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Full-Text Articles in Developmental Biology
The Characterization Of Pb2+ Toxicity In Rat Neural Development: An Assessment Of Pb2+ Effects On The Gaba Shift In Neural Networks And Implications For Learning And Memory Disruption, Lorenz Simon Neuwirth
The Characterization Of Pb2+ Toxicity In Rat Neural Development: An Assessment Of Pb2+ Effects On The Gaba Shift In Neural Networks And Implications For Learning And Memory Disruption, Lorenz Simon Neuwirth
Dissertations, Theses, and Capstone Projects
The toxic effects of Pb2+ on the developing rat nervous system has been investigated to assess early developmental GABAergic disruption and its implications with altering inhibitory learning and memory. This goal was achieved using a multi-systems approach: blood lead levels (clinical physiology), qRT-PCR (molecular genetics), brain and primary neuronal culture immunology (immunohistochemical and cellular approaches), physiological cellular components (synaptosomes and protein expression) and finally through learning and memory assessment with GABA mimetic drug manipulations in the intact animal (behavioral pharmacology). The influence of a 956ppm Pb2+ gestational diet (i.e. from birth to sacrifice) resulted in pup mean blood lead levels …
The Postsynaptic Regulation Of Synaptic Strength In Drosophila, Daniel Michael Gertner
The Postsynaptic Regulation Of Synaptic Strength In Drosophila, Daniel Michael Gertner
Legacy Theses & Dissertations (2009 - 2024)
Postsynaptic Ca2+ plays an important role in synaptic homeostasis and synaptic plasticity. Postsynaptic Ca2+ signals have been shown to regulate synaptic transmission at the Drosophila larval neuromuscular junction (NMJ), however, these signals have not been well characterized. This will explore how these signals regulate synaptic strength and what channels are involved. In previous lab experiments Ca2+ transients were observed during evoked and spontaneous release (Desai and Lnenicka, 2011). It was further demonstrated that a reduction in synaptic strength occurs following synaptic stimulation. It was hypothesized that the increase in postsynaptic Ca2+ following synaptic stimulation activates the gCS and causes a …