Disruptions of endoplasmic reticulum (ER) Ca²⁺ homeostasis are heavily linked to neuronal pathology. Depletion of ER Ca²⁺ stores can result in cellular dysfunction and potentially cell death, although adaptive processes exist to aid in survival. This dissertation examines the age and region-dependence of one postulated adaptive response to ER store depletion, store depletion (SD) HCN channel plasticity, in neurons of the dorsal (DHC) and ventral (VHC) hippocampus from adolescent and adult rats. Using whole-cell patch clamp recordings from the soma and dendrites of CA1 pyramidal neurons, the change in h-sensitive measurements in response to store depletion, induced by treatment with cyclopiazonic acid (CPA), a sarco/endoplasmic reticulum Ca²⁺-ATPase blocker were observed. While DHC and VHC neurons in adolescent animals responded to store depletion with a peri-somatic expression of SD h plasticity, it was found that adult animals express SD h plasticity with a dendritic and somato-dendritic locus of plasticity in DHC and VHC neurons, respectively. Furthermore, SD h plasticity in adults was dependent on membrane voltage and on the activation of L-type voltage gated Ca²⁺ channels. These results suggest that cellular responses to the impairment of ER function, or ER stress, are dependent upon brain region and age, and that the differential expression of SD h plasticity could provide a neural basis for region and age-dependent disease vulnerabilities. / text

Heidelberg, Univ., Diss., 2007.

Berlin, Freie Universiẗat, Diss., 2004. / Dateiformat: zip, Dateien im PDF-Format.

archives@tulane.edu / The broad goal of the following experiments was to determine the mechanisms through which estrogen receptor (ER) α can maintain memory and enhance hippocampal function in the absence of endogenous or exogenously administered ovarian hormones. In Aim 1, we compared the subcellular localization of ERα and the expression of memory-related genes and proteins in the hippocampus following either continuous or previous exposure to estradiol in aging ovariectomized rats. Previous estradiol exposure, like continuous estradiol treatment, immediately following ovariectomy specifically increased the nuclear pool of ERα and resulted in lasting increases in gene transcription and protein expression in the hippocampus. In Aim 2, we demonstrated that insulin-like growth factor-1 (IGF-1) and brain-derived neuroestrogens interact to facilitate activation of hippocampal ERα and enhancement of memory in recently ovariectomized rats. Specifically, we showed that acute infusions of IGF-1 to the brains of ovariectomized middle-aged rats resulted in increased phosphorylation of hippocampal ERα, increased activation of the MAPK signaling pathway, and enhanced performance on the radialarm maze task, but that these effects were dependent on concurrent neuroestrogen synthesis. In Aim 3, we investigated the impacts of long-term ovarian hormone deprivation and previous estradiol treatment on the ability of IGF-1 and neuroestrogen signaling to maintain hippocampal function and memory. Results demonstrated that following long periods of ovarian hormone deprivation, neuroestrogens no longer contribute to ER-dependent transcriptional activity in the brain, a change which coincides with decreased interactions between IGF-1 and neuroestrogen signaling in the hippocampus and the subsequent effects on memory. However, previous exposure to estradiol during midlife maintains the interactions between IGF-1 and neuroestrogen signaling long after termination of estradiol treatment, resulting in long-lasting enhancements in memory and hippocampal function. Together, these experiments demonstrate a complex mechanism through which IGF-1, neuroestrogens, and ERα interact to maintain hippocampal dependent memory in the absence of circulating estrogens. / 1 / Nina E Baumgartner

Zugl.: Marburg, Universiẗat, Diss., 2004.

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.

Proefschrift Universiteit van Amsterdam. / Met bibliogr., lit. opg. - Met samenvatting in het Nederlands.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1966. / Typescript. Vita. Description based on print version record. Includes bibliographical references.