Physiology and Biochemistry of [i]Drosophila[r] Learning Mutants.
Davis, Ronald L..
Dept. of Cell Biology & Neurology, Bayor College of Medicine, Houston, TX
77030
APStracts 2:0025P, 1996.
ABSTRACT
Single gene mutants of [i]Drosophila[r] that are defective in learning/memory
processes have increased substantially our understanding of the physiology,
biochemistry, and anatomy underlying conditioned behaviors. [i]Drosophila[r]
learning mutants can be separated into two general classes, those with
structural defects in the brain and those without (conditioning mutants) any
obvious brain alterations. From studies of brain structural mutants, two
neuroanatomic areas have merged as important for normal conditioned behavior:
the mushroom bodies and the central complex. Biochemical and molecular genetic
studies of the conditioning mutants have implicated numerous types of
molecules in learning, but the adenosine 3[prime],5[prime]-cyclic
monophosphate (cAMP) second messenger pathway has emerged as especially
important. Five different genes in this pathway, amnesiac (a product similar
to adenylate cyclase activating peptides, dunce (cAMP phosphodiesterase),
rutabaga (adenylyl cyclase), DCO (protein kinase A), and dCREB2 (cAMP response
element binding protein), have proven important for normal learning. The
products of many of these learning mutants are enriched in mushroom bodies,
which highlights the importance of mushroom bodies for normal learning and the
cAMP second messenger cascade for the physiology of mushroom body cells in
their role(s) underlying learning. Physiological studies of the mutants have
demonstrated that plastic properties of synaptic transmission, including
facilitation and posttetanic potentiaion, are abnormal in the mutants. An
appendix describing the currently used paradigms to test [i]Drosophila[r]
behavior is included.
APS Manuscript Number P2-5.
Article publication pending April 1996, Physiological Reviews.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 5 November 1996