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This thesis aimed to investigate the role of the perirhinal cortex in object memory in the rat. The first experiment tested the hypothesis that the perirhinal cortex is critical to memory for relationships between objects by testing postoperative learning of novel visual-visual stimulus associations following lesions of the perirhinal cortex. The hypothesis was not supported: postoperative performance was not impaired. Experiments 3.1-3.4 tested the hypothesis that perirhinal cortex is crucial to the integration of multiple features into a representation of an object using spontaneous object recognition with either reconfigured objects or multiple objects. The hypothesis was supported: perirhinal lesions caused disproportionate impairment on tasks involving feature ambiguity. Experiments 4.1-4.7 investigated the effects of, perirhinal, postrhinal or fornix lesions on aspects of memory for object-context associations. The hypothesis that postrhinal and fornix lesioned animals would be more impaired than perirhinal animals was confirmed. Postrhinal lesions impaired memory for object-context associations, as, less severely, did fornix lesions; perirhinal lesions impaired memory when another object was used as the context. Experiment 5.1 used a novel model for episodic-like memory and tested the hypothesis that postrhinal or fornix, but not perirhinal lesions would cause impairment. One of these predictions was supported: fornix but not postrhinal or perirhinal lesions caused severe impairment of episodic-like memory. The fornix impairment was not due to an impairment of memory for object-place associations (experiment 5.2). Finally, experiments 6.1-6.7 investigated the possible function of L-type calcium channels in perirhinal cortex. The dihydropyridine nimodipine was successfully used to reverse the effects of the muscarinic antagonist scopolamine on the spontaneous object recognition task. It is concluded that perirhinal lesions in the rat result in impairments of memory which involve the processing of objects and the relation of their constituent features to each other. They do not impair memory for the association either of distinct objects or of objects and background contexts or locations. This is contrasted with the impairment of memory for object-in-context which results from postrhinal lesions and the impairment of episodic- like memory which results from fornix lesions. The importance of the cholinergic system in object recognition is confirmed and the importance of L-type calcium channels to such memory is suggested.

Although much work has been carried out to identify the mechanisms by which muscle is formed, many of the regulatory pathways involved have yet to be fully elucidated. In creating perturbations during the embryonic period, either nutritionally (with a marginal vitamin A deficiency model) or pharmacologically (with the b₂-adrenerguic agonist clenbuterol), a comparison with 'normal' muscle development may be attained. Differences in the temporal expression of specific regulatory proteins may then enhance the existing knowledge of their function in regulating muscle development. Prior to studying changes in muscle regulatory proteins due to perturbations, it was first necessary to illustrate their temporal pattern in "normal" muscle development. The results indicated that a complex regulatory system operates in myogenesis with a number of proteins appearing to be involved in the process of muscle development. A marginal vitamin A deficiency model was established in which maternal retinol levels were clearly reduced in treatment animals in comparison with controls. This resulted in offspring that showed clearly symptoms of marginal vitamin A deficiency. Changes in the abundance of five proteins were observed in response to marginal vitamin A deficiency. Overall, these changes suggested a potential reduction in secondary myogenesis, based on reduced levels of MHCfast, associated with secondary fibres, following birth. Analysis of RNA, DNA and protein values suggested that neonates from clenbuterol fed dams may have reduced hyperplasia and/or increased hypertrophy. Biochemical analysis revealed that proteins such as GATA-2, PKC and Shh, which have previously been associated with hypertrophy, were altered in response to clenbuterol. Further evidence in support of hypertrophy was indicated in an apparent increase in fibre size of neonates detected by MHC immunolocalisation. In conclusion, it has been demonstrated that both nutritional and pharmacological manipulations throughout are gestation capable of altering myogeneiss <i>in utero</i> by two different mechanisms.

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