The influence of negative emotions on pain: Behavioral effects and neural mechanisms,
NeuroImage (2009), doi:10.1016/j.neuroimage.2009.05.059
Katja Wiech, Irene Tracey
The idea that pain can lead to feelings of frustration, worry, anxiety and depression seems obvious, particularly if it is of a chronic nature. However, there is also evidence for the reverse causal relationship in which negative mood and emotion can lead to pain or exacerbate it. Here, we review findings from studies on the modulation of pain by experimentally induced mood changes and clinical mood disorders. We discuss possible neural mechanisms underlying this modulatory influence focusing on the periaqueductal grey (PAG), amygdala, anterior cingulate cortex (ACC) and anterior insula as key players in both, pain and affective processing.
Replay during sleep
Replay of rule-learning related neural patterns in the prefrontal cortex during sleep
Adrien Peyrache, Mehdi Khamassi, Karim Benchenane, Sidney I Wiener & Francesco P Battaglia
Nature Neuroscience, doi:10.1038/nn.2337
Slow-wave sleep (SWS) is important for memory consolidation. During sleep, neural patterns reflecting previously acquired information are replayed. One possible reason for this is that such replay exchanges information between hippocampus and neocortex, supporting consolidation. We recorded neuron ensembles in the rat medial prefrontal cortex (mPFC) to study memory trace reactivation during SWS following learning and execution of cross-modal strategy shifts. In general, reactivation of learning-related patterns occurred in distinct, highly synchronized transient bouts, mostly simultaneous with hippocampal sharp wave/ripple complexes (SPWRs), when hippocampal ensemble reactivation and cortico-hippocampal interaction is enhanced. During sleep following learning of a new rule, mPFC neural patterns that appeared during response selection replayed prominently, coincident with hippocampal SPWRs. This was learning dependent, as the patterns appeared only after rule acquisition. Therefore, learning, or the resulting reliable reward, influenced which patterns were most strongly encoded and successively reactivated in the hippocampal/prefrontal network.
Adrien Peyrache, Mehdi Khamassi, Karim Benchenane, Sidney I Wiener & Francesco P Battaglia
Nature Neuroscience, doi:10.1038/nn.2337
Slow-wave sleep (SWS) is important for memory consolidation. During sleep, neural patterns reflecting previously acquired information are replayed. One possible reason for this is that such replay exchanges information between hippocampus and neocortex, supporting consolidation. We recorded neuron ensembles in the rat medial prefrontal cortex (mPFC) to study memory trace reactivation during SWS following learning and execution of cross-modal strategy shifts. In general, reactivation of learning-related patterns occurred in distinct, highly synchronized transient bouts, mostly simultaneous with hippocampal sharp wave/ripple complexes (SPWRs), when hippocampal ensemble reactivation and cortico-hippocampal interaction is enhanced. During sleep following learning of a new rule, mPFC neural patterns that appeared during response selection replayed prominently, coincident with hippocampal SPWRs. This was learning dependent, as the patterns appeared only after rule acquisition. Therefore, learning, or the resulting reliable reward, influenced which patterns were most strongly encoded and successively reactivated in the hippocampal/prefrontal network.
Hippocampal theta oscillations are traveling waves
Hippocampal theta oscillations are traveling waves.
Lubenov EV, Siapas AG
Nature 2009;459(7246):534-9.
Theta oscillations clock hippocampal activity during awake behaviour and rapid eye movement (REM) sleep. These oscillations are prominent in the local field potential, and they also reflect the subthreshold membrane potential and strongly modulate the spiking of hippocampal neurons. The prevailing view is that theta oscillations are synchronized throughout the hippocampus, despite the lack of conclusive experimental evidence. In contrast, here we show that in freely behaving rats, theta oscillations in area CA1 are travelling waves that propagate roughly along the septotemporal axis of the hippocampus. Furthermore, we find that spiking in the CA1 pyramidal cell layer is modulated in a consistent travelling wave pattern. Our results demonstrate that theta oscillations pattern hippocampal activity not only in time, but also across anatomical space. The presence of travelling waves indicates that the instantaneous output of the hippocampus is topographically organized and represents a segment, rather than a point, of physical space.
Lubenov EV, Siapas AG
Nature 2009;459(7246):534-9.
Theta oscillations clock hippocampal activity during awake behaviour and rapid eye movement (REM) sleep. These oscillations are prominent in the local field potential, and they also reflect the subthreshold membrane potential and strongly modulate the spiking of hippocampal neurons. The prevailing view is that theta oscillations are synchronized throughout the hippocampus, despite the lack of conclusive experimental evidence. In contrast, here we show that in freely behaving rats, theta oscillations in area CA1 are travelling waves that propagate roughly along the septotemporal axis of the hippocampus. Furthermore, we find that spiking in the CA1 pyramidal cell layer is modulated in a consistent travelling wave pattern. Our results demonstrate that theta oscillations pattern hippocampal activity not only in time, but also across anatomical space. The presence of travelling waves indicates that the instantaneous output of the hippocampus is topographically organized and represents a segment, rather than a point, of physical space.
That Face Looks Familiar
Does Sleep Really Influence Face Recognition Memory?
Bhavin R. Sheth, Ngan Nguyen, Davit Janvelyan
PLoS ONE 4(5): e5496. doi:10.1371/journal.pone.0005496
Mounting evidence implicates sleep in the consolidation of various kinds of memories. We investigated the effect of sleep on memory for face identity, a declarative form of memory that is indispensable for nearly all social interaction. In the acquisition phase, observers viewed faces that they were required to remember over a variable retention period (0–36 hours). In the test phase, observers viewed intermixed old and new faces and judged seeing each before. Participants were classified according to acquisition and test times into seven groups. Memory strength (d′) and response bias (c) were evaluated. Substantial time spent awake (12 hours or more) during the retention period impaired face recognition memory evaluated at test, whereas sleep per se during the retention period did little to enhance the memory. Wakefulness during retention also led to a tightening of the decision criterion. Our findings suggest that sleep passively and transiently shelters face recognition memory from waking interference (exposure) but does not actively aid in its long-term consolidation.
Bhavin R. Sheth, Ngan Nguyen, Davit Janvelyan
PLoS ONE 4(5): e5496. doi:10.1371/journal.pone.0005496
Mounting evidence implicates sleep in the consolidation of various kinds of memories. We investigated the effect of sleep on memory for face identity, a declarative form of memory that is indispensable for nearly all social interaction. In the acquisition phase, observers viewed faces that they were required to remember over a variable retention period (0–36 hours). In the test phase, observers viewed intermixed old and new faces and judged seeing each before. Participants were classified according to acquisition and test times into seven groups. Memory strength (d′) and response bias (c) were evaluated. Substantial time spent awake (12 hours or more) during the retention period impaired face recognition memory evaluated at test, whereas sleep per se during the retention period did little to enhance the memory. Wakefulness during retention also led to a tightening of the decision criterion. Our findings suggest that sleep passively and transiently shelters face recognition memory from waking interference (exposure) but does not actively aid in its long-term consolidation.
Physiological markers of local sleep
Physiological Markers of Local Sleep
David M. Rector, Jennifer L. Schei, Hans P. A. Van Dongen, Gregory Belenky and James M. Krueger
Eur J Neurosci 2009;29(9):1771-8.
Substantial evidence suggests that brain regions that have been disproportionately used during waking will require a greater intensity and/or duration of subsequent sleep. For example, rats use their whiskers in the dark and their eyes during the light which manifests as a greater magnitude of electroencephalogram (EEG) slow wave activity in the somatosensory and visual cortex during sleep in the corresponding light and dark periods respectively. The parsimonious interpretation of such findings is that sleep is distributed across local brain regions and is use-dependent. The fundamental properties of sleep can also be experimentally defined locally at the level of small neural assemblies such as cortical columns. In this view, sleep is orchestrated, but not fundamentally driven, by central mechanisms. We explore two physiological markers of local, use-dependent sleep, namely, an electrical marker apparent as a change in the size and shape of an electrical evoked response, and a metabolic marker evident as an evoked change in blood volume and oxygenation delivered to activated tissue. Both markers, applied to cortical columns, provide a means to investigate physiological mechanisms for the distributed homeostatic regulation of sleep, and may yield new insights into the consequences of sleep loss and sleep pathologies on waking brain function.
David M. Rector, Jennifer L. Schei, Hans P. A. Van Dongen, Gregory Belenky and James M. Krueger
Eur J Neurosci 2009;29(9):1771-8.
Substantial evidence suggests that brain regions that have been disproportionately used during waking will require a greater intensity and/or duration of subsequent sleep. For example, rats use their whiskers in the dark and their eyes during the light which manifests as a greater magnitude of electroencephalogram (EEG) slow wave activity in the somatosensory and visual cortex during sleep in the corresponding light and dark periods respectively. The parsimonious interpretation of such findings is that sleep is distributed across local brain regions and is use-dependent. The fundamental properties of sleep can also be experimentally defined locally at the level of small neural assemblies such as cortical columns. In this view, sleep is orchestrated, but not fundamentally driven, by central mechanisms. We explore two physiological markers of local, use-dependent sleep, namely, an electrical marker apparent as a change in the size and shape of an electrical evoked response, and a metabolic marker evident as an evoked change in blood volume and oxygenation delivered to activated tissue. Both markers, applied to cortical columns, provide a means to investigate physiological mechanisms for the distributed homeostatic regulation of sleep, and may yield new insights into the consequences of sleep loss and sleep pathologies on waking brain function.
Slow waves and information processing
Slow waves, synaptic plasticity and information processing: insights from transcranial magnetic stimulation and high-density EEG experiments
M Massimini, G Tononi, R Huber
European Journal of Neuroscience, Vol. 29, No. 9., pp. 1761-1770.
Sleep slow waves are the main phenomenon underlying NREM sleep. They are homeostatically regulated, they are thought to be linked to learning and plasticity processes and, at the same time, they are associated with marked changes in cortical information processing. Using transcranial magnetic stimulation (TMS) and high-density (hd) EEG we can measure slow waves, induce and measure plastic changes in the cerebral cortex and directly assess corticocortical information transmission. In this manuscript we review the results of recent experiments in which TMS with hd-EEG is used to demonstrate (i) a causal link between cortical plastic changes and sleep slow waves and (ii) a causal link between slow waves and the decreased ability of thalamocortical circuits to integrate information and to generate conscious experience during NREM sleep. The data presented here suggest a unifying mechanism linking slow waves, plasticity and cortical information integration; moreover, they suggest that TMS can be used as a nonpharmacological means to controllably induce slow waves in the human cerebral cortex.
M Massimini, G Tononi, R Huber
European Journal of Neuroscience, Vol. 29, No. 9., pp. 1761-1770.
Sleep slow waves are the main phenomenon underlying NREM sleep. They are homeostatically regulated, they are thought to be linked to learning and plasticity processes and, at the same time, they are associated with marked changes in cortical information processing. Using transcranial magnetic stimulation (TMS) and high-density (hd) EEG we can measure slow waves, induce and measure plastic changes in the cerebral cortex and directly assess corticocortical information transmission. In this manuscript we review the results of recent experiments in which TMS with hd-EEG is used to demonstrate (i) a causal link between cortical plastic changes and sleep slow waves and (ii) a causal link between slow waves and the decreased ability of thalamocortical circuits to integrate information and to generate conscious experience during NREM sleep. The data presented here suggest a unifying mechanism linking slow waves, plasticity and cortical information integration; moreover, they suggest that TMS can be used as a nonpharmacological means to controllably induce slow waves in the human cerebral cortex.
Lessons from fMRI Studies of Emotion, Personality, and Social Cognition
Perspectives on Psychological Science a Journal of the Association for Psychological Science had these recent articles. Posted below are the links to the excellent debate/discussions about fMRI statistical analyses and interesting issues for scientific psychology.
Editor's Introduction to Vul et al. (2009) and Comments
Ed Diener
Puzzlingly High Correlations in fMRI Studies of Emotion, Personality, and Social CognitionEdward Vul, Christine Harris, Piotr Winkielman, and Harold Pashler
Commentary on Vul et al.'s (2009) "Puzzlingly High Correlations in fMRI Studies of Emotion, Personality, and Social Cognition"Thomas E. Nichols and Jean-Baptist Poline
Big Correlations in Little Studies: Inflated fMRI Correlations Reflect Low Statistical Power--Commentary on Vul et al. (2009)
Tal Yarkoni
Correlations in Social Neuroscience Aren't Voodoo: Commentary on Vul et al. (2009)
Matthew D. Lieberman, Elliot T. Berkman, and Tor D. Wager
Discussion of "Puzzlingly High Correlations in fMRI Studies of Emotion, Personality, and Social Cognition" by Vul et al. (2009)
Nicole A. Lazar
Correlations and Multiple Comparisons in Functional Imaging: A Statistical Perspective (Commentary on Vul et al., 2009Martin A. Lindquist and Andrew Gelman
Understanding the Mind by Measuring the Brain: Lessons From Measuring Behavior (Commentary on Vul et al., 2009)
Lisa Feldman Barrett
Reply to Comments on "Puzzlingly High Correlations in fMRI Studies of Emotion, Personality, and Social Cognition"
Edward Vul, Christine Harris, Piotr Winkielman, and Harold Pashler
Editor's Introduction to Vul et al. (2009) and Comments
Ed Diener
Puzzlingly High Correlations in fMRI Studies of Emotion, Personality, and Social CognitionEdward Vul, Christine Harris, Piotr Winkielman, and Harold Pashler
Commentary on Vul et al.'s (2009) "Puzzlingly High Correlations in fMRI Studies of Emotion, Personality, and Social Cognition"Thomas E. Nichols and Jean-Baptist Poline
Big Correlations in Little Studies: Inflated fMRI Correlations Reflect Low Statistical Power--Commentary on Vul et al. (2009)
Tal Yarkoni
Correlations in Social Neuroscience Aren't Voodoo: Commentary on Vul et al. (2009)
Matthew D. Lieberman, Elliot T. Berkman, and Tor D. Wager
Discussion of "Puzzlingly High Correlations in fMRI Studies of Emotion, Personality, and Social Cognition" by Vul et al. (2009)
Nicole A. Lazar
Correlations and Multiple Comparisons in Functional Imaging: A Statistical Perspective (Commentary on Vul et al., 2009Martin A. Lindquist and Andrew Gelman
Understanding the Mind by Measuring the Brain: Lessons From Measuring Behavior (Commentary on Vul et al., 2009)
Lisa Feldman Barrett
Reply to Comments on "Puzzlingly High Correlations in fMRI Studies of Emotion, Personality, and Social Cognition"
Edward Vul, Christine Harris, Piotr Winkielman, and Harold Pashler
Improve creativity while sleeping / dreaming
REM, not incubation, improves creativity by priming associative networks
www.pnas.org/cgi/doi/10.1073/pnas.0900271106
Denise J. Cai, Sarnoff A. Mednick, Elizabeth M. Harrison, Jennifer C. Kanady, and Sara C. Mednick
www.pnas.org/cgi/doi/10.1073/pnas.0900271106
Denise J. Cai, Sarnoff A. Mednick, Elizabeth M. Harrison, Jennifer C. Kanady, and Sara C. Mednick
The hypothesized role of rapid eye movement (REM) sleep, which is rich in dreams, in the formation of new associations, has remained anecdotal. We examined the role of REM on creative problem solving, with the Remote Associates Test (RAT). Using a nap paradigm, we manipulated various conditions of prior exposure to elements of a creative problem. Compared with quiet rest and non-REM sleep, REM enhanced the formation of associative networks and the integration of unassociated information. Furthermore, these REM sleep benefits were not the result of an improved memory for the primed items. This study shows that compared with quiet rest and non-REM sleep, REM enhances the integration of unassociated information for creative problem solving, a process, we hypothesize, that is facilitated by cholinergic and noradrenergic neuromodulation during REM sleep.
False Memory Formation
The role of sleep in false memory formation
Neurobiology of Learning and Memory (2009), doi:10.1016/j.nlm.2009.03.007
Jessica D. Payne, Daniel L. Schacter, Ruth E. Propper, Li-Wen Huang, Erin J. Wamsley, Matthew A. Tucker, Matthew P. Walker, Robert Stickgold
Memories are not stored as exact copies of our experiences. As a result, remembering is subject not only to memory failure, but to inaccuracies and distortions as well. Although such distortions are often retained or even enhanced over time, sleep’s contribution to the development of false memories is unknown. Here, we report that a night of sleep increases both veridical and false recall in the Deese– Roediger–McDermott (DRM) paradigm, compared to an equivalent period of daytime wakefulness. But while veridical memory deteriorates across both wake and sleep, false memories are preferentially preserved by sleep, actually showing a non-significant improvement. The same selectivity of false over veridical memories was observed in a follow-up nap study. Unlike previous studies implicating deep, slow wave sleep (SWS) in declarative memory consolidation, here veridical recall correlated with decreased
SWS, a finding that was observed in both the overnight and nap studies. These findings lead to two counter intuitive conclusions – that under certain circumstances sleep can promote false memories over veridical ones, and SWS can be associated with impairment rather than facilitation of declarative memory consolidation. While these effects produce memories that are less accurate after sleep, these memories may, in the end, be more useful.
Neurobiology of Learning and Memory (2009), doi:10.1016/j.nlm.2009.03.007
Jessica D. Payne, Daniel L. Schacter, Ruth E. Propper, Li-Wen Huang, Erin J. Wamsley, Matthew A. Tucker, Matthew P. Walker, Robert Stickgold
Memories are not stored as exact copies of our experiences. As a result, remembering is subject not only to memory failure, but to inaccuracies and distortions as well. Although such distortions are often retained or even enhanced over time, sleep’s contribution to the development of false memories is unknown. Here, we report that a night of sleep increases both veridical and false recall in the Deese– Roediger–McDermott (DRM) paradigm, compared to an equivalent period of daytime wakefulness. But while veridical memory deteriorates across both wake and sleep, false memories are preferentially preserved by sleep, actually showing a non-significant improvement. The same selectivity of false over veridical memories was observed in a follow-up nap study. Unlike previous studies implicating deep, slow wave sleep (SWS) in declarative memory consolidation, here veridical recall correlated with decreased
SWS, a finding that was observed in both the overnight and nap studies. These findings lead to two counter intuitive conclusions – that under certain circumstances sleep can promote false memories over veridical ones, and SWS can be associated with impairment rather than facilitation of declarative memory consolidation. While these effects produce memories that are less accurate after sleep, these memories may, in the end, be more useful.
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