NDLI: Modulation of the cardiac pacemaker of Drosophila: cellular mechanisms

Content Provider	Springer Nature Link
Author	Johnson, E. Sherry, T. Ringo, J. Dowse, H.
Copyright Year	2002
Abstract	The myogenic cardiac pacemaker of Drosophila melanogaster responds to a range of neurotransmitters and hormones by adjusting heart rate. These cardioactive substances ultimately affect the activity of ion channels comprising the pacemaker. We report here work utilizing genetic variants and pharmacological tools to explore a subset of possible mechanisms for this cellular signaling, specifically: receptors, cAMP, cGMP, G proteins, and calcium. We found that α1 adrenergic and 5-hydroxytryptamine2 (5-HT2) receptors are critical components of mediating modulation of heart rate. There was no evidence that the cAMP system is part of the modulatory mechanism. cGMP is likely to be integral to one active pathway, as non-hydrolyzable forms of this cyclic nucleotide increase heart rate, and flies bearing the mutation sitter, a recessive allele of the foraging gene, which encodes a cGMP-dependent kinase, have tachycardia. Heart rhythm is affected by pertussis toxin and by agonists and antagonists of both α1 adrenergic and 5-HT2 receptors; this suggests involvement of two different types of G proteins. The l(4)16/ciD line, containing a mutation in CaM kinase II, eliminates pacemaker responsiveness to serotonin but is without effect on norepinephrine sensitivity. This result is the same as that for the CaM kinase II enzyme inhibitor KN-93. This work establishes a framework for further investigations into the control of the cardiac pacemaker, and expands the applicability of the Drosophila heart model.
Starting Page	227
Ending Page	236
Page Count	10
File Format	PDF
ISSN	01741578
Journal	Journal of Comparative Physiology B
Volume Number	172
Issue Number	3
e-ISSN	1432136X
Language	English
Publisher	Springer-Verlag
Publisher Date	2002-01-24
Publisher Place	Berlin, Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Content Type	Text
Resource Type	Article
Subject	Physiology Biochemistry Animal Science and Zoology Ecology, Evolution, Behavior and Systematics Endocrinology

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