SLEEP 2011 Abstract Supplement

More documents

Recommendations

Info

A. Basic Science IX. Learning, Memory and Cognition Conclusion: Here we demonstrate that the overnight consolidation of episodic memory normally present in the healthy young brain is impaired in older adults. Moreover, this age-related impairment appears to be mediated by a failure of slow-wave sleep consolidation mechanisms that facilitate systems-level reorganization in hippocampal-neocortical networks. Support (If Any): Supported by National Institutes of Health; NIH NIA [RO1AG031164] (MPW), [F32AG039170](BAM). 0230 IMPAIRED HIPPOCAMPAL-DEPENDENT LEARNING IN OLDER ADULTS MEDIATED BY DEFICIENT SLEEP- SPINDLE GENERATION Mander BA 1 , Rao V 1 , Lu BS 3 , Saletin JM 1 , Jagust WJ 2 , Walker MP 1,2 1 Psychology, University of California, Berkeley, Berkeley, CA, USA, 2 Helen Wills Neuroscience Institute, University of California, Berkeley, Berkeley, CA, USA, 3 Division of Pulmonary and Critical Care Medicine, California Pacific Medical Center, San Francisco, CA, USA Introduction: Recent evidence in young adults suggests that NREM sleep-spindles restore hippocampal-dependent memory encoding ability, promoting efficient post-sleep learning. Aging is associated both with impaired hippocampal-dependent learning and disrupted NREM sleep, yet the causal interaction between these factors remains unknown. Combining EEG and fMRI, here we examine whether age-related deficits in sleep-spindle generation lead to a compromised next-day ability to form hippocampal-dependent episodic memories. Methods: Twenty-three participants, divided between healthy older adults (n=12, 70.5±1.6 years) and healthy young adults (n=11, 20.2±0.6 years) obtained a full night of polysomnographically recorded sleep (whole-head, 19-channel-EEG), followed the next day by a hippocampal-dependent episodic learning task performed during event-related fMRI. Results: Following sleep, older adults exhibited a 49% deficit in nextday episodic learning ability relative to young adults (p=0.013), further paralleled by significant deficits in hippocampal-encoding activation. Co-occurring with these neural and behavioral impairments was a 30% reduction in sleep-spindle density in older adults (p=0.045), most prominent over frontal cortex. In young adults, the density of frontal sleep-spindles accurately predicted next-day hippocampal-encoding activation (r=0.68, p=0.022), and learning ability (r=0.63, p=0.038). In contrast, this mediating spindle relationship with next-day hippocampal activation and concomitant learning ability was lost in old adults (all r0.35). Indeed, the strength of predictive association between frontal sleep-spindles and next-day hippocampal-encoding activity differed significantly between the young and old groups (p=0.018). Conclusion: Here we demonstrate that the restitutive benefit of sleep on next-day hippocampal-dependent encoding ability in the healthy young brain is impaired in older adults. Moreover, such age-related memory impairment appears to be mediated by a failure in the generation of sleep-spindles, specifically over frontal cortex, leading to a compromised ability to form new episodic memories. Such findings suggest that sleep disruption in the elderly is an overlooked but potentially significant mediating factor contributing to cognitive decline in later life. Support (If Any): Supported by National Institutes of Health; NIH NIA [RO1AG031164] (MPW), [F32AG039170](BAM). 0231 DIFFERENCES IN SOCIAL INTERACTION BETWEEN OEXIN/ATAXIN-3 AND WILDTYPE MICE Xie XS 1 , Yang L 1 , Zou B 1 , Sakurai T 2 1 AfaSci Research Laboratory, AfaSci, Inc., Redwood City, CA, USA, 2 Department of Molecular Neuroscience and Integrative Physiology, Kanazawa University, Kanazawa-shi, Japan Introduction: Hypocretins/orexin (Hcrt) regulates general behaviors e.g., wake/sleep, locomotion, feeding, and reward. The Hcrt system has been also implicated in exploring behavior, stress response, learning and memory. To test the hypothesis that Hcrt plays a role in social interaction, we used a validated protocol that two enclosures with either a strange or littermate mouse are placed in a normal home cage to investigate social interaction of the test subject of either wildtype (WT) or orexin/ataxin-3 (AT) mice, in which the Hcrt neurons almost completely degenerated after 4 postnatal weeks. Methods: General behavior and social interaction were automatically quantified using AfaSci’s home cage monitoring system-SmartCage. The social interaction test was conducted in light phase and consisted of three consecutive 10-min sessions: 1) Habituation, the test mouse explored two empty enclosures; 2) Sociability: one stranger (from different cage) or littermate mouse was randomly placed in one enclosure; 3) Preference for social novelty: a new unfamiliar mouse (stranger 2) was placed into the other enclosure. The CageScoreTM software calculated occupancy time of the test mouse in two different zones corresponding to the enclosures. Active counts, active time, traveling distance and velocity, and rearing counts of the test mouse were also automatically analyzed. Results: When using stranger 1 for sociability test and stranger 2 for social novelty test, there were no significant differences in both interactions between the genotypes. When using littermate for sociability test, the WT test subject did not show any sociability. In contrast, the AT subject exhibited a similar degree of sociability as seen with the stranger 1. In the consequent social novelty test using a stranger there were no significant differences between the two genotypes (n=8 per genotype). The AT mice significantly decreased in active counts, active time, travel distance (but not velocity), and rearing counts compared to the WT littermates during the dark period in a 24-h recording. Conclusion: The AT mice have normal social interaction ability as the WT mice. However, the AT mice treat their littermates as strangers and show great interest in exploring during the sociability test, suggesting that the AT mice may have social memory deficits compared to WT littermates. The AT mice displayed a decrease in wake activity, locomotion and rearing during the dark phase compare to their WT littermates. Support (If Any): NIH grants R01 MH078194 and R43NS065555 0232 ELECTROPHYSIOLOGICAL EVIDENCE OF IMPACT ON AUDITORY PRE-ATTENTIVE BRAIN MECHANISM IN HABITUAL SHORT SLEEPERS: STUDY I Gumenyuk V, Roth T, Jefferson C, Drake C Sleep Disorders & Research Center, Henry Ford Hospital, Detroit, MI, USA Introduction: Reduced TIB relative to biological sleep-need is common. The impact of habitual short sleep on automatic (pre-attentive) auditory processing has not been studied to date. An established electrophysiological index of pre-attentive auditory processing is the fronto-centrally distributed event-related potential (ERP) called mismatch negativity (MMN). The current study investigates the effects of chronic - 6h/night of sleep on frontal brain areas involved in auditory attention. Methods: 10 self-defined short sleepers (2-wk diary TST≤6h) (age: 35±10yrs, 5F) and 9 subjects with TST=7-8h, (age: 30±6yrs, 6F) participated. ERPs were recorded via a 64-EEG channel system. Two test conditions: “ignore” and “attend” were implemented in a standard odd- SLEEP, Volume 34, Abstract Supplement, 2011 A82
A. Basic Science IX. Learning, Memory and Cognition ball auditory task utilizing 160 novel sounds (20%) intermixed with tone (75%) and 5% target-sounds. In the ignore task, subjects were asked to ignore the sounds and watch a silent movie. Whereas in the attended task they were instructed to pay attention to the sounds and count target sounds for 7.5 minutes on 2 trials. MMN was analyzed and compared between groups on the two task conditions and frontal/central/parietal electrodes by 3-factor ANOVA. Sleep diary data was compared between groups by t-test. Results: TST was significantly shorter in the short sleepers compared to normal sleeping subjects (7.8h vs. 5.8h, P
Page 1:
JOURNAL OF SLEEP AND SLEEP DISORDER
Page 4 and 5:
EDITORIAL In June of 1986, roughly
Page 6 and 7:
A. Basic Science I. Pharmacology an
Page 8 and 9:
Page 10 and 11:
Page 12 and 13:
A. Basic Science II. Cell and Molec
Page 14 and 15:
Page 16 and 17:
Page 18 and 19:
Page 20 and 21:
Page 22 and 23:
Page 24 and 25:
Page 26 and 27:
A. Basic Science III. Ontogeny/Agin
Page 28 and 29:
Page 30 and 31:
Page 32 and 33:
A. Basic Science IV. Neurobiology S
Page 34 and 35: A. Basic Science IV. Neurobiology o
Page 36 and 37: A. Basic Science IV. Neurobiology
Page 38 and 39: A. Basic Science IV. Neurobiology h
Page 40 and 41: A. Basic Science IV. Neurobiology C
Page 42 and 43: A. Basic Science IV. Neurobiology t
Page 44 and 45: A. Basic Science V. Physiology 0110
Page 46 and 47: A. Basic Science V. Physiology comp
Page 48 and 49: A. Basic Science V. Physiology Resu
Page 50 and 51: A. Basic Science V. Physiology Intr
Page 52 and 53: A. Basic Science V. Physiology 0135
Page 54 and 55: A. Basic Science V. Physiology Conc
Page 56 and 57: A. Basic Science V. Physiology infl
Page 58 and 59: A. Basic Science VI. Chronobiology
Page 70 and 71: A. Basic Science VIII. Behavior 018
Page 72 and 73: A. Basic Science VIII. Behavior 019
Page 74 and 75: A. Basic Science VIII. Behavior a l
Page 76 and 77: A. Basic Science VIII. Behavior Res
Page 78 and 79: A. Basic Science IX. Learning, Memo
Page 94 and 95: A. Basic Science X. Dreaming 0261 P
Page 96 and 97: A. Basic Science XI. Sleep Deprivat
Page 112 and 113: A. Basic Science XII. Instrumentati
Page 118 and 119: B. Clinical Sleep Science I. Sleep
Page 134 and 135:
B. Clinical Sleep Science I. Sleep
Page 136 and 137:
Page 138 and 139:
Page 140 and 141:
Page 142 and 143:
Page 144 and 145:
Page 146 and 147:
Page 148 and 149:
Page 150 and 151:
Page 152 and 153:
Page 154 and 155:
Page 156 and 157:
Page 158 and 159:
Page 160 and 161:
Page 162 and 163:
Page 164 and 165:
B. Clinical Sleep Science II. Sleep
Page 166 and 167:
Page 168 and 169:
Page 170 and 171:
Page 172 and 173:
B. Clinical Sleep Science III. Slee
Page 174 and 175:
Page 176 and 177:
Page 178 and 179:
Page 180 and 181:
Page 182 and 183:
Page 184 and 185:
Page 186 and 187:
Page 188 and 189:
Page 190 and 191:
Page 192 and 193:
Page 194 and 195:
Page 196 and 197:
B. Clinical Sleep Science IV. Sleep
Page 198 and 199:
Page 200 and 201:
Page 202 and 203:
B. Clinical Sleep Science V. Sleep
Page 204 and 205:
Page 206 and 207:
Page 208 and 209:
Page 210 and 211:
B. Clinical Sleep Science VI. Sleep
Page 212 and 213:
Page 214 and 215:
Page 216 and 217:
Page 218 and 219:
B. Clinical Sleep Science VII. Neur
Page 220 and 221:
Page 222 and 223:
Page 224 and 225:
B. Clinical Sleep Science VIII. Med
Page 226 and 227:
Page 228 and 229:
Page 230 and 231:
Page 232 and 233:
Page 234 and 235:
Page 236 and 237:
Page 238 and 239:
Page 240 and 241:
Page 242 and 243:
Page 244 and 245:
B. Clinical Sleep Science IX. Psych
Page 246 and 247:
Page 248 and 249:
Page 250 and 251:
Page 252 and 253:
Page 254 and 255:
Page 256 and 257:
Page 258 and 259:
Page 260 and 261:
Page 262 and 263:
B. Clinical Sleep Science X. Normal
Page 264 and 265:
Page 266 and 267:
Page 268 and 269:
Page 270 and 271:
B. Clinical Sleep Science XI. Pedia
Page 272 and 273:
Page 274 and 275:
Page 276 and 277:
Page 278 and 279:
Page 280 and 281:
Page 282 and 283:
Page 284 and 285:
Page 286 and 287:
Page 288 and 289:
Page 290 and 291:
Page 292 and 293:
Page 294 and 295:
Page 296 and 297:
Page 298 and 299:
Page 300 and 301:
Page 302 and 303:
Page 304 and 305:
B. Clinical Sleep Science XII. Slee
Page 306 and 307:
Page 308 and 309:
Page 310 and 311:
B. Clinical Sleep Science XIII. Sle
Page 312 and 313:
Page 314 and 315:
Page 316 and 317:
Page 318 and 319:
Page 320 and 321:
Page 322 and 323:
Page 324 and 325:
Page 326 and 327:
B. Clinical Sleep Science XIV. Inst
Page 328 and 329:
Page 330 and 331:
Page 332 and 333:
Page 334 and 335:
Page 336 and 337:
B. Clinical Sleep Science XV. Healt
Page 338 and 339:
Page 340 and 341:
Page 342 and 343:
Page 344 and 345:
Page 346 and 347:
j u m p t o : A - B - C - D - E - F
Page 348 and 349:
j u m p t o : A - B - C - D - E - F
Page 350 and 351:
j u m p t o : A - B - C - D - E - F
Page 352 and 353:
j u m p t o : A - B - C - D - E - F
Page 354 and 355:
j u m p t o : A - B - C - D - E - F
Page 356 and 357:
j u m p t o : A - B - C - D - E - F
Page 358 and 359:
j u m p t o : A - B - C - D - E - F
Page 360 and 361:
j u m p t o : A - B - C - D - E - F
Page 362 and 363:
j u m p t o : A - B - C - D - E - F
Page 364 and 365:
j u m p t o : A - B - C - D - E - F
Page 366 and 367:
j u m p t o : A - B - C - D - E - F
Page 368 and 369:
j u m p t o : A - B - C - D - E - F
Page 370 and 371:
j u m p t o : 2 - A - B - C - D - E
Page 372 and 373:
j u m p t o : 2 - A - B - C - D - E
Page 374 and 375:
j u m p t o : 2 - A - B - C - D - E
Page 376 and 377:
j u m p t o : 2 - A - B - C - D - E
Page 378 and 379:
j u m p t o : 2 - A - B - C - D - E
Page 380 and 381:
j u m p t o : 2 - A - B - C - D - E
show all

SLEEP 2011 Abstract Supplement

You also want an ePaper? Increase the reach of your titles

Delete template?

Save as template?