Thesis (Ed. D.)--University of La Verne, 2003. / Includes bibliographical references (p. 184-191).

Thesis (Ph. D.)--University of Wisconsin--Madison, 1969. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 136-140).

Dissertation (Ph.D.)--The University of North Carolina at Greensboro, 2009. / Directed by Stuart Marcovitch; submitted to the Dept. of Psychology. Title from PDF t.p. (viewed May 17, 2010). Includes bibliographical references (p. 87-102).

No description available.

Thesis (M.Sc.)--Memorial University of Newfoundland, 2002. / Bibliography: leaves 78-89.

Thesis (M.S.)--Florida State University, 2006. / Advisor:Thomas A. Houpt, Florida State University, College of Arts and Sciences, Dept. of Biological Science. Title and description from dissertation home page (viewed June 7, 2006). Document formatted into pages; contains vi, 37 pages. Includes bibliographical references.

Judgments of Learning (JOLs) are judgments of the likelihood of remembering recently studied material on a future test. Although JOLs have been extensively studied, particularly due to their important applications in education, relatively little is known about the cognitive and neural processes supporting JOLs and how these processes relate to actual memory processing. Direct access theories describe JOLs as outputs following direct readings of memory traces and hence predict that JOLs cannot be distinguished from objective memory encoding operations. Inferential theories, by contrast, claim JOLs are products of the evaluation of a number of cues, perceived by learners to carry predictive value. This alternative account argues that JOLs are made on the basis of multiple underlying processes, which do not necessarily overlap with memory encoding. In this thesis, the neural and cognitive bases of JOLs were examined in a series of four ERP experiments. Across experiments the study phase ERP data showed that JOLs produce neural activity that is partly overlapping with, but also partly distinct from, the activity that predicts successful memory encoding. Furthermore, the neural correlates of successful memory encoding appear sensitive to the requirements to make a JOL, emphasising the close interaction between subjective and objective measures of memory encoding. Finally, the neural correlates of both JOLs and successful memory encoding were found to vary depending on the nature of the stimulus materials, suggesting that both phenomena are supported by multiple cognitive and neural systems. Although the primary focus was on the study phase ERP data, the thesis also contains two additional chapters reporting the ERP data acquired during the test phases of three of the original experiments. These data, which examined the relative engagements of retrieval processes for low and high JOL items, suggest that encoding processes specifically resulting in later recollection (as opposed to familiarity) form one reliable basis for making JOLs. Overall, the evidence collected in this series of ERP experiments suggests that JOLs are not pure products of objective memory processes, as suggested by direct access theories, but are supported by neural systems that are at least partly distinct from those supporting successful memory encoding. These observations are compatible with inferential theories claiming that JOLs are supported by multiple processes that can be differentially engaged across stimulus contents.

Overexpression of the NR2B subunit of the NMDA receptor in the forebrain has been shown to improve learning and memory in mice (Tang et al 1999), which provides exciting implications for the enhancement of human cognition. However, it was first essential to establish replicability, and since the Tang et al (1999) study used only male mice we wished to investigate possible sex differences. On the hidden platform watermaze, we found a trend for male NR2BOE mice to learn the task more quickly than male wildtype mice (as observed by Tang et al. 1999), but the opposite trend in female mice; female NR2BOE mice were slower to reach the hidden platform than female wildtype mice. This pattern of results was also observed on the spatial reference Y memory task and open field task (for anxiety), although not on the spatial working memory T maze task (despite a sex difference). However, wildtype and NR2BOE mice performed at similar levels on the novel object recognition task, the spatial novelty preference task, visible platform watermaze and visual discrimination task. A battery of tests considering some species typical behaviours of mice demonstrated that wildtype and NR2BOE mice were comparable on tests of motor ability, strength, co-ordination, anxiety, burrowing and nesting. This suggests that our behavioural results are not due to a general impairment or enhancement of species typical behaviours. We considered the possibility that the difference between the results of Tang et al (1999) and those we observed may be caused by age differences; hence we attempted to replicate our results on the hidden platform watermaze, spatial reference Y maze and open field test in age matched mice. However, the second cohort of NR2BOE mice performed at similar levels to wildtype mice, and at significantly improved levels compared to the mice of the first cohort. We also considered the effects of knocking out the NR2B subunit on learning and memory, and NR1 subunit deletion within the hippocampus. On the spatial working memory T maze, these mouse strains performed similarly to their respective wildtype strains. Similarly, on a two beacon watermaze (with one indicating the platform position), mice lacking the NR2B subunit were able to locate the platform in a similar length of time. To ensure that the null results we had observed in the second cohort were not due to loss of the NR2B protein overexpression in the forebrain, we performed polymerase chain reactions (PCR), quantitative real-time PCR, and Western blots. We ascertained that the transgene was indeed present and that NR2B mRNA and protein levels were elevated in the hippocampi of the NR2BOE mice. In conclusion, it is unclear why the behaviours we observed in the NR2BOE mice are different to those published in the literature. It is possible that they may be due to differences in environmental enrichment, but the cause of the genotype by sex differences observed in the mice of cohort 1 is unclear. Nonetheless, we have advanced our knowledge of the effects of modifications in the levels of the NR2B subunit of the NMDA receptor on learning and behaviour.

Made available in DSpace on 2014-12-17T15:37:20Z (GMT). No. of bitstreams: 1 AlineLD_DISSERT.pdf: 1012769 bytes, checksum: dbe4a7a77cff780cc71b4acb54601b4b (MD5) Previous issue date: 2014-04-11 / Coordena??o de Aperfei?oamento de Pessoal de N?vel Superior / The physiologist H. Selye defined stress as the nonspecific response of the body to any factors that endanger homeostasis (balance of internal environment) of the individual. These factors, agents stressors, are able to activate the Hypothalamic-Pituitary-Adrenal (HPA) axis, thus resulting in the physiological responses to stress by the release of glucocorticoids that leads to psychophysiological changes, including effects on cognitive functions such as learning and memory. When this axis is acutely stimulated occurs a repertoire of behavioral and physiological changes can be adaptive to the individual. Notwithstanding, when the HPA axis is chronically stimulated, changes may favor the development of, such as anxiety disorders. Some drugs used in the clinic for the treatment of anxiety disorders these can exert effects on cognitive function, on the HPA axis and on the anxiety. In this context, the aim of our study was to investigate the effects of administration i.p. acute of diazepam (DZP, 2 mg/kg), buspirone (BUS, 3 mg/kg), mirtazapine (MIR, 10 mg/kg) and fluoxetine (FLU, 10 mg/kg) in male mice submitted to acute restraint stress, and evaluated using plus-maze discriminative avoidance task (PMDAT), which simultaneously evaluates parameters such as learning, memory and anxiety. Our results demonstrated that (1) the administration of DZP and BUS, but not FLU, promoted anxiolytic effects in animals; (2) administration mirtazapine caused sedative effect to animals; (3) in the training session, the animals treated with BUS, MIR and FLU learned the task, on the other hand DZP group showed impairment in learning; (4) in the test session, animals treated with DZP, BUS, and MIR showed deficits in relation to discrimination between the enclosed arms, aversive versus non-aversive arm, demonstrating an impairment in memory, however, animals treated with FLU showed no interference in the retrieval of this memory; (5) acute stress did not interfere in locomotor activity, anxiety, or learning on the learning task, but induced impairment in retrieval memory, and the group treated with FLU did not demonstrated this deficit of memory . These results suggest that acute administration of drugs with anxiolytic and antidepressant activity does not interfere with the learning process this aversive task, but impair its retrieval, as well as the acute restraint stress. However, the antidepressant fluoxetine was able to reverse memory deficits promoted by acute stress, which may suggest that modulation, even acutely serotonergic neurotransmission, by selectively inhibiting the reuptake of this neurotransmitter, interferes on the process of retrieval of an aversive memory / O fisiologista H. Selye definiu estresse como a resposta n?o espec?fica do organismo a quaisquer fatores que coloquem em risco a homeostase (equil?brio do meio interno) do indiv?duo. Esses fatores, os agentes estressores, s?o capazes de ativar o eixo Hipot?lamo-Hip?fise-Adrenal (HPA), resultando assim na resposta fisiol?gica ao estresse. Quando esse eixo ? agudamente estimulado, ocorre um repert?rio de mudan?as comportamentais e fisiol?gicas adaptativas ao indiv?duo. Por outro lado, quando o eixo HPA ? cronicamente estimulado, podem ocorrer modifica??es psicofisiol?gicas prejudiciais ao indiv?duo, entre elas, efeitos sobre as fun??es cognitivas, como na aprendizagem e na mem?ria, al?m do desenvolvimento de patologias, como os transtornos de ansiedade. Alguns f?rmacos utilizados na cl?nica para o tratamento de transtornos de ansiedade podem exercer efeitos sobre fun??es cognitivas, sobre o eixo HPA e sobre a ansiedade. Neste contexto, o objetivo de nosso estudo foi verificar os efeitos da administra??o aguda de quatro f?rmacos, o diazepam (DZP, 2 mg/Kg), a buspirona (BUS, 3 mg/Kg), a mirtazapina (MIR, 10 mg/Kg) e a fluoxetina (FLU, 10 mg/Kg) em camundongos machos submetidos ao estresse agudo por conten??o, utilizando a tarefa de esquiva discriminativa em labirinto em cruz elevado, que avalia simultaneamente par?metros de aprendizagem, mem?ria e ansiedade. Nossos resultados demonstraram que (1) a administra??o do DZP e da BUS promoveu efeitos ansiol?ticos nos animais, mas n?o a FLU; (2) a MIR causou efeito sedativo aos animais; (3) durante a sess?o de treino, os animais tratados com BUS, MIR e FLU aprenderam a tarefa, por outro lado o grupo DZP demonstrou preju?zo na aprendizagem; (4) na sess?o teste, animais tratados com DZP, BUS, e MIR mostraram d?ficit na discrimina??o entre os bra?os fechados, aversivo versus n?o aversivo, demonstrando um preju?zo na mem?ria, entretanto, animais que receberam FLU n?o mostraram interfer?ncia na evoca??o dessa mem?ria; (5) o estresse agudo n?o interfere na aprendizagem da tarefa, mas induz preju?zo na evoca??o da mem?ria, sendo este preju?zo revertido apenas para o grupo tratado como FLU. Esses resultados sugerem que a administra??o aguda de f?rmacos com atividade ansiol?tica e antidepressiva n?o interferem no processo de aprendizagem desta tarefa aversiva, mas prejudicam sua evoca??o, bem como o estresse agudo de conten??o. Contudo, o antidepressivo fluoxetina foi capaz de reverter o d?ficit de mem?ria promovido pelo estresse agudo, o que pode sugerir que a modula??o, mesmo que agudamente da neurotransmiss?o serotonin?rgica, por inibidores seletivos da recepta??o desse neurotransmissor, interfere no processo de consolida??o de uma mem?ria aversiva

Made available in DSpace on 2014-12-17T15:37:21Z (GMT). No. of bitstreams: 1 IsabellaMOP_DISSERT.pdf: 1986488 bytes, checksum: 1f1b995fa77d662628cf94f2e167faf0 (MD5) Previous issue date: 2014-05-09 / Conselho Nacional de Desenvolvimento Cient?fico e Tecnol?gico / Lithium (Li) is the first choice to treat bipolar disorder, a psychiatric illness characterized by mood oscillations between mania and depression. However, studies have demonstrated that this drug might influence mnemonic process due to its neuroprotector, antiapoptotic and neurogenic effects. The use of Li in the treatment of cognitive deficits caused by brain injury or neurodegenerative disorders have been widely studied, and this drug shows to be effective in preventing or even alleviating the memory impairment. The effects of Li on anxiety and depression are controversial and the relationship of the effects of lithium on memory, anxiety and depression remain unknown. In this context, this study aims to: evaluate the effects of acute and chronic administration of lithium carbonate in aversive memory and anxiety, simultaneously, using the plus maze discriminative avoidance task (PMDAT); test the antidepressant effect of the drug through the forced swimming test (FS) and analyze brainderived neurotrophic factor (BDNF) expression in structures related to memory and emotion. To evaluation of the acute effects, male Wistar rats were submitted to i.p. administration of lithium carbonate (50, 100 or 200 mg/kg) one hour before the training session (PMDAT) or lithium carbonate (50 or 100 mg/kg) one hour before the test session (FS). To evaluation of the chronic effects, the doses administered were 50 or 100 mg/kg or vehicle once a day for 21 days before the beginning of behavioral tasks (PMDAT and FS). Afterwards, the animals were euthanized and their brains removed and submitted to immunohistochemistry procedure to quantify BDNF. The animals that received acute treatment with 100 and 200 mg/kg of Li did not discriminated between the enclosed arms (aversive and non-aversive) in the training session of PMDAT, showing that these animal did not learned the task. This lack of discrimination was also observed in the test session, showing that the animals did not recall the aversive task. We also observed an increased exploration of the open arms of these same groups, indicating an anxiolytic effect. The same groups showed a reduction of locomotor activity, however, this effect does not seem to be related with the anxiolytic effect of the drug. Chronic treatment with Li did not promote alterations on learning or memory processes. Nevertheless, we observed a reduction of open arms exploration by animals treated with 50 mg/kg when compared to the other groups, showing an anxiogenic effect caused by this dose. This effect it is not related to locomotor alterations since there were no alterations in these parameters. Both acute and chronic treatment were ineffective in the FS. Chronic treatment with lithium was not able to modify BDNF expression in hippocampus, amygdala and pre-frontal cortex. These results suggest that acute administration of lithium promote impairments on learning in an aversive task, blocking the occurrence of memory consolidation and retrieval. The reduction of anxiety following acute treatment may have prevented the learning of the aversive task, as it has been found that optimum levels of anxiety are necessary for the occurrence of learning with emotional context. With continued, treatment the animals recover the ability to learn and recall the task. Indeed, they do not show differences in relation to control group, and the lack of alterations on BDNF expression corroborates this result. Possibly, the regimen of treatment used was not able to promote cognitive improvement. Li showed acute anxiolytic effect, however chronic administration 4 promoted the opposite effect. More studies are necessary to clarify the potential beneficial effect of Li on aversive memory / L?tio (Li) ? o f?rmaco de escolha para o tratamento do transtorno bipolar, doen?a psiqui?trica caracterizada por oscila??es de humor entre mania e depress?o. Entretanto, estudos mostram que essa droga pode ter influ?ncia sobre os processos mnem?nicos devido a seu car?ter neuroprotetor, antiapopt?tico e neurog?nico. O emprego no l?tio para o tratamento de d?ficits cognitivos provocados por les?es cerebrais ou doen?as neurodegenerativas vem sendo amplamente estudado, visto que esse f?rmaco mostra-se capaz de prevenir ou at? mesmo aliviar preju?zos na mem?ria. Os efeitos do Li na ansiedade e depress?o s?o controversos e a rela??o entre os efeitos do Li na mem?ria, ansiedade e depress?o s?o ainda desconhecidos. Neste contexto, os objetivos deste estudo foram: avaliar os efeitos da administra??o aguda e cr?nica de carbonato de l?tio na mem?ria aversiva e ansiedade, simultaneamente, utilizando a esquiva discriminativa no labirinto em cruz elevado (ED); testar o efeito antidepressivo do f?rmaco atrav?s do teste do nado for?ado (NF); avaliar a express?o de fator neurotr?fico derivado do enc?falo (BDNF) em estruturas relacionadas com mem?ria e emo??o. Para a avalia??o do efeito agudo, ratos Wistar machos foram submetidos ? administra??o intraperitoneal de carbonato de l?tio 50, 100 ou 200 mg/kg uma hora antes do treino (ED) ou carbonato de l?tio 50 ou 100 mg/kg uma hora antes do teste (NF). Para a avalia??o cr?nica, foram administradas as doses de 50 ou 100 mg/kg ou ve?culo por 21 dias antes do in?cio das tarefas comportamentais (ED e NF). Ap?s o t?rmino dessas tarefas, os animais foram eutanasiados e seus enc?falos removidos para realiza??o de imunohistoqu?mica para quantificar BDNF. Os animais que receberam tratamento agudo com Li nas doses de 100 e 200 mg/kg n?o demonstraram discrimina??o entre os bra?os fechados (aversivo e n?o-aversivo) na sess?o treino da ED, mostrando que esses animais n?o aprenderam a tarefa. Essa aus?ncia na discrimina??o foi observada tamb?m na sess?o teste, mostrando que n?o houve evoca??o da mem?ria aversiva. Foi ainda observado um aumento da explora??o dos bra?os abertos para essas mesmas doses, apontando um efeito ansiol?tico do f?rmaco. Os mesmos grupos apresentaram ainda uma redu??o na atividade locomotora, no entanto, esse efeito parece n?o estar relacionado com o efeito ansiol?tico do f?rmaco. O tratamento cr?nico com l?tio n?o promoveu altera??es nos processos de aprendizado e mem?ria. No entanto, foi observado uma redu??o da explora??o dos bra?os abertos pelos animais tratados com a dose de 50 mg/kg em rela??o aos outros grupos, mostrando um efeito ansiog?nico causado pelo tratamento cr?nico. Esse efeito n?o est? relacionado a altera??es locomotoras, visto que n?o foi detectado altera??es nesses par?metros. Ambos os tratamentos (agudo e cr?nico) foram ineficazes em demonstrar o efeito antidepressivo do l?tio na tarefa do NF. O tratamento cr?nico com l?tio tamb?m n?o foi capaz de alterar a express?o de BDNF no hipocampo, am?gdala e c?rtex pr?-frontal. Esses resultados sugerem que a administra??o aguda de l?tio promove preju?zos no aprendizado em uma tarefa aversiva, impedindo a ocorr?ncia de consolida??o e evoca??o da mem?ria. A redu??o da ansiedade no tratamento agudo pode ter impedido o aprendizado da tarefa aversiva, visto que j? foi verificado que n?veis adequados de ansiedade s?o necess?rios para que ocorra aprendizado com contexto 2 emocional. Com a continuidade do tratamento os animais recuperam a capacidade de aprender e evocar a tarefa, mas n?o apresentam altera??es em rela??o ao grupo controle e a aus?ncia de altera??o na express?o de BDNF corrobora esse resultado. Possivelmente, o regime de tratamento utilizado n?o foi capaz de promover melhora cognitiva nos animais. O l?tio demonstrou efeito ansiol?tico agudo, todavia a administra??o cr?nica promoveu efeito oposto. Mais estudos s?o necess?rios para esclarecer o potencial efeito ben?fico do l?tio sobre a mem?ria