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Recent evidence suggests a possible role for the prefrontal cortex (PFC) in sleep/wake regulation and sleep-related electroencephalogram (EEG) activity. This study investigated the effects of cell-specific ibotenic acid lesions to the PFC on sleep-wake patterns and the EEG under baseline conditions and during recovery from a 6 h period of sleep deprivation (SD) using gentle handling in rats. Control rats were injected with saline. PFC lesions had no effects on overall amounts of wake, non rapid-eye movement (NREM) sleep, or rapid-eye movement sleep. However, lesioned animals had fewer wake and NREM sleep episodes and longer mean durations of these episodes particularly during the dark phase. Following SD, no significant lesion effects were observed in sleep rebound or homeostatic increase in NREM EEG delta power (a measure of sleep intensity). These results suggest a role for the PFC in sleep-wake regulation, in particular behavioural state stability.

Introduction: Cataplexy - the sudden involuntary loss of skeletal muscle tone – is a defining feature of narcolepsy. The current study aimed to determine if cataplexy is influenced by direct manipulation of REM sleep circuitry. We did this by pharmacogenetically inhibiting the REM sleep center, subcoeruleus (Sub-C). Methods: Inhibitory DREADD (hM4D-Gi) was bilaterally targeted to the Sub-C in hypocretin knockout mice (n=7). Intraperitoneal administration of clozapine-n-oxide was used to inhibit Sub-C cells expressing hM4D-Gi. Electrophysiological and behavioral criteria were used to characterize cataplexy and REM sleep. Results: Sub-C inhibition increased REM sleep and cataplexy amounts (p<0.05). Sub-C inhibition increased time spent in cataplexy amounts by increasing the number of cataplexy attacks (p<0.05). This intervention triggered increases in basal muscle tone during REM sleep, but had negligible effects on muscle tone during cataplexy (p>0.05). Conclusion: Pharmacogenetic manipulation of the Sub-C suggest that REM sleep and cataplexy are mediate by similar neural mechanism.

The underlying mechanism for the origin of ultradian rhythms is not clearly understood at present. Based on a recent study from our laboratory, we have conceptualized a model for the origin of quasiperiodic ultradian rhythms in sleep-wake state. This model hypothesizes that the ultradian rhythms of sleep-wake state may be generated by a mechanism that includes the sleep-wake homeostat. The main purpose of the present study was to test the hypothesis that sleep homeostasis and sleep-wake ultradian rhythms share a common underlying mechanism. The present study has refuted that hypothesis. I conclude that: (1) the proposed model for the generation of quasiperiodic ultradian rhythms in sleep-wake state in mammals is overly simplistic in its present form, (2) the generation of ultradian rhythms in sleep-wake state probably arise from a more complex systemic interactions between the sleep-wake oscillatory network and other internal/external inputs, rather than the simple expression of sleep homeostat.

The underlying mechanism for the origin of ultradian rhythms is not clearly understood at present. Based on a recent study from our laboratory, we have conceptualized a model for the origin of quasiperiodic ultradian rhythms in sleep-wake state. This model hypothesizes that the ultradian rhythms of sleep-wake state may be generated by a mechanism that includes the sleep-wake homeostat. The main purpose of the present study was to test the hypothesis that sleep homeostasis and sleep-wake ultradian rhythms share a common underlying mechanism. The present study has refuted that hypothesis. I conclude that: (1) the proposed model for the generation of quasiperiodic ultradian rhythms in sleep-wake state in mammals is overly simplistic in its present form, (2) the generation of ultradian rhythms in sleep-wake state probably arise from a more complex systemic interactions between the sleep-wake oscillatory network and other internal/external inputs, rather than the simple expression of sleep homeostat.

Introduction: Cataplexy - the sudden involuntary loss of skeletal muscle tone – is a defining feature of narcolepsy. The current study aimed to determine if cataplexy is influenced by direct manipulation of REM sleep circuitry. We did this by pharmacogenetically inhibiting the REM sleep center, subcoeruleus (Sub-C). Methods: Inhibitory DREADD (hM4D-Gi) was bilaterally targeted to the Sub-C in hypocretin knockout mice (n=7). Intraperitoneal administration of clozapine-n-oxide was used to inhibit Sub-C cells expressing hM4D-Gi. Electrophysiological and behavioral criteria were used to characterize cataplexy and REM sleep. Results: Sub-C inhibition increased REM sleep and cataplexy amounts (p<0.05). Sub-C inhibition increased time spent in cataplexy amounts by increasing the number of cataplexy attacks (p<0.05). This intervention triggered increases in basal muscle tone during REM sleep, but had negligible effects on muscle tone during cataplexy (p>0.05). Conclusion: Pharmacogenetic manipulation of the Sub-C suggest that REM sleep and cataplexy are mediate by similar neural mechanism.

Pontomesencephalic tegmental cholinergic neurons were destroyed in cats by local injections of kainic acid in order to assess the role of these neurons in sleep-wakefulness states and in the defining variables of these states: EEG (electroencephalographic) and EMG (electromyographic) amplitude, PGO (ponto-geniculo-occipital) spike rate, REMs (rapid eye movements) and (OBS) olfactory bulb spindles. Loss of cholinergic innervation to forebrain and brainstem structures was also assessed by histochemistry. Histological and histochemical analysis of the brains after the lesion showed a major destruction of the pontomesencephalic cholinergic neurons and a major loss of innervation to thalamic nuclei and brainstem regions, including the reticular formation. Whereas the states of waking and slow wave sleep were relatively unaffected, paradoxical sleep (PS) was reduced or eliminated immediately following the lesions. Two to three weeks later, incipient PS-like episodes returned with a reduced PGO spike rate and REMs, and an elevated EMG amplitude, marking the loss of muscle atonia. Such results suggest pontomesencephalic cholinergic neurons and their projections to thalamic and brainstem regions are important for the expression of PS and its defining variables.

Despite high prevalence rates of insomnia among the elderly, very few treatment options adapted to the characteristics and needs of this population group exist. This study aims to investigate the efficacy of a thermal biofeedback based technique in treating sleep onset insomnia in an elderly sample. Eight healthy elderly good sleepers and eight healthy elderly sleep onset insomniacs participated in the study. The effect of the thermal biofeedback on participants' forehead temperature, clavicular temperature, right hand temperature, left hand temperature, stomach temperature, thigh temperature, right foot temperature, core body temperature, and sleep latency was assessed. Furthermore, the impact of the thermal biofeedback technique on participants' subjective ratings of biofeedback proficiency and sleepiness was investigated. The thermal biofeedback protocol failed to generate adequate and consistent changes in participants' body temperature, indicating that it is of limited practical used as a treatment of sleep onset insomnia in its present form. Several interesting trends observed during the current study are explored and areas for further research identified. / Thesis (MPsy(Clinical))--University of South Australia, 2006.

Thesis (MAppSc in Physiotherapy) -- University of South Australia, 1993

Thesis (Ph.D.) - Carleton University, 2002. / Includes bibliographical references (p. 152-169). Also available in electronic format on the Internet.