Thesis (M.Sc.)--York University, 2005. Graduate Programme in Kinesiology and Health Science. / Typescript. Includes bibliographical references (leaves 59-63). Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://gateway.proquest.com/openurl?url%5Fver=Z39.88-2004&res%5Fdat=xri:pqdiss &rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:MR11744

Thesis (M.Sc.)--York University, 2005. Graduate Programme in Kinesiology and Health Science. / Typescript. Includes bibliographical references (leaves 46-52). Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://gateway.proquest.com/openurl?url%5Fver=Z39.88-2004&res%5Fdat=xri:pqdiss &rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:MR11898

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Since the field-defining patient HM, consistent links have been made between a region of the brain called the hippocampus and memories that can be consciously declared - so called declarative memories. Declarative memories fall into two categories (1) episodic memories, memories that are highly detailed and re-experiential, and (2) semantic memories, fact-based memories for personal and public information but that have no sense of re-experiencing. It is believed that the intrinsic anatomy of the hippocampus supports episodic memory but not semantic memory. The hippocampus consists of five regions (cornu Ammonis, CA, 1-3, dentate gyrus, subiculum) with each purported to have a specific role in episodic memory acquisition and retrieval. However, controversy surrounds the temporal extent to which episodic memories rely on the hippocampus for retrieval: current consensus suggests the hippocampus supports these memories for five-10 years post-acquisition, but some suggest that it is required for retrieval across the lifetime. Voltage-gated potassium channel-complex antibody-mediated limbic encephalitis (VGKC-complex LE) is a recently described autoimmune disease that causes chronic hippocampal atrophy and mild amnesia on standardized neuropsychological assessment. Two subfields of the hippocampus - CA1 and CA3 - contain the antigenic targets of the disease but it is unknown if specific atrophy of these subfields underlies the hippocampal damage in humans. Here, the human hippocampal subfield volumes of VGKC-complex LE patients (n = 19, mean age: 64.0±2.55; range: 24-71) were investigated using ultra-high spatial resolution MRI at 7.0-Tesla. Assessment also included standardized neuropsychology to examine the impact of the pathology on hippocampal-dependent and -independent memory performance, as well as attention, language, executive function, and perception Declarative memory assessment measured semantic and episodic memory performance across the lifespan. Manual segmentation detected lesions to just CA3, with no volume loss noted elsewhere in the hippocampus or brain. Patients were impaired on hippocampal-dependent memory domains but not the hippocampal-independent and non-memory domains. Notably, episodic memory assessment revealed episodic amnesia across the lifetime except for their earliest memories. This counters the received convention that the hippocampus has a temporally limited role in episodic retrieval. Conversely, the performance of the VGKC-complex LE patients for semantic memory, including a new test developed herein, was comparable to controls across the lifespan. It was then shown that CA3 volume predicted episodic memory performance across the lifetime. Together, the results suggest that VGKC-complex LE provides a novel model of human hippocampal subfield pathology, with which to explore the roles of hippocampal subfields in episodic memory acquisition and retrieval.

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It has been reported previously that systemic administration of clonidine, an agonist of α-2 receptors for noradrenaline, significantly retards amygdaloid kindling, by delaying the emergence from partial seizure, Conversely, systemic administration of α-2 antagonists has been reported to facilitate amygdaloid kindling, The experiments I conducted attempted to discover whether α-2 adrenoceptors in the amygdala participated in these effects, I examined the effect of either systemic administration (i,p.) or intraamygdaloid infusions of a variety of noradrenergic drugs on the kindling of seizures with electrical stimulation of the amygdala, Rats received either low-frequency stimulation of the amygdala, to induce rapid kindling, or conventional high-frequency stimulation, Drugs and electrical stimulation were administered once every 48 hrs, I observed a significant retardation of kindling in rats receiving i,p. injections of clonidine (0.1 mg/kg) or unilateral infusions of clonidine in concentrations of [special characters omitted] to [special characters omitted] M, regardless of the stimulation frequency. The prophylactic effect was due to a delay in the progression out of partial seizure. I observed similar effects with infusions of xylazine, also an α-2 adrenoceptor agonist, The effect was specific to the amygdala/pyriform region, because infusions of clonidine dorsal lo the amygdala were without effect. Power spectral analysis of the AD from the stimulated and the contralateral amygdala during the initial occurrence of bilateral AD failed to reveal differences attributable to clonidine, Therefore, clonidine might retard kindling by modifying the propagation of AD from the stimulated amygdala to a midbrain or pontine brainstem area critical, for the expression of generalized seizures. Clonidine had no effect on established generalized seizures, suggesting that it was producing a genuine prophylactic effect against kindling. Unexpectedly, intraamygdaloid infusions of either idazoxan, yohimbine, or SK&F 104856, antagonists of α-2 receptors, failed to accelerate kindling. Simultaneous infusion of idazoxan blocked clonidine’s prophylactic effect, which suggests strongly that this effect was mediated at the α-2 adrenoceptor. Blockade of amygdaloid α-1 adrenoceptors with corynanthine failed to affect kindling. I conclude that the population of α-2 adrenoceptors in the amygdala/pyriform region contributes to the antiepileptogenic effect observed after systemic administration of clonidine and that the facilitation of kindling observed after systemic administration of α-2 antagonists reported previously may have been mediated by the blockade of a population of α -2 adrenoceptors in addition to, or outside of, the amygdala/pyriform region. / Graduate

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