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Thesis (M.A.)--Baylor University, 2007. / In abstract "h and 2" are subscript. Includes bibliographical references (p. 43-52).

The role of the forebrain commissures in the developing and developed kindled amygdaloid seizure in the rat was investigated. In the first two experiments, bisection of the corpus callosum, hippocampal commissure, and anterior commissure prior to kindling caused a significant facilitation in the rate of primary-site kindled seizure development. In the last experiment, bisection of the corpus callosum and hippocampal commissure after primary-site kindling facilitated the subsequent rate of secondary-site kindling. It is evident, that in the intact animal, the nonstimulated hemisphere is able to exert an inhibitory influence over the development of seizure activity in a stimulated hemisphere and that this effect is, in turn, mediated via the forebrain commissures. The corpus callosum and hippocampal commissure were found to participate in the interference phenomenon since bisection of these structures either before or after primary-site kindling caused a facilitation in the rate of primary-site rekindling. In the first two experiments, an extracommissural, possibly brainstem, mechanism is suggested to mediate the transfer effect between the primary and secondary sites since bisection of the forebrain commissures prior to kindling had no effect on the rate of secondary-site kindling. The development of primary generalized motor seizures is in part dependent on the integrity of the corpus callosum and hippocampal commissure. Bisection of these structures after primary-site kindling, however, abolished the subsequent development of primary generalized seizures in a significant number of rats. Therefore, it appears that if the commissures are bisected prior to kindling, alternate pathways able to mediate the development of primary generalized seizures evolve. / Medicine, Faculty of / Graduate

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Thesis (B.A.)--Haverford College, Dept. of Psychology, 2004. / Includes bibliographical references.

Learned taste avoidance (LTA) was studied by allowing rats to drink a novel sweet solution followed by induction of gastric malaise (training). When the solution was presented again (test), normal rats reduced their consumption. Ultrasonic vocalizations indicated that the rats experienced positive affect during training which shifted to negative affect during the test. Basolateral amygdala lesions eliminated the LTA and the negative affective shift when the rats were 23 hr water deprived during both training and test suggesting amygdala-based Pavlovian conditioning, but only attenuated the LTA and eliminated the aversive shift when the rats were 3 hr deprived on the test, suggesting instrumental learning. When rats were 3 h deprived during training the lesions had no effect on either the LTA or the negative affective shift, suggesting an amygdala-independent form of LTA based on latent learning.

Temporal lobe epileptics often experience interictal (i.e., between-seizure) emotional disturbances such as fear and anxiety. Despite the problem that these disturbances present, little progress has been made in characterizing their nature and etiology because they are not amenable to experimental analysis in clinical populations. Accordingly, the general purpose of the experiments in this thesis was to demonstrate the potential of long-term amygdala kindling in rats as a model of the interictal hyperemotionality of temporal lobe epileptics. Seven experiments comprise this thesis. Experiments 1 and 2 established that longterm amygdala kindling (i.e., 100 stimulations) results in large and reliable increases in emotionality. In Experiment 1, the long-term amygdala-kindled rats displayed more resistance to capture from an open field and more open-arm activity on an elevated plus maze than did the sham-stimulated rats; in Experiment 2, the magnitude of this hyperemotionality was shown to be dependent on the number of amygdala stimulations that the rats received. Experiment 3 showed that kindling-induced hyperemotionality is enduring; the hyperemotionality present 1 day after the final stimulation did not decline significantly over the ensuing month although some amelioration of symptoms was observed. Experiment 4 established that kindling-induced hyperemotionality is not unique to amygdala stimulation. Although increases in emotionality were greatest in amygdalakindled rats, hippocampal-kindled, but not caudate-kindled, rats also displayed significant increases. Experiments 5 and 6 showed that kindling-induced hyperemotionality is fundamentally defensive in nature. In Experiment 5, amygdala-kindled rats displayed high levels of emotionality in an unfamiliar, but not in a familiar, situation; in Experiment 6, amygdala-kindled rats displayed more defensive, but less aggressive behaviour, in their interactions with other rats. Finally, Experiment 7 showed that 8-OH-DPAT binding to serotonin 5HT1A receptors is increased in the dentate gyrus of amygdala-kindled rats, but not in the amygdala, periaqueductal grey, perirhinal cortex, or CA1 or CA3 hippocampal subfields. Together, the results of these experiments establish the potential of long-term amygdala kindling as a useful animal model of interictal emotionality in temporal lobe epileptics.

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