Thesis (M.A.)--University of Wisconsin--Madison, 1967. / eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1982. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 185-196).

Thesis (Ph. D.)--Washington State University, December 2006. / Includes bibliographical references (p. 100-110).

Thesis (M.S.)--Montana State University--Bozeman, 2007. / Typescript. Chairperson, Graduate Committee: A. Michael Babcock. Includes bibliographical references (leaves 28-31).

Thesis (M.S.)--Montana State University--Bozeman, 2007. / Typescript. Chairperson, Graduate Committee: Michael Babcock. Includes bibliographical references (leaves 49-57).

No description available.

Limbic structures, including the hippocampus, are thought to be involved in pain though not much is known of their neuronal responses to noxious stimuli. Experiments were therefore performed in lightly anaesthetized rats to determine the effect of noxious heat stimuli on the excitability of dorsal hippocampal field CA1 pyramidal neurones. A prolonged and substantial depression of the CA1 population spike was produced by a brief but intense noxious stimulus applied to the tail. This depression was temperature-dependent and habituated to subsequent noxious stimuli applied more than 1 hr later. In other animals, a similar depression and habituation was also obtained with noxious heat stimuli applied to the left hind paw. However, following this habituation of the hind paw, a persistent depression of the CA1 population spike was seen if the tail was exposed to a noxious heat stimulus. The persistent depression was absent when noxious heat was applied in the presence of hippocampal theta rhythm. If, however, the hippocampal electroencephalographic ( EEG ) activity was in an irregular pattern at the time noxious heat was applied, a 4-6 Hz theta rhythm was produced along with the depression of the population spike. The latency and intensity of the reflex response was combined into a reflex-reaction score. There appeared to be a relationship between the reflex-reaction score and the duration of theta rhythm induced by different intensities of noxious heat stimuli but there was no habituation to these responses. The CA1 population spike evoked either by ipsilateral or contralateral CA3 stimulation was similarly depressed following a noxious stimulus. Concomitantly, the persistent depression and habituation of the commissural CA1 population spike was also accompanied by similar changes in the corresponding dendritic field excitatory postsynaptic potential ( EPSP ). However, the amplitude of the CA1 antidromic spike was increased in the majority of cases. These findings suggest that a presynaptically mediated decrease in synaptic transmission may account for the depression of the population spike and dendritic field EPSP. There is evidence to suggest that the noxious stimulus-induced persistent depression of CA1 pyramidal cell synaptic excitability is due to a cholinergic projection from the medial septal-vertical limb of the diagonal band of Broca complex ( MS-VLDBB ). Thus, atropine sulphate ( 40 mg/kg, i.p. ) prevented the persistent depression of the CA1 population spike to a noxious stimulus. It also antagonized the septal tetanus-evoked, cholinergic mediated facilitation of the CA1 commissural population spike but had no effect on the corresponding paired-pulse facilitation. Atropine, applied iontophoretically to the cell body region antagonized the iontophoretic acetylcholine-induced facilitation of the CA1 population spike but not its depression to a noxious stimulus. On the other hand, apical dendritic application of atropine antagonized iontophoretic acetylcholine and noxious stimulus-induced depression of the CA1 dendritic field EPSP. However, such iontophoretic application of atropine had no effect on dendritically applied gamma aminobutyric acid ( GABA )-induced depression of the CA1 dendritic field EPSP. These results support the notion that acetylcholine release in the dendritic region of CA1 neurones is involved in the depression of synaptic excitability of these neurones evoked by a noxious stimulus. / Pharmaceutical Sciences, Faculty of / Graduate

This study was undertaken to resolve the conflict between two existing studies regarding the layer in the dentate gyrus where the septal fibers terminate. This was accomplished by injecting radioact ively labelled amino acids into the medial septum where they were incorporated into protein by the cell bodies and transported to the nerve terminals. Autoradiographic grain counts showed labelling was moderately heavy in the subgranular zone of the dentate gyrus, whereas labelling was scant in the molecular layer. These findings support the work of Raisman et al., (1965), but indicate the degeneration seen by Mosko, et al., (1973) in the molecular layer may have been artefactual. The ultrastructure of the septal terminals in the subgranular zone of the dentate gyrus was described. These terminals formed asymmetrical synapses onto dendrites and spines, and contained clear round vesicles. They resembled cholinergic nerve terminals described in other regions of the brain. These findings agree with accumulating evidence that the septo-dentate pathway is cholinergic. / Medicine, Faculty of / Graduate

Table of Contents: Chapter 1 - Remembrance of places past: a history of theories of space / Chapter 2 - Spatial behaviour / Chapter 3 - Anatomy / Chapter 4 - Physiology / Chapter 5 - Introduction to the lesion review / Chapter 6 - Exploration / Chapter 7 - Discrimination and maze learning / Chapter 8 - Aversively motivated behaviour / Chapter 9 - Operants: the limited role of the locale system / Chapter 10 - Reactions to reward change / Chapter 11 - Maintenance behaviours / Chapter 12 - Stimulation studies / Chapter 13 - Long-term memory / Chapter 14 - An extension of the theory to humans / Chapter 15 - The amnesic syndrome

No description available.