Thesis (Ph. D.)--University of Texas at Austin, 2007. / Vita. Includes bibliographical references.

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Dysfunction of cholinergic and dopaminergic systems has been implicated in memory function de cits that are core pathology and associated features of several neurological disorders. However, in order to develop more effective treatments, it is crucial to better understand how different aspects of learning and memory are modulated by these neuromodulatory systems. Using optogenetic stimulation or silencing, this thesis aims to investigate the effects of cholinergic and dopaminergic modulation on various hippocamal learning and memory processes. To understand how these neuromodulatory systems modulate hippocampal network activity, I first examined their effects on hippocampal local field potentials in urethane-anaesthetised mice. I demonstrated that optogenetic cholinergic activation suppressed slow oscillations, shifting brain activity to a state dominated by theta and gamma oscillations. In contrast, dopaminergic activation suppressed gamma oscillations. Second, to directly probe the effects of neuromodulation on different stages of spatial learning, I acutely activated or inactivated cholinergic or dopaminergic neurons during various behavioural tasks. My findings suggested that cholinergic activation, solely during the reward phase of a long-term spatial memory task, slowed place learning, highlighting the importance of temporally-precise neuromodulation. Moreover, dopaminergic stimulation may enhance place learning of a food rewarded task, supporting a role for dopamine in spatial learning. In addition, I tested the effects of cholinergic and dopaminergic modulation on reversal learning and found that cholinergic inactivation and dopaminergic activation appear to impair this process. Together, these findings emphasise the importance of cholinergic and dopaminergic modulation in learning and memory. They suggest that precise timing of neuromodulator action is critical for optimal learning and memory performance, and that acetylcholine and dopamine support complementary processes that allow for effective learning and adaptation to changing environments.

Thesis (Ph. D.)--University of Texas at Austin, 2007. / Vita. Includes bibliographical references.

Thesis (Ph. D.)--UCLA, 2009. / Vita. Description based on print version record. Includes bibliographical references.

This thesis investigates the effects of in-application relaxation and memory technique instructions on effectiveness of human–computer interaction (HCI) in a computer-based learning (CBL) set-up. The literature survey identifies a general absence of a clear definition of effectiveness of human–computer interaction, and even more scarcity of direct reference to the connection between effectiveness of human–computer interaction and learning.

Traumatic Brain Injury (TBI) is a global health problem and concussion, or mild TBI (mTBI), accounts for up to 75% of all brain injuries occurring annually in the US. There is also growing awareness that repeated mild traumatic brain injury (r-mTBI) can result in cumulative neuropathology and learning and memory deficits, however there is a paucity of preclinical data as to the extent these deficits manifest. R-mTBI in juvenile populations is of special interest as not only is this a high risk group, but this is also a time period when the human brain continues to mature. The hippocampus is a brain region important for learning and memory processes, and r-mTBI during the juvenile period may particularly disrupt the development of cognitive processes. To examine this issue we used a model of awake closed head injury (ACHI), and administered 8 impacts over a 4 day period to juvenile male and female rats (P25-28). At 1 or 7 days after the last injury, a cohort of rats was used for behavioural testing to study anxiety and risk-taking behaviours and cognitive abilities. From a different cohort, hippocampal slices were generated and used for in vitro electrophysiological recordings, and the capacity for long-term depression (LTD) and long-term potentiation (LTP) was examined in the medial perforant path (MPP)-dentate gyrus (DG) synapse. Our results showed that r-mTBI impaired hippocampal-dependent spatial learning and memory and that r-mTBI significantly impaired the capacity for LTD but not LTP in both sexes. These data are the first to describe the negative impact of r-mTBI on LTD in the juvenile DG in both males and females, and provide evidence for the delayed development of neurological deficits with r-mTBI. / Graduate

Learning and memory offer animals the ability to modify their behavior in response to changes in the environment. A main target of neuroscience is to understand mechanisms underlying learning, memory formation and memory maintenance. Honeybees and bumblebees exhibit remarkable learning and memory abilities with a small brain, which makes them popular models for studying the neurobiological basis of learning and memory. However, almost all of previous molecular level research on bees' learning and memory has focused on the olfactory domain. Our understanding of the neurobiological basis underlying bee visual learning and memory is limited. In this thesis, I explore how synaptic organization and gene expression change in the context of visual learning. In Chapter 2, I investigate the effects of color learning and experience on synaptic connectivity and find that color learning result in an increase of the density of synaptic complexes (microglomeruli; MG), while exposure to color information may play a large role in experience-dependent changes in microglomerular density increase. In addition, microglomerular surface area increases as a result of long-term memory formation. In Chapter 3, I investigate the correlations between synaptic organizations and individual performance and the results show that bees with a higher density of microglomeruli in visual association areas of the brain are predisposed to faster learning and better long-term memory during a visual discrimination task. In Chapter 4, I explore the genes involved in visual learning and memory by transcriptome sequencing and I show the unique gene expression patterns at different times after visual learning. In summary, my findings shed light on the relationship between synaptic connections and visual learning and memory in bees at the group and individual level and show new candidate genes involved in visual learning, which provide new avenue for future study.

Long-term depression (LTD) induced by low frequency stimulation (LFS; 900x1Hz) at medial perforant path (MPP) synapses in the rat dentate gyrus (DG) has been described as both developmentally regulated and N-methyl D-aspartate receptor (NMDAr) independent, yet sufficient evidence suggest that the processes is not entirely independent of NMDAr activity. In the present study, in vitro DG-LTD LFS was induced in hippocampal slices prepared from rats at postnatal day (PND) 14, 21 and 28 to investigate how the sensitivity of DG-LTD~LFS to the NMDAr antagonist amino-5-phosphonovaleric acid (AP5; 50µM) changes throughout the juvenile developmental period (jDP; PNDs 12-29) that occurs immediately after the period of peak neurogenesis. We further examined the acute effects of the partial NMDAr antagonist ethanol (EtOH) on DG-LTD LFS and NMDAr excitatory post synaptic currents (NMDAr-EPSCs) in dentate granule cells (DGCs) using 50 and 100mM concentrations (50mM ~0.2%BAC) of EtOH. The magnitude of LTD induced at all three time points was not statistically different between age groups, but the probability of successfully inducing LTD did decrease with age. We found that AP5 was insufficient to inhibit DG-LTD LFS at PND14, but significantly inhibited DG-LTD LFS at PND21 and PND28. We also found that 50mM EtOH, but not 100mM EtOH, significantly attenuated the mag-nitude of DG-LTD LFS induced at each time point. Acute effects of 50mM EtOH had relatively little effect on NMDAr-EPSCs at PND14, and showed a slight potentiation of the response at PND21. 50mM EtOH at PND28, and 100mM EtOH at all three developmental time points showed inhibition of the NMDAr-EPSC. These findings provide insight on how developmental changes to the DG network and dentate gran-ule cells (DGCs) influences mechanisms and processes involved in the induction and expression of synaptic plasticity in the DG. / Graduate

Lidée selon laquelle la mémoire déclarative à long terme celle qui nous permet dencoder et de récupérer sur un mode « déclaratif » des connaissances et des souvenirs acquis par le passé renvoie à deux réalités fondamentalement différentes nest pas neuve. Il y a plus de trente ans, en effet, Tulving (1972)proposait de distinguer la mémoire sémantique de la mémoire épisodique. Cette distinction est toujours admise aujourdhui et constitue une référence pour les pratiques dévaluation en neuropsychologie. Non seulement elle fournit une structure pour lanalyse clinique des troubles de la mémoire, mais elle sert également de cadre théorique pour la compréhension du syndrome amnésique (Verfaellie, 2000). Les relations quentretiennent ces deux systèmes mnésiques ainsi que les réseaux neuronaux qui les sous-tendent restent cependant encore lobjet de débats. De plus, les mécanismes impliqués dans lacquisition de nouvelles connaissances sémantiques sont peu connus. Bien que plusieurs études suggèrent que lapprentissage de nouvelles informations sémantiques dépend de mécanismes implicites (par ex., Ashby & Gott, 1988; Ashby & Maddox, 1990, 1992, Ashby, Alfonson-Reese, Turken, & Waldron, 1998; Hinton, 1981) dautres suggèrent que les mécanismes impliqués pourraient être à la fois implicite et explicites (par ex., Gopnik & Meltzoff, 1997) ou encore uniquement explicites (OConnor, Cree, & McRae, in press). En fait, limplication des mécanismes explicites et implicites pourrait dépendre du type de connaissances sémantiques à apprendre : lacquisition de labels pourrait dépendre de mécanismes plus explicites tandis que lapprentissage de catégories ou des caractéristiques de celles-ci pourrait dépendre de mécanismes plus implicites (Pitel et al., 2009). Dans cette perspective, si les mécanismes dapprentissage implicite interviennent dans lacquisition de connaissances sémantiques, il apparaît intéressant de déterminer leur rôle et les relations quentretiennent lacquisition de connaissances sémantiques et le domaine de lapprentissage implicite. Au plan théorique, cette mise en relation permettrait une meilleure compréhension du rôle joué par les processus dapprentissage implicite dans larchitecture cognitive ; par ailleurs, outre les répercussions que lon pourrait en attendre sur le plan des méthodes pédagogiques, une meilleure compréhension du rôle joué par les mécanismes dapprentissage implicite dans lapprentissage de nouvelles connaissances sémantiques devrait conduire au développement de pratiques de revalidation plus adaptées aux capacités de mémoire préservées ou résiduelles présentées par certains patients amnésiques. Dans ce travail, nous commencerons par développer les principaux modèles de la mémoire qui permettront de situer le système sémantique par rapport aux autres systèmes mnésiques. Nous développerons ensuite les modèles plus spécifiques de la mémoire sémantique qui nous aideront à mieux comprendre comment les connaissances sémantiques sont organisées et comment de nouveaux apprentissages peuvent survenir. Enfin, nous mettrons en évidence les éléments qui permettent de penser que les mécanismes dapprentissage implicite sont directement impliqués dans lacquisition de nouvelles connaissances sémantiques.