Publications by authors named "Douglas J Brusich"

Mutation of the gene or pharmacological agents targeting it are commonly used to assess homeostatic synaptic function at the larval neuromuscular junction (NMJ). The commonly used mutation, , is a null allele created by a large and imprecise excision of a P-element which affects and multiple upstream genes. Here we mapped the exact bounds of the allele, refined a multiplex PCR strategy for positive identification of in homozygous or heterozygous backgrounds, and sequenced and characterized three new CRISPR-generated mutants.

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Repetitive mild TBI (rmTBI) events are common in the U.S. However, rmTBI is challenging to study and this contributes to a poor understanding of mechanistic bases for disease following these injuries.

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Several million traumatic brain injury (TBI) events are reported in the United States annually. However, mild TBI events often go unreported, and mild and repetitive mild TBI conditions are challenging to model. Fruit flies () have gained traction for the study of TBI.

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Gain-of-function mutations in the human CaV2.1 gene CACNA1A cause familial hemiplegic migraine type 1 (FHM1). To characterize cellular problems potentially triggered by CaV2.

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Forms of homeostatic plasticity stabilize neuronal outputs and promote physiologically favorable synapse function. A well-studied homeostatic system operates at the Drosophila melanogaster larval neuromuscular junction (NMJ). At the NMJ, impairment of postsynaptic glutamate receptor activity is offset by a compensatory increase in presynaptic neurotransmitter release.

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Homeostatic synaptic plasticity (HSP) helps neurons and synapses maintain physiologically appropriate levels of output. The fruit fly Drosophila melanogaster larval neuromuscular junction (NMJ) is a valuable model for studying HSP. Here we introduce a genetic tool that allows fruit fly researchers to examine the lifelong maintenance of HSP with a single cross.

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