Members of the Dlg/PSD-95 protein family have a modular organization with multiple protein interaction domains and are thought to be important in the organization of synapses. A degenerate primer PCR strategy was used to screen for members of this family in the central nervous system of Apteronotus leptorhynchus, which possesses an electrosensory system that is well-suited for the study of synaptic organization and the subcellular localization of proteins. A. leptorhynchus was found to express at least four Dlg/PSD-95 family genes as in mammals, and the full coding sequences of the homologues of mammalian PSD-95 and SAP102 were determined. In situ hybridization experiments performed for the A. leptorhynchus Dig/PSD-95 family members in brain showed that they have a differential pattern of expression.

Transmission at an identified chemical synapse between two giant molluscan neurones, in the snail Achatina fulica, was sampled continuously from late embryogenesis to adulthood. The laboratory culture and reproductive life-cycle of the snail are described. The propagation of spontaneous excitatory postsynaptic potentials (Epsps) into the postsynaptic soma was documented throughout development. Short-term facilitation (Epsp(,2)/Epsp(,1)) was present at the identified synapse at all ages studied. Over a series of 100 trials, embryonic synapse showed a net synaptic depression; while, postembryonically, there was a progressive increase in frequency-facilitation with increasing age. A quantal analysis of transmission indicates that the amplitude of the quantal unit declines in parallel with the decrease in the postsynaptic input resistance. There is a progressive (20-fold) increase in quantal content from embryos to adults. The developmental increase in transmission at the synapse is primarily presynaptic in origin. Structural correlates for the electrophysiological findings were discussed.

Diss. (sammanfattning) Uppsala : Univ., 2004. / Härtill 4 uppsatser.

Thesis (M.Phil.)--Hong Kong University of Science and Technology, 2008. / Includes bibliographical references (leaves 118-147). Also available in electronic version.

Thesis (Ph. D.)--Carleton University, 2004. / Includes bibliographical references (p. 118-146). Also available in electronic format on the Internet.

Thesis (Ph.D.)--University of California, San Francisco, 2004. / Bibliography: leaves 157-175. Also available online.

Thesis (Ph. D.)--University of Chicago, Committee on Immunology, June 2003. / Includes bibliographical references. Also available on the Internet.

Thesis (Ph.D.)--Hong Kong University of Science and Technology, 2005. / Includes bibliographical references (leaves 136-146). Also available in electronic version.

Thesis (Ph. D.)--University of Texas at Austin, 2004. / Supervisor: Wesley J. Thompson. Vita. Includes bibliographical references.

The molecular mechanisms of synaptic function and development have been studied extensively, but little is known about the energy requirements of synapses, or the mechanisms that coordinate their energy production with their metabolic demands. These are oversights, as synapses with high energy demands are more susceptible to degeneration and degrade in the early stages of diseases such as amyotrophic lateral sclerosis, spinal muscle atrophy and Parkinson’s disease. Here, in a structure-function study at Drosophila motor neuron terminals, a neurophysiological model was generated to investigate how power (ATP/s) supply is integrated to satisfy the power demand of presynaptic terminals. Power demands were estimated from six nerve terminals through direct measurements of neurotransmitter release and Ca2+ entry, as well as theoretical estimation of Na+ entry and power demands at rest (cost of housekeeping). The data was leveraged with a computational model that simulated the power demands of the terminals during their physiological activity, revealing high volatility in which power demands can increase 15-fold within milliseconds as neurons transition from rest to activity. Another computational model was generated that simulated ATP production scenarios regarding feedback to the power supply machinery (Oxphos and glycolysis) through changes in nucleotide concentrations, showing that feedback from nucleotides alone fail to stimulate power supply to match the power demands of each terminal. Failure of feedback models invokes the need for feed forward mechanisms (such as Ca2+) to stimulate power supply machinery to match power demands. We also quantified mitochondrial volume, density, number and size in each nerve terminal, revealing all four features positively correlate with the terminals power demands. This suggests the terminals enhance their oxidative capacity by increasing mitochondrial content to satisfy their power demands. And lastly, we demonstrate that abolishing an ATP buffering system (the phosphagen system) does not impair neurotransmission in the nerve terminals, suggesting motor nerve terminals are capable of satisfying their power demands without the ATP buffering system. / Includes bibliography. / Dissertation (Ph.D.)--Florida Atlantic University, 2019. / FAU Electronic Theses and Dissertations Collection