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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

The role of targets and growth factors in neuronal ageing

Andrews, Timothy John January 1993 (has links)
No description available.
2

Characterization of the Functional Domains of a Novel Vertebrate-Specific Presynaptic Protein-Mover

Akula, Asha Kiran 28 July 2015 (has links)
No description available.
3

Optimizing Genetically Encoded Calcium Indicators to Measure Presynaptic Calcium Transients

Gilyan, Andrew 27 September 2012 (has links)
Neurotransmitter release is modulated by multiple regulatory mechanisms that control several stages of synaptic vesicle (SV) exocytosis. At the final stage, SV fusion with the presynaptic membrane requires calcium influx through voltage-gated calcium channels, and regulatory mechanisms that alter the surface expression or conductance of calcium channels have large effects on neurotransmitter release. To determine how these mechanisms contribute to synapse-specific modulations of neurotransmitter release and synaptic strength, we require a means to monitor presynaptic calcium transients at individual synapses. Genetically encoded calcium indicators (GECIs), engineered proteins that change their fluorescence emission properties upon calcium binding, generally lack the sensitivity to measure such transients in response to isolated stimuli. Therefore, we modified the GECI, GCaMP3, by altering its sensitivity for calcium. Our results suggest the modified GCaMP-based presynaptically targeted GECIs are excellent tools to quantify presynaptic calcium transients at individual synapses in response to isolated action potentials.
4

Is zinc a new class of neurotransmitter? a presynaptic model /

Ketterman, Joshua K. January 2006 (has links)
Thesis (M.S.)--Ohio University, August, 2006. / Title from PDF t.p. Includes bibliographical references.
5

Signal transduction mechanism in xenopus presynaptic differentiation /

Hung, Hiu Wai. January 2003 (has links)
Thesis (M. Phil.)--Hong Kong University of Science and Technology, 2003. / Includes bibliographical references. Also available in electronic version. Access restricted to campus users.
6

Rhythmic arm cycling differentially modulates stretch and H-reflex amplitudes in soleus muscle

Palomino, Andres Felipe 08 July 2011 (has links)
During rhythmic arm cycling soleus H-reflex amplitudes are reduced by modulation of group Ia presynaptic inhibition (Frigon et al, 2004). This reflex suppression is graded with the frequency of arm cycling (Loadman & Zehr 2007; Hundza & Zehr 2009) and 0.8 Hz is the minimum frequency to significantly reduce the soleus H-reflex (Hundza & Zehr 2009). Despite the data on modulation of the soleus H-reflex amplitude induced by rhythmic arm cycling, comparatively little is known about the modulation of stretch reflexes due to remote limb movement. Therefore, the present study was intended to explore the effect of arm cycling on stretch and H-reflex amplitudes in the soleus muscle. In so doing, additional information on the mechanism of action during rhythmic arm cycling would be revealed. Although both reflexes share the same afferent pathway, we hypothesized that stretch reflex amplitudes would be less suppressed by arm cycling because they are less inhibited by presynaptic inhibition (Morita et al, 1998). Failure to reject this hypothesis would add additional strength to the argument that Ia presynaptic inhibition is the mechanism modulating soleus H-reflex amplitude during rhythmic arm cycling. Participants were seated in a customized chair with feet strapped to footplates. Three motor tasks were performed: static control trials and arm cycling at 1 and 2 Hz. Soleus H-reflexes were evoked using single 1 ms pulses of electrical stimulation delivered to the tibial nerve at the popliteal fossa. A constant M-wave and ~6% MVC activation of soleus was maintained across conditions. Stretch reflexes were evoked using a vibratory shaker (ET-126; Labworks Inc). The shaker was placed over the triceps surae tendon and controlled by a custom written LabView program (single sinusoidal pulse at 100Hz). Results demonstrated that rhythmic arm cycling that was effective for conditioning soleus H-reflexes did not show a suppressive effect on the amplitude of the soleus stretch reflex. We suggest this indicates that stretch reflexes are less sensitive to conditioning by rhythmic arm movement, as compared to H-reflexes, due to the relative insensitivity of Ia presynaptic inhibition. / Graduate
7

Presynaptic differentiation at the neuromuscular junction : regulation by a novel bFGF-p120 catenin signaling pathway /

Chen, Cheng. January 2007 (has links)
Thesis (Ph.D.)--Hong Kong University of Science and Technology, 2007. / Includes bibliographical references (leaves 115-123). Also available in electronic version.
8

Development of the presynaptic nerve terminal during neuromuscular synaptogenesis /

Lee, Chi Wai. January 2005 (has links)
Thesis (Ph.D.)--Hong Kong University of Science and Technology, 2005. / Includes bibliographical references (leaves 136-146). Also available in electronic version.
9

A Framework for Understanding Power Supply and Demand in Presynaptic Nerve Terminals

Unknown Date (has links)
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
10

Effects of m-CPP in Altering Neuronal Function: Blocking Depolarization in Invertebrate Motor and Sensory Neurons but Exciting Rat Dorsal Horn Neurons

Sparks, Garrett M., Brailoiu, Eugen, Brailoiu, G. Cristina, Dun, Nae J., Tabor, Jami, Cooper, Robin L. 18 April 2003 (has links)
The compound m-chlorophenylpiperazine (m-CPP) is used clinically to manipulate serotonergic function, though its precise mechanisms of actions are not well understood. m-CPP alters synaptic transmission and neuronal function in vertebrates by non-selective agonistic actions on 5-HT1 and 5-HT2 receptors. In this study, we demonstrated that m-CPP did not appear to act through a 5-HT receptor in depressing neuronal function in the invertebrates (crayfish and Drosophila). Instead, m-CPP likely decreased sodium influx through voltage-gated sodium channels present in motor and primary sensory neurons. Intracellular axonal recordings showed that m-CPP reduced the amplitude of the action potentials in crayfish motor neurons. Quantal analysis of excitatory postsynaptic currents, recorded at neuromuscular junctions (NMJ) of crayfish and Drosophila, indicated a reduction in the number of presynaptic vesicular events, which produced a decrease in mean quantal content. m-CPP also decreased activity in primary sensory neurons in the crayfish. In contrast, serotonin produces an increase in synaptic strength at the crayfish NMJ and an increase in activity of sensory neurons; it produces no effect at the Drosophila NMJ. In the rat spinal cord, m-CPP enhances the occurrence of spontaneous excitatory postsynaptic potentials with no alteration in evoked currents.

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