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Resources » Paper

Vera Hapiak et al. (2006) Neuronal Development, Synaptic Function, and Behavior Meeting "Tyramine abolishes 5-HT dependent increases in octanol sensitivity in Caenorhabditis elegans"

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  • Comments on Vera Hapiak et al. (2006) Neuronal Development, Synaptic Function, and Behavior Meeting "Tyramine abolishes 5-HT dependent increases in octanol sensitivity in Caenorhabditis elegans" (0)

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    Status:
    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00028229

    Vera Hapiak, Gareth Harris, Rachel Wragg, Robert Hobson, & Richard Komuniecki (2006). Tyramine abolishes 5-HT dependent increases in octanol sensitivity in Caenorhabditis elegans presented in Neuronal Development, Synaptic Function, and Behavior Meeting. Unpublished information; cite only with author permission.

    Tyramine (TA) regulates a number of key processes in nematodes, including pharyngeal pumping, egg-laying, and locomotion. Previously, we have identified two C. elegans TA receptors, SER-2 and TYRA-2. In the present study, we have identified a third C. elegans gene, mo3f4.3, that also appears to encode for a TA receptor. mo3f4.3 is conserved in the parasitic nematode, Brugia malayi and is expressed as multiple isoforms with different N-termini. Membranes from COS-7 cells expressing M03F4.3a bind [3H]-LSD in the low nM range (Kd, 30 +/- 4 nM) with higher affinity for TA than other classical biogenic amines. For example, IC50s for TA, octopamine, dopamine and 5-HT are 0.5 +/- 0.07, 59.5 +/- 16.5, 83 +/- 23, and 540 +/- 127 uM, respectively. M03F4.3 does not appear to play any obvious role in TA-dependent hyperactivity or decreases in 5-HT stimulated egg-laying or pharyngeal pumping, based on an analysis of these phenotypes in putative mo3f4.3 null mutants. Interestingly, TA abolished 5-HT increases in sensitivity to 30% octanol and this TA-dependent inhibition was absent in animals containing null mutations in mo3f4.3, but not ser-2 or tyra-2. These studies are continuing to examine the G-protein coupling and downstream signaling of MO3F4.3 and the neuron-specific rescue of the TA dependent phenotypes observed in mo3f4.3 null mutants.


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