Thesis (B.Psy.Sc.(Hons.)) - University of Queensland, 2006. / Includes bibliography.

Memories are gradually consolidated after learning, and subsequent offline periods containing sleep are suggested to support the stabilisation, enhancement, reorganisation and integration of representations within long-term memory networks. The spontaneous reactivation of specific memory traces during sleep is proposed as a key mechanism underlying sleep-dependent consolidation, but the neurophysiological underpinnings of this ‘memory replay’ remain unclear. The research described in this thesis utilised a method of manipulating memory reactivation during sleep (targeted memory reactivation), in combination with behavioural experimentation, polysomnography (PSG), electroencephalography (EEG), and functional magnetic resonance imaging (fMRI), to refine current understanding of the neural processes underlying sleep-dependent memory consolidation. In Chapter 2 we developed a motor sequence learning paradigm that combined visuo-motor performance with sound stimuli, which enabled the targeted memory reactivation (TMR) of specific motor memories during sleep in subsequent chapters via the replay of the associated sounds during sleep. Chapter 3 used this task to cue the reactivation of a learned motor sequence during slow-wave sleep (SWS), which enhanced motor skill for the cued sequence relative to an uncued sequence, and also made the sequence of motor movements more available for conscious recall. Furthermore, these effects were associated with key neural features of sleep (slow oscillations and spindles). These findings indicate that reactivation not only enhances procedural memories, but plays a part in the reorganisation of representations that leads to the emergence of explicit knowledge. A great deal of research has shown that the neural systems supporting procedural memories evolve over time, particularly within cortico-striatal and cortico-cerebellar networks. Chapter 4 used fMRI to show that reactivation is instrumental to this neural plasticity by comparing brain activity at retrieval of a sequence that was cued during SWS with a sequence that was not. The cued sequence showed increased activation in bilateral caudate nucleus and left hippocampus, mediated by time spent in slow-wave sleep, while functional connectivity was also altered by TMR between caudate and hippocampus. These findings indicate that the behavioural enhancements associated with TMR of procedural learning are related to overnight plasticity in motor memory networks. Lastly, Chapter 5 expanded on the reorganisation of memories investigated in Chapter 3, asking whether reactivation mediates the generalisation of representations that can sometimes create false memories. Learned lists of semantically associated words were reactivated during NREM sleep, but revealed no evidence that TMR effected false memory formation. However TMR was found to reduce the recognition of studied items, which may indicate that certain TMR procedures can interfere with consolidation rather than enhance it. Collectively these results provide new insights to the role played by reactivation in memory consolidation. We have provided evidence for both the enhancement and reorganisation of procedural memories during sleep, and indicate that such effects are supported by alterations to underlying neural plasticity. We also show the importance of slow-wave sleep and associated neural features in this consolidation process.

No description available.

Thesis (Ph.D.)--University of Alberta, 2009. / A thesis submitted to the Faculty of Graduate Studies and Research in partial fulfillment of the requirements for the degree of Doctor of Philosphy, Centre for Neuroscience. Title from pdf file main screen (viewed on November 6, 2009). Includes bibliographical references.

No description available.

Any disruption of homeostasis causes a stress response that serves to restore balance in the body. Stress hormone levels, such as glucocorticoids, strongly influence the consolidation of episodic memory dependent on the hippocampus. Sleep has beneficial effects on individual types of memory and is necessary for the proper course of consolidation of newly acquired information. Little is known, however, about neuronal processes of memory consolidation for a traumatic event. The topic of this work is to study the combination of these two factors and to determine the effect of elevated levels of corticosterone and sleep on the consolidation of traumatic memory in rats. The theoretical part of this work summarizes the knowledge about memory, sleep and stress. The practical part deals with the experimental procedure combining behavioral (fear conditioning), electrophysiological methods (EEG recording and determination of sleep stages) and pharmacological manipulation (intrahippocampal administration of corticosterone). In summary, we found the effect of high levels of corticosterone in the hippocampus on contextual memory consolidation and on the amount of slow wave sleep. These results can bring new features in the field of traumatic memory consolidation and associated post-traumatic stress disorder....

Made available in DSpace on 2014-12-17T14:03:42Z (GMT). No. of bitstreams: 1 LarissaMA_DISSERT.pdf: 2537553 bytes, checksum: 12f02428f3ae0866d5e225dc96048ea4 (MD5) Previous issue date: 2013-05-20 / Conselho Nacional de Desenvolvimento Cient?fico e Tecnol?gico / Dopamine (DA) is known to regulate both sleep and memory formations, while sleep plays a critical role in the consolidation of different types of memories. We believe that pharmacological manipulation of dopaminergic pathways might disrupt the sleep-wake cycle, leading to mnemonic deficits, which can be observed in both behavioral and molecular levels. Therefore, here we investigated how systemic injections of haloperidol (0.3 mg/kg), immediately after training in dark and light periods, affects learning assessed in the novel object preference test (NOPT) in mice. We also investigated the hippocampal levels of the plasticity-related proteins Zif-268, brain-derived neurotrophic factor (BDNF) and phosphorylated Ca2+/calmodulin-dependent protein kinases II (CaMKII-P) in non-exposed (na?ve), vehicle-injected controls and haloperidol-treated mice at 3, 6 and 12 hours after training in the light period. Haloperidol administration during the light period led to a subsequent impairment in the NOPT. In contrast, preference was not observed during the dark period neither in mice injected with haloperidol, nor in vehicle-injected animals. A partial increase of CaMKII-P in the hippocampal field CA3 of vehicle-injected mice was detected at 3h. Haloperidol-treated mice showed a significant decrease in the dentate gyrus of CaMKII-P levels at 3, 6 and 12h; of Zif-268 levels at 6h, and of BDNF levels at 12h after training. Since the mnemonic effects of haloperidol were only observed in the light period when animals tend to sleep, we suggest that these effects are related to REM sleep disruption after haloperidol injection / A dopamina (DA) regula tanto o sono quanto o processo de forma??o de mem?rias, enquanto o sono desempenha uma fun??o essencial na consolida??o de diferentes tipos de mem?rias. Acreditamos que a manipula??o farmacol?gica das vias dopamin?rgicas possa afetar o ciclo sono-vig?lia, acarretando d?ficits mnem?nicos, os quais podem ser observados tanto em n?vel comportamental quanto molecular. Dessa forma, no presente estudo, investigamos o efeito do haloperidol (halo - 0,3 mg/kg; i.p.), administrado imediatamente ap?s sess?es de treino no per?odo da manh? e da noite, sobre o desempenho de camundongos no teste de prefer?ncia por objetos novos (TPON). Observamos que esse tratamento causou um preju?zo mnem?nico apenas nos camundongos testados pela manh?. Devido ? maior ocorr?ncia de epis?dios de sono durante a fase clara dos roedores, acreditamos que esse d?ficit pode estar associado a uma cascata de plasticidade hipocampal, a qual envolve a express?o de diferentes mol?culas em per?odos distintos ap?s a exposi??o ao est?mulo mnem?nico inicial. Para testar tal hip?tese, realizamos imunohistoqu?mica (IHQ) em tecidos de animais na?ve n?o expostos (NV), bem como de animais expostos aos objetos com posterior inje??o de halo ou salina (ve?culo - VH), perfundidos 3, 6 e 12h ap?s o est?mulo inicial. Quantificamos a express?o hipocampal (CA1, CA3 e GD) das prote?nas CaMKII-P, Zif-268 e BDNF, atrav?s de densitometria e contagem de c?lulas (somente para Zif-268). Observamos um aumento parcial na express?o de CaMKII-P em animais VH 3h, na regi?o CA3. Quanto ao grupo halo, houve uma redu??o dos n?veis de CaMKII-P nos tr?s hor?rios analisados; de Zif-268 em 6h, tanto em CA1 quanto CA3; e de BDNF em 12h, apenas no GD. Considerando-se o melhor desempenho diurno na consolida??o de mem?rias, associado ? fun??o do halo na regula??o do sono, propomos que a redu??o de plasticidade sin?ptica e os d?ficits no processo mnem?nicoocorreram devido ? supress?o do sono REM mediada pelo tratamento com haloperidol