenergic antagonist, nadolol, were administered to Wistar rats after passive avoidance fear conditioning training in the Gemini Avoidance System. Wistar rats were used because of their recognised enhanced sensitivity to stress. Evidence from this pilot study confirmed that propranolol 10 mg/kg significantly inhibits the consolidation of learned fear in rats, whereas nadolol is ineffective. This effectively validated our protocol and the apparatus for further application in this study and also confirmed the importance of a central mechanism of action for –adrenoceptor blockade in the possible application of these drugs in preventing the development of PTSD posttrauma. The second objective of this study was to investigate the role of 1–, 2–, 1–, and 2–receptors in a conditioned fear passive avoidance paradigm. This was done in order to investigate how selective pharmacological modulation of these receptors may modify the conditioned fear response, and whether any of these receptor systems might exert opposing effects in passive fear conditioning. Various centrally active noradrenergic agents were employed over a 3–tiered dose response design, including the 1–antagonist, prazosin, the 2–agonist, guanfacine, the 2–antagonist, yohimbine, the 1–antagonist, betaxolol and the 2–antagonist ICI 118551. The effect of post–exposure administration of these drugs on conditioned fear was compared to that of propranolol 10 mg/kg. Selected doses of betaxolol (10 mg/kg) and ICI 118551 (1 mg/kg) attenuated fear conditioning to an extent comparable to propranolol, as did prazosin (0.1 mg/kg). Yohimbine tended to boster fear learning at all doses tested, albeit not significantly, while guanfacine did not produce any significant effect on memory retention at any of the doses studied. This latter observation was surprising since yohimbine tended to bolster fear conditioning while earlier studies indicate that 2–agonism impairs conditioned fear. Concluding, this study has conferred validity to our passive avoidance model and has provided greater insight into the separate roles of noradrenergic receptors in contextual conditioned fear learning. The study has provided supportive evidence for a key role for both 1– and 2–antagonism, as well as 1–antagonism, in inhibiting fear memory consolidation and hence as viable secondary treatment options to prevent the development of PTSD posttrauma. However, further study is required to delineate the precise role of the 2–receptor in this regard. / Thesis (M.Sc. (Pharmacology))--North-West University, Potchefstroom Campus, 2012.

Posttraumatic stress disorder is a debilitating anxiety disorder that can develop in the aftermath of a traumatic or life–threatening event involving extreme horror, intense fear or bodily harm. The disorder is typified by a symptom triad consisting of re–experiencing, hyperarousal and avoidance symptoms. Approximately 15–25% of trauma–exposed individuals go on to develop PTSD, depending on the nature and severity of the trauma. Although dysfunctional adaptive responses exist in multiple neurobiological pathways in the disorder, e.g. glutamate, GABA, glucocortocoids and serotonin, the noradrenergic system is particularly prominent and represents an important pharmacological target in attempts at preventing the development of PTSD posttrauma. However, current literature shows opposing and conflicting results regarding the effect of selective noradrenergic agents in memory processing, and the effect of modulation of selective noradrenergic receptors are spread over diverse protocols and paradigms of learning and fear also employing different strains of animals. Fear conditioning is a behavioural paradigm that uses associative learning to study the neural mechanisms underlying learning, memory and fear. It is useful in investigating the underpinnings of disorders associated with maladaptive fear responses. Performing fear conditioning experiments with the aim of applying it to an animal model of PTSD, and relating these behavioural responses to a defined neural mechanism, will assist both in the elucidation of the underlying pathology of the disease, as well as the development of more effective treatment. This project has set about to re–examine the diverse and complex role of noradrenergic receptors in the conditioned fear response with relevance to PTSD. To the best of my knowledge, this study represents the first attempt at studying a range of noradrenergic compounds with diverse actions and their ability to modify conditioned fear in a single animal model. This work thus introduces greater consistency and comparative relevance not currently available in the literature, and will also provide much needed pre–clinical evidence in support of treatment strategies targeting the noradrenergic system in the prevention of PTSD posttrauma. The first objective of this study was to set up and validate a passive avoidance fear conditioning protocol under our laboratory conditions using the Gemini Avoidance System. The noradrenergic system plays a prominent role in memory consolidation and fear conditioning, while administration of –adrenergic blockers, such as propranolol, have been shown to abolish learning and fear conditioning in both humans and animals. Propranolol has also demonstrated clinical value in preventing the progression of acute traumatic stress syndrome immediately posttrauma to full–blown PTSD. To confer predictive validity to our model, the centrally active –adrenergic antagonist, propranolol, and the non–centrally acting –adrenergic antagonist, nadolol, were administered to Wistar rats after passive avoidance fear conditioning training in the Gemini Avoidance System. Wistar rats were used because of their recognised enhanced sensitivity to stress. Evidence from this pilot study confirmed that propranolol 10 mg/kg significantly inhibits the consolidation of learned fear in rats, whereas nadolol is ineffective. This effectively validated our protocol and the apparatus for further application in this study and also confirmed the importance of a central mechanism of action for –adrenoceptor blockade in the possible application of these drugs in preventing the development of PTSD posttrauma. The second objective of this study was to investigate the role of 1–, 2–, 1–, and 2–receptors in a conditioned fear passive avoidance paradigm. This was done in order to investigate how selective pharmacological modulation of these receptors may modify the conditioned fear response, and whether any of these receptor systems might exert opposing effects in passive fear conditioning. Various centrally active noradrenergic agents were employed over a 3–tiered dose response design, including the 1–antagonist, prazosin, the 2–agonist, guanfacine, the 2–antagonist, yohimbine, the 1–antagonist, betaxolol and the 2–antagonist ICI 118551. The effect of post–exposure administration of these drugs on conditioned fear was compared to that of propranolol 10 mg/kg. Selected doses of betaxolol (10 mg/kg) and ICI 118551 (1 mg/kg) attenuated fear conditioning to an extent comparable to propranolol, as did prazosin (0.1 mg/kg). Yohimbine tended to boster fear learning at all doses tested, albeit not significantly, while guanfacine did not produce any significant effect on memory retention at any of the doses studied. This latter observation was surprising since yohimbine tended to bolster fear conditioning while earlier studies indicate that 2–agonism impairs conditioned fear. Concluding, this study has conferred validity to our passive avoidance model and has provided greater insight into the separate roles of noradrenergic receptors in contextual conditioned fear learning. The study has provided supportive evidence for a key role for both 1– and 2–antagonism, as well as 1–antagonism, in inhibiting fear memory consolidation and hence as viable secondary treatment options to prevent the development of PTSD posttrauma. However, further study is required to delineate the precise role of the 2–receptor in this regard. / Thesis (M.Sc. (Pharmacology))--North-West University, Potchefstroom Campus, 2012.

No description available.