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Poster Full Abstracts - Neurophysiology and Behavior
Poster board number is above title. The first author is the presenter
300
631A
Dopamine neurons signal reward for odour memory in Drosophila.
Chang Liu
1,2
, Anja Friedrich
1
, Igor Siwanovicz
1
, Hiromu Tanimoto
1
. 1) Max-Plank
Institute of Neurobiology, Martinsried, Germany; 2) Kunming Institute of Zoology, Chinese Academy of Science, Kunming, China.
Animals tend to approach stimuli that predict pleasant outcome. Following the paired presentation of an odour and a reward, Drosophila melanogaster can
develop a conditioned approach towards that odour. Despite recent advances in understanding the neural circuits for associative memory and appetitive
motivation, the cellular mechanisms for reward processing in the fly brain are unknown. Dopamine (DA) plays important roles in variety of behaviors in
both vertebrates and invertebrates. However, unlike in mammals, DA is widely accepted as the critical neurotransmitter for signaling the punishment in
aversive associative learning in insects. Recent studies suggested that DA may also contribute to appetitive learning in adult flies and larvae. In this study,
we tried to evaluate the role of DA neurons in appetitive learning and memory in Drosophila. By transient activation and inactivation of DA neurons in
behavioral fly, we found that a specific group of DA neurons are required for the formation of appetitive memory. Activation of these neurons could induce
appetitive memory. These neurons convey reward information to the medial lobes of the mushroom bodies. Our results demonstrate that a specific group of
DA neurons are responsible for appetitive learning and memory in Drosophila.
632B
Effect of LIMK1 isoform ratio on Drosophila melanogaster courtship behavior.
Ekatherina Nikitina, Alena Kaminskaya, Dmitry Molotkov, Gennady
Zakharov, Tatyana Payalina, Elena Savvateeva-Popova. Dept Neurogenetics, Pavlov Inst Physiology, St Petersburg, Russian Federation.
Motile processes at the origin of cell migration, cell division, morphogenesis, synaptic plasticity and endocytosis are governed by spatially and temporally
controlled assembly of actin filaments. Increased attention of neurobiologists to the signal cascade of actin remodeling, integration of different
neurodegenerative disorders under the name «cophilinopathies» pointed to wide spectrum of inner adaptive processes related to this cascade. The signal
cascade of actin remodeling: receptors of neurotransmitters - small Rho GTPases (RhoA, Cdc42 and Rac1) - LIM kinase 1 (LIMK1) - cofilin - actin - is
believed to play the main role in dendrite- and synaptogenesis. LIMK1 - is the key enzyme of actin remodeling which controls dendritic spine morphology
necessary for synaptic plasticity during learning and memory formation. Conditioned courtship suppression paradigm was used to asses learning acquisition
and memory formation in four Drosophila strains polymorphic for the limk1 gene harbored by the agnostic locus: the wild type strains Canton-S, Berlin,
Oregon-R and the mutant agnts3. Wild type strains Canton-S and Berlin are characterized by normal learning acquisition and 3-h (intermediate) memory
formation. Oregon-R proved to be disabled in learning; we observed a failure of 3-h memory formation in this strain too. Also agnts3 mutants showed 3-h
(intermediate) memory and learning ability that were three-fold lower than those in Canton S flies. Behavioral performances were compared to the ratio of
two LIMK1 isoforms in these Drosophila strains. Quantity of D- and C-isoforms of LIMK1 in agnts3 multiplied thrice as compared to the same level in
Canton-S, but their ration was identical. Quantity of D-isoform in Berlin doubled the same in Canton-S, but in Oregon-R decreased twice as compared to
Canton-S. Apparently, observed disturbances of learning acquisition and memory formation in flies may be linked to the alteration in ratio of LIMK1 D/C
isoforms.
633C
Tip60 HAT activity regulates synaptic plasticity: Implications for epigenetics in learning and memory.
Jessica Sarthi, Felice Elefant. Biology, Drexel
Univ, Philadelphia, PA.
Age-associated cognitive decline and neurodegenerative disorders such as Alzheimer’s disease (AD) are associated with misregulation of synaptic
plasticity linked genes; however the mechanisms underlying decline of such gene control during aging are unknown. Histone acetylation of chromatin
promotes dynamic transcriptional responses in neurons that influence neuroplasticity critical for cognitive ability. Accordingly, aberrant changes to histone
acetylation patterns in the aging brain epigenome are linked to memory loss. It is therefore critical to identify and study the histone acetyltransferases (HAT)
that create such marks. One promising candidate is Tip60, a HAT implicated in AD and shown by our laboratory to be critical in regulating neuronal
processes linked to cognition (Genetics, 2007; PLoS ONE, 2010; PLoS ONE, 2011).To explore a direct role for Tip60 in synaptic plasticity, here we explore
the consequences of misregulating Tip60 HAT activity in the Drosophila neuromuscular junction (NMJ). We show that the HAT dTip60 is concentrated
both pre and post-synaptically within the NMJ. Presynaptic targeted reduction of dTip60 HAT activity significantly increases synaptic bouton number that
specifically affects type Is boutons while postsynaptic reduction results in significant loss of these boutons. The excess boutons show a suppression of the
active zone synaptic function marker bruchpilot, suggesting defects in neurotransmission function. Analysis using immunohistochemical staining to the
MAP, futsch reveals a significant increase in the rearrangement of microtubule loop architecture that is required for bouton division. Moreover, α-tubulin
acetylation levels of microtubules are also reduced in response to dTip60 HAT reduction. Our results are the first to demonstrate a causative role for the
HAT dTip60 in the control of synaptic plasticity that is achieved, at least in part, via regulation of the synaptic microtubule cytoskeleton. These findings
have implications for dTip60 HAT dependant epigenetic mechanisms underlying cognitive function. NIH grant HD045292-01 to F.E.
634A
An epigenetic role for dTip60 in locomotion and axonal vesicle transport.
Ashley Zervos, William Reube, Felice Elefant. Dept Biol, Drexel Univ,
Philadelphia, PA.
Histone acetyltransferases (HATs) are a key class of enzymes that control chromatin accessibility to regulate gene expression profiles critical for diverse
cellular processes. Tip60 is one such HAT that has been shown by our laboratory to play a critical role in regulating neuronal genes linked to
neurodevelopment and cognition (Genetics, 2007; PLoS ONE, 2010; PLoS ONE, 2011). Consistent with our findings, Tip60 has been implicated in the age-
related neurodegenerative disorder Alzheimer’s disease (AD) via its interaction with the AD linked amyloid precursor protein intracellular domain (AICD).
This complex is essential for the epigenetic regulation of certain genes critical for neuronal function. Inappropriate complex formation may contribute to pre-
clinical AD-related pathology by misregulation of target genes involved in neurogenesis; however a direct epigenetic based role for Tip60 in this process
remains unclear. Here, we investigate a causative role for Tip60 in axonal vesicle transport, a process affected in the pre-clinical stages of AD. We show that
reduction of Tip60 HAT activity specifically in the nervous system of the fly leads to locomotor defects and a distinctive tail flipping phenotype. These
phenotypes are reminiscent of nervous system defects linked to mutations in genes required for axonal vesicle transport machinery. Confocal imaging of