The posterior parietal cortex (PPC) is a cortical region receiving inputs from different sensory modalities which has been shown to subserve a visuospatial function. The potential contribution of PPC in audiospatial behaviours and recognition of amodal spatial correspondences were postulated and assessed in the present study. Adult male Long- Evans rats received PPC lesions by aspiration, and they were compared to sham operated control rats on three behavioural tasks. In the Morris water maze, the rats had to learn to use the distal visual cues to locate an escape platform hidden in the pool. In an open field task, the rats were assessed on their reactions to a spatial relocation of a visual or an auditory object. In a spatial cross-modal transfer (CMT) task (Tees & Buhrmann, 1989), rats were trained to respond to light signals using spatial rules, and were then subjected to transfer tests using comparable sound signals. Results from the Morris water maze, the open field, and the initial training phase of the spatial CMT task confirmed a visuospatial deficit in PPC lesioned rats. However, if given sufficient training, PPC lesioned rats could learn the location of a hidden platform in the Morris water maze, and they could also acquire spatial rules in the CMT task. Such results indicated that the visuospatial deficits in PPC lesioned rats were less severe than previously thought. On the other hand, a persistent navigational difficulty characterized by a looping pattern of movement was observed in the PPC lesioned rats in the Morris water maze. Results from the open field indicated that PPC was less involved in audiospatial behaviours. Moreover, results also indicated that PPC was not necessary for spatial CMT. Hence, data from the present study did not support the idea that PPC played an essential role in supramodal spatial abilities in the rats. Instead, data from the spatial CMT task seemed to imply a role of PPC in managing conflicting spatial information coming from different sensory modalities. / Arts, Faculty of / Psychology, Department of / Graduate

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The current interest in the secretions of the adrenal cortex is shared by physiologist, physician and pharmacologists alike. such attention is not surprising in the case of a gland which is immediately essential to life, which can produce syndromes as varied as precocious puberty, virilisation; Addison's disease; Cushing's syndrome, and the newly described hyperaldosteronism syndrome of Conn (1955), a gland which has been implicated in the parthenogenesis of diabetes (Hoet and Lukens, 195; Jackson, 1955), hypertension (Sepeika, 1948, 1955), pre-eclampsia, and atherosclerosis, and which profoundly effects so many of the metabolic processes of the body. The need for accurate measurement of adrenocortical function has therefore been accentuated in recent years. The purpose of this study was to find out as direct a method as possible for determining the rate of secretion of this gland and to define with this method the norms and normal variations.

The study of motor cortex (dorsal premotor cortex and primary motor cortex) has been greatly aided by the development of a conceptual paradigm that has emerged over the past decade. In contrast to established frameworks, which view neural activity within motor cortex as a representation of particular movement parameters, the ‘dynamical systems paradigm’ posits that motor cortex is best understood via the low-dimensional neural processes that allow the generation of motor commands. This framework largely evolved from, and has been most successfully applied to, simple reaching tasks, where the sequential stages of movement generation are largely separated in time – motor cortex absorbs an input that specifies the identity of the upcoming reach, a second input initiates the movement, and strong, autonomous dynamics generate time-varying motor commands. However, while the dynamical systems paradigm has provided a useful scaffolding for interrogating motor cortex, our understanding of the mechanisms that generate movement is still evolving, and many questions remain unanswered. Prior work has established that the neural processes within motor cortex that generate descending commands are initiated by a large, condition-invariant input. But are movements made under different behavioral contexts initiated via the same mechanisms? Lesion studies suggest that the generation of so-called ‘self-initiated movements’ is uniquely dependent on the supplementary motor area (SMA), a premotor region immediately upstream of motor cortex. In contrast, SMA is thought to be less critical for generating externally-cued movements. To characterize the degree to which SMA is able to impact movement initiation across behavioral contexts, we trained two monkeys to make reaches that were either internally or externally cued. On a subset of trials, we disrupted activity within SMA via microstimulation and asked how this perturbation impacted the monkeys’ behavior. Surprisingly, we found that the effect of stimulation was largely preserved across contexts; the behavioral effects of stimulation could be explained by a simple model in which a context-invariant, time-varying kernel multiplicatively altered the odds of movement initiation. These results suggest that SMA is able to impact movement initiation across behavioral contexts. The question of how sequences of discrete actions are generated has been investigated for over one hundred years. It is commonly thought that once a given sequence (particularly a rapid sequence) becomes well-learned, individual actions that were once produced separately become ‘merged’, such that multiple actions are generated as a single, holistic unit. But what does it mean to generate multiple actions as a single unit? The dynamical systems paradigm offers the ability to translate this notion into specific predictions about the timing and structure of neural activity within motor cortex during sequence production. Importantly, it also offers predictions for the alternative hypothesis – that motor cortex generates the component actions of a sequence independently. To determine whether the production of rapid sequences requires motor cortex to merge multiple actions into a single ‘movement’, we trained monkeys to make sequences of two reaches. Surprisingly, we found that the same set of neural events are used to produce rapid sequences and isolated reaches. Rather than merging individual actions into a single unit, motor cortex generated rapid sequences by overlapping the neural activity related to reach preparation and execution. These results demonstrate that the performance of extremely fast, well-learned movement sequences does not require motor cortex to implement a sequence-specific strategy; the same neural motif that produces a simple reach can also generate movement sequences.

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Human visual perception changes across the lifespan that relies on changes in synaptic plasticity in the visual cortex. Anatomical studies of the visual cortex, however, suggest human V1 develops early and remains relatively constant from childhood and on. Animal models have pin-pointed specific neurobiological mechanisms that are necessary for the development of visual plasticity and receptive field properties in the visual cortex. Very little is known, however, about how those synaptic mechanisms develop in the human visual cortex to support plasticity and perception across the lifespan. This thesis addresses this gap by providing new studies on the development of those neurobiological mechanisms in postmortem human visual cortex cases that range in age from 20 days to 79 years. The main findings from this thesis support prolonged development of plasticity mechanisms in human V1 that could be characterized in 5 stages of change across the lifespan: booting up synaptic function in infancy, high neural variability in young childhood, peaks of development in older childhood, prolonged plasticity in adulthood, and return to juvenile-like state in aging. In addition, I show a contrasting development of synaptic plasticity mechanisms in V1 and extrastriate areas that suggest higher order visual perception is processed differently. I also highlight a modernized technique for isolating synaptoneurosomes in human brain that helps quantify synaptic proteins using postmortem human tissue. Together these findings aid in the translation of neurobiological mechanisms in animal models for identifying new therapeutic targets for recovery in human visual disorders and vision loss. / Thesis / Doctor of Philosophy (PhD) / The ability to see the world constantly changes from birth to old age, and depends on the health and function of our brain. The visual cortex is the part of the brain that processes vision, and it is made up of millions of cells that connect to each other through billions of synapses. Fine-tuning those connections and networks in the brain leads to better vision. The ability for connections to be fine-tuned by experience is called plasticity, and it is necessary for developing good vision. This thesis addresses the development of plasticity in the human brain by measuring levels of proteins that are responsible for controlling plasticity and vision. My findings suggest that humans have a longer period of plasticity for developing good vision than previously thought. These findings will help identify new targets to rescue vision loss that occurs in aging or visual disorders across the lifespan.