Vowel perception primarily depends on the overall shape of the speech spectrum, which is imposed by the positions of the primary speech articulators. Voiced vowels also have a harmonic fine structure due to the activity of the vocal folds, and these harmonics give rise to synchronized activity in the brainstem. This synchronous firing may be useful for speech perception in noise and speaker discrimination, although it is unknown if the synchronized neural response to the harmonic increases perceptual audibility of the harmonic. The focus of the current study was to examine the relationship between the audibility of harmonics and the brainstem response to harmonics. The individual harmonics were found to be encoded in the brainstem, determined using brainstem frequency-following response recording, and the individual harmonics were audible to the individual, as determined using the pulsation threshold technique; however there was minimal relationship between the frequency-following response and perception of harmonics.

An important function of the brain is to inhibit irrelevant behaviors. This thesis examines the role of the basal ganglia in response suppression using saccadic eye movements as a model of behavior. We measured the activity of single saccade-related neurons in primate Substantia Nigra pars reticulata (SNr), a main output structure of the basal ganglia, while the context surrounding the initiation and suppression of saccades was manipulated. Inserting a temporal gap of no stimuli between the disappearance of a central visual fixation point and the appearance of a peripheral visual target leads to a reduction in saccadic reaction times (SRT); the ‘gap’ effect. SNr pause neurons decreased their activity during the gap and this decrease correlated with SRT. This finding suggests the SNr may contribute directly to producing the gap effect and that signals related to the effect are propagating through a frontal-basal ganglia circuitry to impact pre-saccade processing. Interleaving pro-saccade (look towards a visual stimulus) and anti-saccade (look away from visual stimulus) trials allowed us to investigate how neural processes change when preparing to suppress a saccade instead of making one automatically. We show that SNr neurons exhibit activity consistent with both suppression of automatic responses and facilitation of voluntary responses, during anti-saccades. These data provide direct neurophysiological evidence for a dual role of inhibitory and disinhibitory basal ganglia outputs in the flexible shaping of behavior. Parkinson’s disease (PD) is a neurodegenerative disorder that impairs motor function due to depletion of dopamine in the striatum. Using an oculomotor countermanding paradigm, we found that PD patients were unable to suppress saccades to a peripheral target, providing evidence that the SNr performs a gating function that mediates the initiation and suppression of saccades. When pathology to the circuitry occurs, inhibitory control over saccades is affected. In Conclusion, using a variety of behavioral contexts, this thesis has demonstrated that the basal ganglia, specifically the SNr, mediates the suppression and voluntary initiation of saccades, possibly via an inhibitory gating mechanism, and that this role is important for successful interaction with a dynamic environment. / Thesis (Ph.D, Physiology) -- Queen's University, 2008-07-16 12:06:19.188

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No description available.

No description available.

Despite substantial progress in the area of depression research, the current treatments for Major Depressive Disorder (MDD) remain suboptimal. Therefore, various medications are often used as augmenting agents in pharmacotherapy of treatment-resistant MDD. Despite the relative clinical success, little is known about the precise mechanisms of their antidepressant action. The present work was focused on describing the effects of three drugs with distinctive pharmacological properties (pramipexole, aripiprazole, and quetiapine) on function of the monoaminergic systems involved in the pathophysiology and treatment of MDD. Reciprocal interactions between the monoamines serotonin, norepinephrine, and dopamine systems allow the drugs targeting one neuronal entity to modify the function of the other two chemospecific entities. Electrophysiological experiments were carried out in anaesthetized rats after 2 and 14 days of drug administration to determine their immediate and the clinically-relevant long-term effects upon monoaminergic systems. Pramipexole is a selective D2-like agonist with no affinity for any other types of receptors. It is currently approved for use in Parkinson’s disorder and the restless leg syndrome. Long-term pramipexole administration resulted in a net increase in function of both dopamine and serotonin systems. Aripiprazole is a unique antipsychotic medication. Unlike all other representatives of this pharmacological class that antagonize D2 receptor, this drug acts as a partial agonist at this site. Chronic administration of aripiprazole elevated the discharge rate of the serotonin neurons, presumably increasing the overall serotonergic neurotransmission. Like aripiprazole, quetiapine is one of three atypical antypsicotic drugs approved for use in MDD. Prolonged administration of quetiapine led to a significant increase in both noradrenergic and serotonergic neurotransmission. Importantly, the clinically counter-productive decrease in the spontaneous firing of catecholaminergic neurons, induced by SSRIs, was overturned by the concomitant administration of both aripiprazole and quetiapine. The increase in serotonergic neurotransmission was a consistent finding between all three drugs studied herein. In every case this enhancement was attained in a distinctive manner. Understanding of the precise mechanisms leading to the amplification/normalization of function of monoamines enables potential construction of optimal treatment strategies thereby allowing clinicians greater pharmacological flexibility in the management of depressive symptoms.

Thesis (Ph.D.)--Tufts University, 1999. / Adviser: Phillip J. Holcomb. Submitted to the Dept. of Psychology. Includes bibliographical references (leaves 103-113). Access restricted to members of the Tufts University community. Also available via the World Wide Web;

Thesis (Ph. D.)--University of Hong Kong, 2007. / Also available in print.

Thesis (Ph. D.)--University of Sydney, 2001. / Includes published articles. Title from title screen (viewed Apr. 24, 2008). Submitted in fulfilment of the requirements for the degree of Doctor of Philosophy to the School of Physics, Faculty of Science. Includes bibliography. Also available in print form.

Thesis (Ph. D.)--University of Hong Kong, 2007. / Also available online.