Thesis (doctoral)--Umeå Universitet, Sweden, 1990. / Extra t.p. with thesis statement inserted. Includes bibliographical references.

Thesis (doctoral)--Umeå Universitet, Sweden, 1990. / Extra t.p. with thesis statement inserted. Includes bibliographical references.

Thesis (M.S.)--Brigham Young University. Dept. of Physiology and Developmental Biology, 2006. / Includes bibliographical references (p. 49-52).

Aims: Test the putative contribution of 17-beta-estradiol in the development of spreading depression (SD) events and head pain in awake, non-restrained rats. Main Methods: Female, Sprague-Dawley rats were intact or underwent ovariectomy followed one week later by surgery to place electrodes onto the dura to detect epidural electroencephalographic activity (dEEG). dEEG activity was recorded two days later for 12 hours after systemic administration of 17-beta-estradiol (180 mu g/kg, i.p.). A separate set of rats were observed for changes in exploratory, ambulatory, fine, and rearing behaviors; periorbital allodynia was also assessed. Key Findings: A bolus of 17-beta-estradiol significantly elevated serum estrogen levels, increased SD episodes over a 12-hour recording period and decreased rearing behaviors in ovariectomized rats. Pre-administration of ICI 182,780, an estrogen receptor antagonist, blocked 17-beta-estradiol-evoked SD events and pain behaviors; similar results were observed when the antimigraine therapeutic sumatriptan was used. Significance: These data indicate that an estrogen receptor-mediated mechanism contributes to SD events in ovariectomized rats and pain behaviors in both ovariectomized -and intact-rats. This suggests that estrogen plays a different role in each phenomenon of migraine where intense fluctuations in concentration may influence SD susceptibility. This is the first study to relate estrogen peaks to SD development and pain behaviors in awake, freely moving female rats, establishing a framework for future preclinical migraine studies.

No description available.

No description available.

This study aimed to examine whether trigeminal nerve injury induces chronic nociceptive behaviour and central sensitization (CS) in functionally identified medullary dorsal horn (MDH) nociceptive neurons in mice, and whether CS in acute and chronic orofacial pain models and nociceptive behaviour in the chronic model are affected by systemic administration of pregabalin. Infraorbital nerve injury induced chronic facial mechanical allodynia as well as MDH CS; acute noxious tooth pulp stimulation also induced MDS CS. Systemic administration of pregabalin attenuated the nerve injury-induced allodynia as well as the MDH CS in both the chronic and acute pain models. These findings reveal that MDH CS occurs in mouse models of acute and chronic orofacial pain and that pregabalin may prove useful clinically in acute and chronic orofacial pain states.

This study aimed to examine whether trigeminal nerve injury induces chronic nociceptive behaviour and central sensitization (CS) in functionally identified medullary dorsal horn (MDH) nociceptive neurons in mice, and whether CS in acute and chronic orofacial pain models and nociceptive behaviour in the chronic model are affected by systemic administration of pregabalin. Infraorbital nerve injury induced chronic facial mechanical allodynia as well as MDH CS; acute noxious tooth pulp stimulation also induced MDS CS. Systemic administration of pregabalin attenuated the nerve injury-induced allodynia as well as the MDH CS in both the chronic and acute pain models. These findings reveal that MDH CS occurs in mouse models of acute and chronic orofacial pain and that pregabalin may prove useful clinically in acute and chronic orofacial pain states.

Thesis (M.S.)--University of Michigan, 2003. / Includes bibliographical references.

Thesis (Ph. D.)--Brigham Young University. Dept. of Physiology and Developmental Biology, 2006. / Includes bibliographical references (p. 109-113).