Publications by authors named "I M Morrow"
Article Synopsis
- The study investigates how the cricket species Gryllus pennsylvanicus can distinguish between two different compound visual motifs using an operant conditioning method.
- It employs a Y-maze setup where the crickets are exposed to colored visual cues linked to a water reward.
- Findings indicate that the crickets successfully learned to differentiate the visual patterns and associated them with the reward, demonstrating their ability to recognize visuo-spatial regularities.
By 2050, 1 in 4 people worldwide will be living with hearing impairment. We propose a digital Speech Hearing Screener (dSHS) using short nonsense word recognition to measure speech-hearing ability. The importance of hearing screening is increasing due to the anticipated increase in individuals with hearing impairment globally.
View Article and Find Full Text PDFOur understanding of endocytic pathway dynamics is severely restricted by the diffraction limit of light microscopy. To address this, we implemented a novel technique based on the subdiffractional tracking of internalized molecules (sdTIM). This allowed us to image anti-green fluorescent protein Atto647N-tagged nanobodies trapped in synaptic vesicles (SVs) from live hippocampal nerve terminals expressing vesicle-associated membrane protein 2 (VAMP2)-pHluorin with 36-nm localization precision.
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- Munc18-1 and syntaxin-1A are essential for the process of neuroexocytosis in neurons, and their organization in specific areas on the cell membrane is crucial for vesicle fusion.
- A mutant form of Munc18-1 that lacks certain residues leads to increased docking time of secretory vesicles, indicating the importance of its structure in facilitating vesicle fusion.
- Changes in the movement of Munc18-1 and syntaxin-1A in response to stimulation suggest that a specific region of Munc18-1 regulates the engagement of syntaxin-1A in forming SNARE complexes, which are necessary for the release of neurotransmitters.
Munc18-1 is a key component of the exocytic machinery that controls neurotransmitter release. Munc18-1 heterozygous mutations cause developmental defects and epileptic phenotypes, including infantile epileptic encephalopathy (EIEE), suggestive of a gain of pathological function. Here, we used single-molecule analysis, gene-edited cells, and neurons to demonstrate that Munc18-1 EIEE-causing mutants form large polymers that coaggregate wild-type Munc18-1 in vitro and in cells.
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