Research over the past several decades has revealed that the amygdala is involved in aversive, or fear, conditioning. However, the precise nature of this involvement remains a matter of debate. One hypothesis suggests that disrupting amygdala function eliminates the storage of memories formed during aversive conditioning, eliminating the production of internal responses that alter the expression of observable behaviors. Alternatively, lesions or inactivation of the amygdala may impair the modulation of memories in other brain regions and disrupt the ability to perform certain observable behaviors. The experiments reported in the present thesis examined these arguments by making multiple behavioral measures during exposure to unconditioned (US) or conditioned (CS) aversive cues. Amygdala activity was inferred from changes in c-Fos protein expression or activity was temporarily suppressed with muscimol injections. The relationship between the behavioral measures and the role of the amygdala in producing them was examined. Amygdala neurons expressing the c-Fos protein tracked exposure to the US and CS but did not coincide with expression of freezing. Temporary inactivation of the amygdala with muscimol injections before presentation of the US or exposure to the CS attenuated the expression of freezing and active place avoidance; two incompatible behaviors. Finally, temporary inactivation of amygdala activity blocked freezing, place avoidance, and memory modulation produced by the same posttraining exposure to an aversive CS. Since amygdala activation alone was not sufficient to produce freezing and inactivation of the amygdala eliminated freezing, place avoidance, and memory modulation, the results cannot be interpreted as reflecting a direct role for the amygdala in production of observable behaviors. The results also preclude the idea that memory modulation is the only function of the amygdala. Rather, the results of all three studies suggest that the amygdala stores an aversive representation of the US which promotes the expression of various behaviors, possibly through the production of internal responses reflecting an aversive affective state.

Thesis (Ph.D.). / Written for the Dept. of Psychology. Title from title page of PDF (viewed 2008/08/04). Includes bibliographical references.

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. / Arts, Faculty of / Psychology, Department of / Graduate

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Thesis (Ph. D.)--Michigan State University. Neuroscience Program, 2008. / Title from PDF t.p. (viewed on Mar. 26, 2009). Includes bibliographical references (p. 109-119). Also issued in print.

Thesis (M.A.)--Baylor University, 2007. / Includes bibliographical references (p. 34-38).

Thesis (Ph. D.)--Rutgers University, 2010. / "Graduate Program in Integrative Neuroscience." Includes bibliographical references (p. 111-123).

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