Magister Artium (Social Work) - MA(SW) / Julian Rotter (1966, 1975) het die persoonlikheidskonstruk lokus van kontrole beskryf as die mate waartoe.die individu glo dat versterking die gevolg is van sy eie gedrag (interne lokus van kontrole) of die gevolg is van gelukkige toeval, kans, of die noodlot (eksterne lokus van kontrole) . Sedert Rotter (1966) die konstruk "lokus van kontrole" gedefinieer en as integrale komponent van sy sosiale leerteorie voorgestel het, het velerlei navorsers ook hierdie konstruk indringend ondersoek en met talle aspekte in verband probeer bring. Een van die veranderlikes wat veral aandag geniet het, is akademiese prestasie en die verband wat ditmet lokus van kontrole sou toon. Alhoewel daar nie ooreenstemming bestaan met betrekking tot hierdie verband nie, blyk dit asof die meerderheid navorsers wel bevind dat 'n interne lokus van kontrole verband hou met hoê akademiese prestasie (byvoorbeeld Kishor, 1983; Maqsud, 1980; Messer, 1972). Verskeie tersiêre inrigtings (waaronder die Universiteit van Wes-Kaapland, waar hierdie studie beslag vind) bied dan ook studiebegeleidingsprogramme aan ten einde studente van studievaardighede te voorsien wat hulle in staat sou stelom akademies beter te presteer. Hierdie programme neem egter selde persoonlikheidsveranderlikes in aanmerking en fokus veel eerder op die verskaffing van studiewenke en -vaardighede. Hierdie studie het dus In unieke studiebegeleidingsprogram probeer ontwerp wat In interne lokus van kontrole by die deelnemende proefpersone wil bevorder. Dit is dan die primêre studiebegeleidingsprogram van die U.W.K. te evalueer ten opsigte van die invloed daarvan op die persoonlikheidskonstruk lokus van kontrole by die deelnemende proefpersone. Sekondêre doelstellings behels die volgende ii) om die samehang tussen die konstruk lokus van kontrole met die volgende veranderlikes te bepaal: a) Geslag b) Geografiese herkoms, naamlik plattelandse vs. stedelike studente • c) Ouderdom d) Sosio-ekonomiese status e) Studierigting f) Taalgroep g) Politieke betrokkenheid, organisatoriese affiliasie en organisatoriese betrokkenheid h) Akademiese prestasie i) Akademiese studiejaar iii) om vergelykings te tref met Westerse navorsingsbevindinge Die huidige studie was ondersoekend van aard weens die afwesigheid van soortgelyke voorafgaande navorsing. In Voortoets-natoets kontrole groep-ontwerp is gebruik om die verband tussen lokus van kontrole en die studiebegeleidingsprogram na te vors. Altesaam Proefpersone het aan die ondersoek deelgeneem Collins (1974) se aanpassing van Rotter (1966) se interneeksterne lokus van kontrole skaal is as meetmiddel gebruik. Herdie skaal het deel gevorm van In vraelys wat ook informasie ingewin het omtrent die persoon huistaal, studiedoelstellings, se geslag, politieke studentestatus, betrokkenheid, betrokkenheid, organisatoriese affiliasie, organisatoriese akademiese prestasie en geografiese herkoms. Die resultate van die huidige navorsing het aangedui dat daar geen beduidende verband bestaan tussen die lokus van kontrole geneigdheid van die proefpersone en die ervaring van die studiebegeleidingsprogram nie. Die huidige navorsing het voorts geen verband gevind waar dit die samehang van lokus van kontrole en die veranderlikes van geslag, geografiese herkoms, ouderdom, sosio-ekonomiese status, studierigting, taalgroep, politieke affiliasie, en organisatoriese betrokkenheid aangaan nie. Beduidende verbande is wel bespeur ten opsigte van die lokus van kontrole-tellings van manlike en vroulike proefpersone wat In Afrika-taal besig, asook ten opsigte van die veranderlikes politieke betrokkenheid, akademiese prestasie en akademiese studiejaar. Hierdie bevindinge is bespreek met verwysing na die geneigdheid van die proefpersone en die ervaring van die studiebegeleidingsprogram nie. Die huidige navorsing het voorts geen verband gevind waar dit die samehang van lokus van kontrole en die veranderlikes van geslag, geografiese herkoms, ouderdom, sosio-ekonomiese status, studierigting, taalgroep, politieke affiliasie, en organisatoriese betrokkenheid aangaan nie. Beduidende verbande is wel bespeur ten opsigte van die lokus van kontrole-tellings van manlike en vroulike proefpersone wat In Afrika-taal besig, asook ten opsigte van die veranderlikes politieke betrokkenheid, akademiese prestasie en akademiese studiejaar. Literatuuroorsig, asook met inagneming van die unieke aard van die studentebevolking aan die Universiteit van Wes-Kaapland. Die unieke suid-Afrikaanse sosio-politieke realiteit is ook in aanmerking geneem. Ten slotte word sekere aanbevelings gemaak met die oog op verdere navorsing .

Text in Afrikaans / Die doel van die studie is om die leefwereld van die aggressiewe adolessente seun te verken. Aggressie word beskou as 'n gedragsafwyking wat op fisieke, verbale of passiewe wyses kan manifesteer. Die oorsake van aggressiewe gedragsmanifestasies by die adolessente seun word hoofsaaklik gevind in die ontoereikende gesinsrelasies. Gevoelens van ongeborgenheid, verwardheid en verwerping is dan die gevolg. 'n Onrealisties positiewe of -negatiewe selfkonsep kan hieruit voortvloei en kan daartoe lei dat die aggressiewe adolessente seun betrokke raak by negatiewe portuurrelasies, waar onder andere rook, dwelm- en drankmisbruik asook roekelose gedrag manifesteer. Ult hierdie literatuurbevindinge is twaalf postulate gestel en bespreek. Vyf idiografiese studies is onderneem, waarvan drie volledig bespreek is. Die bevindings uit hierdie studies sluit aan by die feite wat ult die literatuurstudie oor die leefwereld van die aggressiewe adolessente seun verkry is. Vroee uitkenning, ouerleiding en navorsing met betrekking tot hulpprogramme aan terapeute word aanbeveel om aggressiewe gedragsmanlfestasles by die adolessente seun te voorkom / The purpose of this study is to explore the lifeworld of the aggressive adolescent boy. Aggression is regarded as deviant behaviour, that may manifest itself physically, verbally or passively. The causes of aggressive behaviour in the adolescent boy can be due to inadequate family relationships. Feelings of insecurity, confusion and rejection are the results of the problematic relationships. An unrealistic positive or negative self concept may develop that might lead to involvement with the negative peer group. Smoking, alcohol and drug abuse, as well as reckless behaviour may occur. Twelve postulates have been determined and discussed. Five idiographic studies have been done. Three are discussed in detail. Deductions made from these studies are in agreement with findings in existing literature of the life world of the adolescent boy. Early identification parental guidance and research regarding therapeutical programmes are recommended to prevent aggressive behaviour with the adolescent / Psychology of Education / M. Ed. (Spesialisering in Voorligting)

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.

Text in Afrikaans / Die doel van die studie is om die leefwereld van die aggressiewe adolessente seun te verken. Aggressie word beskou as 'n gedragsafwyking wat op fisieke, verbale of passiewe wyses kan manifesteer. Die oorsake van aggressiewe gedragsmanifestasies by die adolessente seun word hoofsaaklik gevind in die ontoereikende gesinsrelasies. Gevoelens van ongeborgenheid, verwardheid en verwerping is dan die gevolg. 'n Onrealisties positiewe of -negatiewe selfkonsep kan hieruit voortvloei en kan daartoe lei dat die aggressiewe adolessente seun betrokke raak by negatiewe portuurrelasies, waar onder andere rook, dwelm- en drankmisbruik asook roekelose gedrag manifesteer. Ult hierdie literatuurbevindinge is twaalf postulate gestel en bespreek. Vyf idiografiese studies is onderneem, waarvan drie volledig bespreek is. Die bevindings uit hierdie studies sluit aan by die feite wat ult die literatuurstudie oor die leefwereld van die aggressiewe adolessente seun verkry is. Vroee uitkenning, ouerleiding en navorsing met betrekking tot hulpprogramme aan terapeute word aanbeveel om aggressiewe gedragsmanlfestasles by die adolessente seun te voorkom / The purpose of this study is to explore the lifeworld of the aggressive adolescent boy. Aggression is regarded as deviant behaviour, that may manifest itself physically, verbally or passively. The causes of aggressive behaviour in the adolescent boy can be due to inadequate family relationships. Feelings of insecurity, confusion and rejection are the results of the problematic relationships. An unrealistic positive or negative self concept may develop that might lead to involvement with the negative peer group. Smoking, alcohol and drug abuse, as well as reckless behaviour may occur. Twelve postulates have been determined and discussed. Five idiographic studies have been done. Three are discussed in detail. Deductions made from these studies are in agreement with findings in existing literature of the life world of the adolescent boy. Early identification parental guidance and research regarding therapeutical programmes are recommended to prevent aggressive behaviour with the adolescent / Psychology of Education / M. Ed. (Spesialisering in Voorligting)