My research focuses on understanding the genetic basis of swimming by studying a set of zebrafish mutants recently isolated in the lab. Zebrafish exhibit many similarities to humans in the genes and circuits that underlie movement. Therefore, zebrafish motility mutants provide useful models for human genetic disaeses that impact nerve and muscle function.The lab also studies mutants for which the culprit gene has been identified, to better understand homeostatic mechanisms triggered in response to mutation. The zebrafish motility mutant shocked has a point mutation in the glial glycine transporter (GlyT1). Consequently, the inhibitory neurotransmitter glycine builds up in the nervous system and the mutant larvae fail to escape when touched. However,as the larvae mature, they naturally recover the ability to mount a normal escape response. We have found that mutant recovery is associated with a dramatic decrease in the post-synaptic glycine receptors. We hope to further study this mutant with the aim of understanding the mechanisms causal to glycine receptor down-regulation. This study is medically relevant because glycine transporter antagonists are currently being tested as atypical anti-psychotics and similar forms of homeostasis are likely to occur in humans with chronic use of GlyT1 inhibitors
