The CaM kinase, CMK-1, mediates a negative feedback mechanism coupling the C. elegans AMPA receptor, GLR-1, with its own transcription.

Moss, Benjamin.

Abstract: Chronic changes in synaptic activity result in compensatory alterations in AMPA-type glutamate receptors (AMPARs), but the mechanisms underlying this process have not been fully elucidated. In this thesis, I investigate a feedback mechanism that bidirectionally regulates transcription of the C. elegans AMPAR GLR-1 in response to chronic changes in synaptic activity. It was previously sho... read more

Sackler School of Graduate Biomedical Sciences. Department of Neuroscience.
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ID: tufts:20469
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