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Poster Full Abstracts - Neurophysiology and Behavior
Poster board number is above title. The first author is the presenter
301
third-instar larval motor axons reveals abnormal vesicle aggregation and clogging in response to Tip60 HAT reduction. These defects are exacerbated by
APP overexpression and dependent upon AICD, the region of APP that interacts with Tip60. Importantly, treatment of larvae with ms-275, a nervous system
specific class 1 HDAC inhibitor, rescues both vesicle clogging in motor axons as well as locomotion defects. In addition to providing new biological insight
into epigenetic gene control mechanisms underlying neurodegeneration in AD, these studies will be fundamental in exploring the utility of novel epigenetic-
based therapeutics to improve healthcare and quality of life in the elderly. NIH grant HD045292-01 to F.E.
635B
ROS-mediated detection of epidermal mechanical stress by larval peripheral nociceptors.
Wayne A. Johnson, Justin Carder. Dept Molec
Physiol/Biophysics, Univ of Iowa Carver College of Medicine, Iowa City, IA.
Wandering stage larvae are particularly susceptible to dessication displaying a strong aversion to locomotion on dry surfaces to prevent movement into
areas of potentially lethal low humidity. This aversion is manifested by the humidity-dependent height of pupation within a culture vial. This high friction
aversion is mediated by the class IV multiple dendritic(mdIV) nociceptor neurons expressing the DEG/ENaC subunit, Pickpocket1(PPK1), within complex
dendritic arbors tiling the larval body wall. Direct electrophysiological recordings showed that the mdIV neurons are activated by nanomolar levels of the
reactive oxygen species(ROS), H
2
O
2
. Both the aversion behavior and ROS-mediated mdIV nociceptor activation are dependent upon the PPK1 protein. We
have further investigated the source and role of an endogenous ROS signal by genetic and transgenic manipulation of various components of the cellular
redox machinery resulting in modifications of larval aversion behavior. Transgenic overexpression of catalase in epidermal cells to increase breakdown of
endogenous H
2
O
2
duplicated phenotypes associated with mdIV nociceptor inactivation or
ppk1
loss-of-function. Knockdown of endogenous epidermal
catalase using transgenic RNAi, to increase ROS levels, caused a reciprocal mdIV nociceptor hypersensitization. Similar opposite phenotypes were observed
due to either overexpression or RNAi-based knockdown of superoxide dismutase(SOD) which catalyzes the conversion of superoxide to H
2
O
2
. A potential
source of endogenous H
2
O
2
may be the Duox(NADPH oxidase dual peroxidase) protein capable of producing H
2
O
2
in response to a variety of chemical
and/or mechanical stimuli. Transgenic RNAi-based knockdown of Duox in larval epidermis caused striking effects upon mdIV nociceptor and PPK1-
dependent larval behaviors. These results support a model describing ROS-mediated signaling from the larval epidermis undergoing high friction mechanical
stress to activate the mdIV nociceptors and mediate a larval aversion behavior to move away from potentially lethal low humidity environments.
636C
The temporal pattern of neural activity underlying ecdysis behavior is regulated by neuropeptides downstream of Ecdysis Triggering Hormone.
John Ewer, Wilson Mena. Centro Interdisciplinario de Neurociencias, Universidad de Valparaiso, Valparaiso, CHILE.
The insect molt culminates with ecdysis, an innate behavior that is used to shed the remains of the old cuticle. Ecdysis includes several behavioral
subroutines that are expressed sequentially to loosen and then shed the old cuticle, then expand and harden the new one. Ecdysis is triggered by the
neuropeptide, Ecdysis-Triggering Hormone (ETH), which activates sequentially a number of peptidergic neurons, all of which express the A isoform of the
ETH receptor (ETHR). Current models propose that each class of peptidergic neurons then activates or modulates the different phases of the ecdysis motor
programs. We examined ecdysis behavior and used the calcium sensitive GFP, GCaMP, to monitor the activation of ETH targets in wild-type animals as
well as in animals in which ETHR was disabled using RNAi or were mutant for specific neuropeptides. All these manipulations affected ecdysis behavior.
However, whereas decreasing ETHR expression using RNAi caused a quantitative reduction in the neural response to ETH, eliminating neuropeptides
downstream of ETH caused qualitative changes to the pattern of neural activity induced by this triggering hormone. Thus, unlike the model in which
neuropeptides downstream of ETH are the outputs that are sequentially activated to then turn on specific ecdysial subroutines, our results suggest that these
neuropeptides configure the network’s response to ETH, which then controls the ensuing behaviors. In addition to contributing to the further understanding
of how this critical insect behavior is regulated, our results provide insights for understanding how multiple peptides regulate complex physiological and
behavioral responses.
637A
Differential Recruitment of Dopamine Neurons into the Stress Response Circuitry.
Kathryn J. Argue, Wendi S. Neckameyer. Pharmacological and
Physiological Sciences, Saint Louis University School of Medicine, St. Louis, MO.
Sex, sexual maturity, and reproductive status have been shown to affect whether a mutant Drosophila strain with specific anatomical defects limited to
critical brain regions modifies its response to stress relative to wild-type flies (Neckameyer and Matsuo, 2008). Our results suggest that for each population
(sexually immature and mature males and females), unique subsets of neurons are recruited into the stress response circuitry and differentially affect
behavior. By knocking down dopamine (DA) synthesis in subsets of DA neurons and assaying for behavioral changes in response to starvation and oxidative
stress in these lines, we will be able to identify DA neurons that are important for a given behavioral response to stress within a given population. This work
has been funded by NIMH 1RO1MN083771 and NSF 0616062.
638B
Dissection of the Dopaminergic Circuitry Regulating Sleep/Wake in
Drosophila
.
Qili Liu
1
, Sha Liu
1
, Lay Kodama
1
, Maria Driscoll
1
, Shahnaz Lone
1
,
Mark Wu
1,2
. 1) Department of Neurology, Johns Hopkins University, Baltimore, MD; 2) Department of Neuroscience, Johns Hopkins University, Baltimore,
MD.
Dopamine (DA) has been shown to regulate a wide variety of behaviors, including arousal and locomotion, in animals ranging from worms to mammals.
There are around 200 dopaminergic neurons, divided into 13 subgroups in the adult
Drosophila
brain. To identify specific DA neurons involved in
sleep/wake regulation, we generated novel transgenic Gal4 lines labeling subsets of DA neurons. Analysis of the activation of these specific DA subsets
using
UAS-dTrpA
suggests that 1 subgroup in particular is important for promoting wakefulness, by reducing the arousal threshold. We are now carrying out
MARCM analysis using these drivers to identify the few DA cells that are most critical for arousal. We have also carried out loss-of-function experiments
with these restricted DA drivers, by using
UAS-Shi
TS
. These studies suggest that several DA neurons in the thoracic ganglion may promote locomotion
specifically. These findings are now being confirmed by the concomitant use of
Tsh-Gal80
, which blocks Gal4 function specifically in the thoracic ganglion.
On the postsynaptic side, there are 4 DA receptors in Drosophila. We find that the dramatic decrease of sleep seen when activating all DA cells using dTrpA