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| This page was produced using the Society for Neuroscience Abstract Viewer and Itinerary Planner . The correct citation for abstracts presented at the 35th meeting of the Society for Neuroscience in Washington DC is:[Authors], [Title], Program No. xxx.xx. 2005 Abstract Viewer/Itinerary Planner. Washington, DC: Society for Neuroscience, 2005. Online. Permission to reprint abstracts after the 2005 SFN meeting was granted by the Society for Neuroscience. |
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ABSTRACTS OF POSTERS
PRESENTED BY 2005 FUN TRAVEL AWARDEES - WASHINGTON DC |
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| TOP OF PAGE | ITINERARY | ABSTRACTS | HOME | BACK TO TRAVEL AWARDS HOME | |
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The genetic background of ( Na+,K+ ) - ATPase, a-
2 knock-out mice affects the distribution of a-
2 and a-
3 isoforms of this enzyme in brain and the survival time of homozygous newborns
A.M.Baran 1; T.M.Spranger1; A.E.Moseley2; J.B.Lingrel2; M.L.Caspers1*
1. Chemistry and Biochemistry, Univ. of Detroit Mercy, Detroit, MI, USA; 2. Molecular Genetics, Biochemistry and Microbiology, Univ. of Cincinnati, Cincinnati, OH, USA
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The (Na+,K+)-ATPase maintains Na+ and K+ gradients in cells through the active transport of these ions across the plasma membrane. [3H]Ouabain, which binds with high affinity to the a-
2 and a-
3 isoforms of the (Na+,K+)-ATPase, was used to study the distribution of these isoforms in the brains of adult wild type and heterozygous a-
2 knockout mice of FVBN genetic background. Frozen, coronal brain sections (24 micron) were prepared and were assayed in a 100 mM Tris-HCl buffer containing 10 mM NaCl, 10 mM MgCl2, 5 mM ATP and 29 nM [3
H]ouabain. The sections were exposed to Kodak BioMax Scientific Imaging film and the images were subjected to computer-assisted densitometry. In a-
2 heterozygotes, significant decreases in the relative density of [3H]ouabain binding sites were observed in the cerebral cortex (5.1%) and hippocampus (4.4%) compared to wild-type mice. These findings are similar to results obtained with C57BL6 mice where small decreases in [3
H]ouabain binding sites were observed in the cerebral cortex, hippocampus and thalamus of heterozygous a-
2 knockout mice but are dissimilar to results using a-
2 heterozygous 129/Black Swiss (mixed) mice where larger decreases in [3
H]ouabain binding, relative to wild-type animals, were seen in all brain regions tested (Program #517.10, 2004 Abstract Viewer/Itinerary Planner, Washington, DC: Society for Neuroscience, CD-ROM). Strain differences also are seen in the survival time of homozygous a-
2 knockout mice; FVBN knockout mice live approximately 1 day whereas the mixed and C57BL6 knockout mice die at birth.
Support Contributed By: NIH grants HL28573 and HL66062 and a gift from J.D. Rose. Citation: A.M.Baran, T.M.Spranger, A.E.Moseley, J.B.Lingrel, M.L.Caspers. The genetic background of ( Na+,K+ ) - ATPase, a- 2 knock - out mice affects the distribution of a- 2 and a- 3 isoforms of this enzyme in brain and the survival time of homozygous newborns. Program No. 736.12. 2005 Abstract Viewer/Itinerary Planner. Washington, DC: Society for Neuroscience| TOP OF PAGE | ITINERARY | ABSTRACTS | HOME | BACK TO TRAVEL AWARDS HOME | |
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Spatial learning and memory in male and female rats is not affected by chronic oral Accutane ( ACC )
K.J.Berry 1; F.J.Cisneros1; B.Gough1; L.C.Schmued1*; J.P.Hanig2; S.A.Ferguson1 1. Neurotoxicology, NCTR/FDA, Jefferson, AR, USA; 2. CDER/FDA, Silver Spring, MD, USA |
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Use of the anti-acne drug, ACC (isotretinoin, 13-cis-retinoic acid), is associated with depression and/or suicide ideation in humans. Adult mice treated with ACC exhibited decreased cell proliferation in the hippocampus and subventricular zone (Crandall et al., 2004), areas of the brain associated with learning and memory processing. However, the full effects of ACC treatment on spatial learning and memory have not been adequately explored. Here, male and female Sprague-Dawley rats (n=15/sex/dose) were gavaged daily with 0 (soy oil), 7.5, or 30 mg/kg/day ACC beginning on postnatal day 59. 7.5 mg/kg/day ACC in rats has been shown to produce blood levels similar to therapeutic levels seen in humans. Morris water maze activity (three 2-minute trials/day) was evaluated over 5 consecutive days after 7 weeks of treatment. Complex maze activity (15-minute water-reinforced session) was evaluated for 5 consecutive days after 13 weeks of treatment. Latency to reach the platform, swim speed, proximity index, and path length in the Morris water maze were not affected by ACC treatment. Concomitantly, ACC treatment had no significant effects on complex maze performance; however, the typical sex difference effects in complex maze were exhibited (i.e., females were more active than males (p<.001) and earned more rewards (p<.001)). These data suggest that ACC treatment which produces blood levels in adult rats similar to those achieved in humans does not significantly affect learning and memory. Citation: K.J.Berry, F.J.Cisneros, B.Gough, L.C.Schmued, J.P.Hanig, S.A.Ferguson. Spatial learning and memory in male and female rats is not affected by chronic oral Accutane ( ACC ) Program No. 886.1. 2005 Abstract Viewer/Itinerary Planner. Washington, DC: Society for Neuroscience| TOP OF PAGE | ITINERARY | ABSTRACTS | HOME | BACK TO TRAVEL AWARDS HOME | |
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Reactive oxygen species accelerate and antioxidants delay loss of dopaminergic neurons and motor impairments in a Drosophila
model for Parkinson's disease.
S.P.Bothwell ; E.R.Reynolds* Department of Biology, Program in Neuroscience, Lafayette Col., Easton, PA, USA |
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Parkinson's disease is the second most common neurodegenerative disorder, characterized by a progressive loss of dopaminergic neurons in the substantia nigra, the formation of Lewy bodies, and motor impairments. While the cause of this disease is unknown, high levels of oxidative stress caused by reactive oxygen species (ROS) are thought to contribute to dopaminergic cell death. The current study used a Drosophila
model of Parkinson's disease to examine the effects of the ROS producing compounds paraquat and iron and the antioxidants melatonin and tocopherol on the degeneration of dopaminergic neurons and on motor deficits in a climbing assay. Flies expressing alpha-synuclein in a pan-neural distribution and chronically exposed to paraquat or iron exhibited motor deficits at an earlier age than transgenic controls, had more severe deficits in climbing ability over time, and had a more pronounced loss of dopaminergic neurons by 30 days of age. Motor impairment was delayed in transgenic flies chronically treated with melatonin or tocopherol, and these flies had more dopaminergic neurons remaining on days 30 and 40 than transgenic controls. The results support the proposed role of oxidative stress on dopaminergic cell loss and indicate that prolonged exposure to either paraquat or iron may induce symptoms at an earlier age and cause more pronounced deficits over time in those with a genetic form of Parkinson's disease. Chronic administration of melatonin or tocopherol may be therapeutic by alleviating symptoms for a period of time and by slowing down their progression.
Support Contributed By: Lafayette College Program in Neuroscience Citation: S.P.Bothwell, E.R.Reynolds. Reactive oxygen species accelerate and antioxidants delay loss of dopaminergic neurons and motor impairments in a Drosophila model for Parkinson's disease Program No. 425.14. 2005 Abstract Viewer/Itinerary Planner. Washington, DC: Society for Neuroscience |
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Modulation of reactive gliosis by siRNA
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B.G.Cordero *; M.C.Davidson; J.Schallhorn; G.A.Silva 1. Bioengineering, 2. Ophthalmology, Univ. of California, San Diego, San Diego, CA, USA |
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Reactive gliosis and glial scarring are ubiquitous neuropathological processes associated with all major forms of central nervous system (CNS) and neural retinal traumatic and degenerative disorders. Gliosis is caused by reactive glial cells, astrocytes in the CNS and astrocytes and Muller cells in the retina. Although there is no way to regulate or limit gliosis in vivo, in vitro studies suggest that it can be suppressed by down regulating the expression of the intermediate filament proteins glial fibrillary acidic protein (GFAP) and vimentin. We developed siRNA oligonucleotide probes against GFAP and vimentin and investigated their ability to limit the effects of gliosis by measuring the down regulation of GFAP expression in an rMC-1 Muller cell induced gliosis model developed in our lab. Three different siRNA oligonucleotides were designed targeting GFAP and vimentin at two different concentrations. siRNA's were delivered to reactive Muller cells by the use of a lipid passed transfection reagent into 24-well plates, and immunocytochemistry was performed at varying time points. The reactive state of the cells was determined by measuring an upregulation of GFAP and vimentin immunoreactivity. Reactive Muller cells treated with all our siRNA oligos showed a measurable knockdown in GFAP and vimentin by day five. All cells retained normal morphology and viability although their growth rate decreased compared to untreated control cells. This suggests that anti-GFAP and ani-vimentin siRNA mediated approaches may provide a clinically useful approach for limiting gliosis and glial scarring.
Support Contributed By: Sigma Xi Scientific Research Society Grants in Aid of Research, University of California San Diego Undergraduate Research Grants Citation: B.G.Cordero, M.C.Davidson, J.Schallhorn, G.A.Silva. Modulation of reactive gliosis by siRNA Program No. 836.3. 2005 Abstract Viewer/Itinerary Planner. Washington, DC: Society for Neuroscience| TOP OF PAGE | ITINERARY | ABSTRACTS | HOME | BACK TO TRAVEL AWARDS HOME | |
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Early postnatal exposure to polybrominated diphenyl ethers alters the cholinergic modulation of attention.
C.Dufault ; G.Poles; L.L.Driscoll* Psychology, Colorado Col., Colorado Springs, CO, USA |
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Polybrominated diphenyl ethers (PBDEs) are flame retardants commonly used in the United States. Although they are readily leached into the environment and rapidly bioaccumulate in humans and wildlife, little is known about their potential toxicological properties. In the current study, Male Long-Evans rats were orally administered the commercial PBDE mixture DE-71 for one week beginning at postnatal day (PND) 6. As adults, the PBDE-exposed rats and control littermates were tested on a visual discrimination task and two sustained attention tasks. Following completion of these tasks, the rats were administered a drug challenge with the muscarinic antagonist scopolamine (0, 0.01, 0.03, 0.05 mg/kg), which was injected subcutaneously 30 minutes prior to testing on the second sustained attention task. Prior to the drug challenge, the PBDE-exposed rats demonstrated deficits in learning but not in sustained attention. However, they showed subsensitivity to the effects of scopolamine on sustained attention. The lack of sustained attention deficits in the absence of the drug, coupled with the subsensitivity to scopolamine, suggest possible alterations of the cholinergic system in the PBDE-exposed animals that were overcome by the development of compensatory neural mechanisms or response strategies in adulthood.
Support Contributed By: Colorado College Research and Development Grant (LLD), Faculty-Student Collaborative Research Grant (GP and LLD), and Howard Hughes Undergraduate Research Fellowship (CD). Citation: C.Dufault, G.Poles, L.L.Driscoll. Early postnatal exposure to polybrominated diphenyl ethers alters the cholinergic modulation of attention Program No. 644.10. 2005 Abstract Viewer/Itinerary Planner. Washington, DC: Society for Neuroscience| TOP OF PAGE | ITINERARY | ABSTRACTS | HOME | BACK TO TRAVEL AWARDS HOME | |
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Nicotine does not improve spatial working memory in mice with hippocampal damage
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H.N.Foozer ; M.S.Griffith; M.E.Bardgett* Psychology, Northern Kentucky Univ., Highland Heights, KY, USA |
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People with schizophrenia, depression, and Alzheimer's disease have hippocampal abnormalities as well as memory loss. Our goal is to develop an animal model of hippocampal abnormalities that mimic those found in these psychiatric disorders. The present study was designed to determine if the memory impairment produced by hippocampal damage could be reversed or improved by nicotine, since it enhances performance in other models of memory loss. Eighteen adult male C57BL/J mice were used in this experiment and housed four per cage. N-methyl-D-aspartate (NMDA, 8 mg/ml) was used to produce hippocampal damage. Stereotaxic surgery was performed to infuse vehicle (sterile saline) or NMDA (0.08 ml volume per infusion) into four bilateral locations within the dorsal hippocampus. Two months later, behavior was assessed in a delayed spatial alternation task. Three different doses of nicotine (0.03, 0.06, & 0.12 mg/kg, IP) were compared with saline. When mice were injected with saline, the lesioned mice performed significantly worse than the unlesioned mice in the delayed spatial alternation task. However, nicotine did not improve performance in mice with or without hippocampal lesions. Two main conclusions can be drawn from this research. First, even though nicotine improves memory in other animal models, it does not improve memory in mice with hippocampal damage. This would suggest that cholinergic agonists, such as nicotine, require an intact hippocampus in order to improve memory. Second, it will be important to continue using this lesion model as a screen for drugs that can improve memory deficits associated with hippocampal dysfunction.
Support Contributed By: The KY-BRIN program funded through NIH-NCRR P20 RR-16481 Citation: H.N.Foozer, M.S.Griffith, M.E.Bardgett. Nicotine does not improve spatial working memory in mice with hippocampal damage Program No. 885.2. 2005 Abstract Viewer/Itinerary Planner. Washington, DC: Society for Neuroscience| TOP OF PAGE | ITINERARY | ABSTRACTS | HOME | BACK TO TRAVEL AWARDS HOME | |
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Thalamic high - frequency stimulation abolishes network oscillations I: electrophysiologic analysis on mechanism of action.
F.L.Hitti 1; C.C.McIntyre3; D.C.Lee4; M.H.Shalinsky1*; D.W.Roberts2; J.C.Leiter1; K.H.Lee2 1. Physiology, 2. Neurosurgery, Dartmouth-Hitchcock Med. Ctr., Lebanon, NH, USA, 3. Biomedical Engineering, Cleveland Clinic Foundation, Cleveland, OH, USA; 4. Center for Neuroscience and Neurological Recovery, Methodist Rehabilitation Ctr., Jackson, MS, USA |
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The mechanism of action of high frequency deep brain stimulation (DBS) in the thalamus for the treatment of tremor and epilepsy is unknown. Here, we tested the hypothesis that high frequency stimulation (HFS) abolishes synchronized oscillations such as spindle waves and 3 Hz absence seizure-like discharges generated within the thalamic neural network. Electrophysiological recordings were made in the thalamocortical relay (TC) neurons and in the GABAergic nucleus Reticularis thalami (nRt) neurons in the in vitro slice preparation of the ferret lateral geniculate nucleus (LGN). This slice preparation spontaneously generates spindle oscillations, and in the presence of GABA-A antagonists generates 3 Hz absence seizure-like discharges. Electrical stimulation (1-10 s; 10-2000 µA; 100 Hz) was delivered using a bipolar stimulating electrode placed within 100 µm of the recording electrodes in the slice preparation. Extracellular recordings from the A1 laminae of the LGN and the nRt revealed that synchronized oscillations were abolished at both locations when HFS was applied to either the LGN or nRt. Intracellular recordings from TC neurons resulted in an initial inhibitory post-synaptic potential (IPSP) followed by excitatory post-synaptic potentials (EPSPs) during HFS. In contrast, intracellular recordings from the GABAergic nRt neurons during HFS displayed only EPSPs; IPSPs were not observed. In both TC and nRt neurons, HFS resulted in membrane depolarization, decrease in the apparent input resistance, and abolition of spontaneous spindle and 3 Hz absence seizure-like oscillations. These results suggest that the mechanism of action of HFS involves release of neurotransmitters which profoundly affect the whole neural network.
Support Contributed By: NIH NS-47388, NREF Citation: F.L.Hitti, C.C.McIntyre, D.C.Lee, M.H.Shalinsky, D.W.Roberts, J.C.Leiter, K.H.Lee. Thalamic high - frequency stimulation abolishes network oscillations I: electrophysiologic analysis on mechanism of action Program No. 668.6. 2005 Abstract Viewer/Itinerary Planner. Washington, DC: Society for Neuroscience| TOP OF PAGE | ITINERARY | ABSTRACTS | HOME | BACK TO TRAVEL AWARDS HOME | |
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Basolateral amygdala modulation of consolidation and reconsolidation of inhibitory avoidance memory
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J.D.Rudoy *; G.M.Gunasekera; E.K.Williams; N.J.Sandstrom Dept. of Psychology & Neurosci. Prog., Williams Col., Williamstown, MA, USA |
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Evidence from recent studies suggests that, following reactivation of a consolidated fear memory, the memory enters a reconsolidation period during which it is susceptible to amnestic insult. The basolateral amygdala (BLA) modulates the consolidation of inhibitory avoidance fear memories, but no studies as yet have addressed the effects of functional inactivation of the BLA on reconsolidation of these memories. The present studies therefore examine the role of the (BLA) in the consolidation process following inhibitory avoidance training and the reconsolidation processes following reactivation. In Experiment 1, adult male rats received a single training trial on an inhibitory avoidance task. Immediately after conditioning, they received bilateral infusions of saline or the GABA agonist, muscimol, directed to the BLA. When tested 24 hr later, rats that received muscimol exhibited significantly shorter cross-over latencies than rats that received saline, replicating previous studies (Wilensky et al., 2000). In Experiment 2, rats were trained on the inhibitory avoidance task. Twenty-four hours later, they received a 1-min exposure to either the bright side of the conditioning apparatus (reactivation) or a novel environment (no reactivation) after which they received bilateral infusions of saline or muscimol. Animals infused with muscimol after reactivation had lower latencies than animals infused with muscimol after no reactivation. Animals infused with saline after either reactivation or no reactivation did not differ from each other. These findings suggest that the BLA plays a critical role in both consolidation and reconsolidation processes.
Support Contributed By: Essel Foundation and Williams College Science Center Citation: J.D.Rudoy, G.M.Gunasekera, E.K.Williams, N.J.Sandstrom. Basolateral amygdala modulation of consolidation and reconsolidation of inhibitory avoidance memory Program No. 650.5. 2005 Abstract Viewer/Itinerary Planner. Washington, DC: Society for NeuroscienceTOP OF PAGE | ITINERARY | ABSTRACTS | HOME | BACK TO TRAVEL AWARDS HOME | |
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The genetic background of ( Na+,K+ ) - ATPase,
a
-2 knock-out mice affects the distribution of
a
-2 and
a
-3 isoforms of this enzyme in brain and the survival time of homozygous newborns.
A.M.Baran 1; T.M.Spranger 1; A.E.Moseley2; J.B.Lingrel2; M.L.Caspers1*
1. Chemistry and Biochemistry, Univ. of Detroit Mercy, Detroit, MI, USA; 2. Molecular Genetics, Biochemistry and Microbiology, Univ. of Cincinnati, Cincinnati, OH, USA
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The (Na+,K+)-ATPase maintains Na+ and K+ gradients in cells through the active transport of these ions across the plasma membrane. [3 H]Ouabain, which binds with high affinity to the a -2 and a -3 isoforms of the (Na+,K+)-ATPase, was used to study the distribution of these isoforms in the brains of adult wild type and heterozygous a -2 knockout mice of FVBN genetic background. Frozen, coronal brain sections (24 micron) were prepared and were assayed in a 100 mM Tris-HCl buffer containing 10 mM NaCl, 10 mM MgCl2, 5 mM ATP and 29 nM [3 H]ouabain. The sections were exposed to Kodak BioMax Scientific Imaging film and the images were subjected to computer-assisted densitometry. In a -2 heterozygotes, significant decreases in the relative density of [3 H]ouabain binding sites were observed in the cerebral cortex (5.1%) and hippocampus (4.4%) compared to wild-type mice. These findings are similar to results obtained with C57BL6 mice where small decreases in [3 H]ouabain binding sites were observed in the cerebral cortex, hippocampus and thalamus of heterozygous a -2 knockout mice but are dissimilar to results using a -2 heterozygous 129/Black Swiss (mixed) mice where larger decreases in [3H]ouabain binding, relative to wild-type animals, were seen in all brain regions tested (Program #517.10, 2004 Abstract Viewer/Itinerary Planner, Washington, DC: Society for Neuroscience, CD-ROM). Strain differences also are seen in the survival time of homozygous a -2 knockout mice; FVBN knockout mice live approximately 1 day whereas the mixed and C57BL6 knockout mice die at birth. Support Contributed By: NIH grants HL28573 and HL66062 and a gift from J.D. Rose. Citation: A.M.Baran, T.M.Spranger, A.E.Moseley, J.B.Lingrel, M.L.Caspers. The genetic background of ( Na+,K+ ) - ATPase, a- 2 knock-out mice affects the distribution of a- 2 and a- 3 isoforms of this enzyme in brain and the survival time of homozygous newborns. Program No. 736.12. 2005 Abstract Viewer/Itinerary Planner. Washington, DC: Society for Neuroscience | TOP OF PAGE | ITINERARY | ABSTRACTS | HOME | BACK TO TRAVEL AWARDS HOME | |
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Kinematics of larval locomotion in mutant Drosophila
V.M.Woods ; P.K.Rivlin; B.R.Land; R.Wyttenbach*; R.R.Hoy Dept. of Neurobiology and Behavior, Cornell Univ., Ithaca, NY, USA
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As part of an ongoing investigation in our lab to study how bioamine and neural activity mutations influence larval and adult behaviors in Drosophila
, we have developed Matlab code to analyze digital images of crawling larvae and to compute a number of locomotor parameters that include path length, average speed, turning angle, turning direction and frequency, and percent body area change. Here we report the analysis of TßhM18
Sh
5
, a double mutant generated by combining Shaker
, a potassium ion channel mutant that results in increased neurotransmission with an octopamine deficient mutant, TßhM18. Studies have shown that larval locomotor behavior is altered in Shaker
and TßhM18
mutants with Shaker
displaying decreased speed and fewer changes in direction (Wang et al. 2002), and TßhM18
displaying increased turning and decreased speed (Saraswati et al. 2003). Our preliminary analysis of TßhM18
Sh
5
indicates that path length and speed are reduced and turning frequency is increased as compared to Sh
5
and TßhM18
alone, thus suggesting that these mutations act synergistically to alter locomotor behavior. To better understand the mechanisms that underlie these locomotor phenotypes, we are extending our Matlab code to analyze two additional aspects of Drosophila
locomotion: a "searching and decision-making" behavior which accompanies a change in direction, and the underlying energetic mechanisms of larval locomotion.
Support Contributed By: HHMI Professor Award to RRH Citation: V.M.Woods, P.K.Rivlin, B.R.Land, R.Wyttenbach, R.R.Hoy. Kinematics of larval locomotion in mutant Drosophila Program No. 55.1. 2005 Abstract Viewer/Itinerary Planner. Washington, DC: Society for Neuroscience| TOP OF PAGE | ITINERARY | ABSTRACTS | HOME | BACK TO TRAVEL AWARDS HOME | |
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SFN ITINERARY - WASHINGTON, DC - 2005
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Presentation Day / Time |
Location Washington Conv. Ctr. Hall A-C |
Prog. #/ Type |
Authors Institutions |
Abstract Title Session #/Title |
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Saturday Nov. 12 1:00 - 2:00 PM |
X4 |
55.1 Poster |
V.M.Woods
;
P.K.Rivlin; B.R.Land; R.Wyttenbach*
; R.R.Hoy Dept. of Neurobiology and Behavior, Cornell Univ., Ithaca, NY, USA |
Kinematics of larval locomotion in mutant Drosophila
55 Kinetics and EMG: Locomotion |
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Presentation Day / Time |
Location Washington Conv. Ctr. Hall A-C |
Prog. #/ Type |
Authors Institutions |
Abstract Title Session #/Title |
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Monday Nov. 14 9:00 - 10:00 AM |
NN21 |
425.14 Poster |
S.P.Bothwell
;
E.R.Reynolds*
Department of Biology, Program in Neuroscience, Lafayette Col., Easton, PA, USA |
Reactive oxygen species accelerate and antioxidants delay loss of dopaminergic neurons and motor impairments in a Drosophila
model for Parkinson's disease 425 Parkinson's Disease Models: Environmental Toxins |
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Tuesday, Nov. 15 (AM) - Poster Presentations
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Presentation Day / Time |
Location Washington Conv. Ctr. Hall A-C |
Prog. #/ Type |
Authors Institutions |
Abstract Title Session #/Title |
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Tuesday Nov. 15 9:00 - 10:00 AM |
GG32 |
644.10 Poster |
C.Dufault
;
G.Poles; L.L.Driscoll*
Psychology, Colorado Col., Colorado Springs, CO, USA |
Early postnatal exposure to polybrominated diphenyl ethers alters the cholinergic modulation of attention 644 Attention: Pharmacology and Gene Action |
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Tuesday Nov. 15 8:00 - 9:00 AM |
JJ30 |
650.5 Poster |
J.D.Rudoy
*
;
G.M.Gunasekera; E.K.Williams; N.J.Sandstrom Dept. of Psychology & Neurosci. Prog., Williams Col., Williamstown, MA, USA |
Basolateral amygdala modulation of consolidation and reconsolidation of inhibitory avoidance memory 650 Consolidation and Reconsolidation |
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Tuesday Nov. 15 9:00 - 10:00 AM |
SS22 |
668.6 Poster |
F.L.Hitti
1
;
C.C.McIntyre3
; D.C.Lee4
; M.H.Shalinsky1*
; D.W.Roberts2
; J.C.Leiter1
; K.H.Lee2
1. Physiology, 2. Neurosurgery, Dartmouth-Hitchcock Med. Ctr., Lebanon, NH, USA, 3. Biomedical Engineering, Cleveland Clinic Foundation, Cleveland, OH, USA; 4. Center for Neuroscience and Neurological Recovery, Methodist Rehabilitation Ctr., Jackson, MS, USA |
Thalamic high - frequency stimulation abolishes network oscillations I: electrophysiologic analysis on mechanism of action 668 Epilepsy: Animal Models |
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Presentation Day / Time |
Location Washington Conv. Ctr. Hall A-C |
Prog. #/ Type |
Authors Institutions |
Abstract Title Session #/Title |
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Tuesday Nov. 15 4:00 - 5:00 PM |
V3 |
736.12 Poster |
A.M.Baran
1
; T.M.Spranger1
;
A.E.Moseley2
; J.B.Lingrel2
; M.L.Caspers1*
1. Chemistry and Biochemistry, Univ. of Detroit Mercy, Detroit, MI, USA; 2. Molecular Genetics, Biochemistry and Microbiology, Univ. of Cincinnati, Cincinnati, OH, USA |
The genetic background of ( Na+
,K+
) - ATPase, a-
2 knock-out mice affects the distribution of a-
2 and a-
3 isoforms of this enzyme in brain and the survival time of homozygous newborns. 736 Modulation of Firing Properties |
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Presentation Day / Time |
Location Washington Convention Ctr. Hall A-C |
Prog. #/ Type |
Authors Institutions |
Abstract Title Session #/Title |
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Wednesday Nov. 16 10:00 - 11:00 AM |
D59 |
836.3 Poster |
B.G.Cordero
*
;
M.C.Davidson; J.Schallhorn; G.A.Silva 1. Bioengineering, 2. Ophthalmology, Univ. of California, San Diego, San Diego, CA, USA, |
Modulation of reactive gliosis by siRNA 836 Regeneration: CNS IV |
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Wednesday
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LL5 |
885.2 Poster |
H.N.Foozer
;
M.S.Griffith; M.E.Bardgett*
Psychology, Northern Kentucky Univ., Highland Heights, KY, USA |
Nicotine does not improve spatial working memory in mice with hippocampal damage 885 Learning and Memory: Nicotine and Alcohol |
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Wednesday Nov. 16 8:00 - 9:00 AM |
LL18 |
886.1 Poster |
K.J.Berry
1
;
F.J.Cisneros1
; B.Gough1
; L.C.Schmued1*
; J.P.Hanig2
; S.A.Ferguson1
1. Neurotoxicology, NCTR/FDA, Jefferson, AR, USA; 2. CDER/FDA, Silver Spring, MD, USA |
Spatial learning and memory in male and female rats is not affected by chronic oral Accutane ( ACC ) 886 Learning and Memory: Pharmacology III |
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