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"Vecsey, Christopher"
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High-Resolution Positional Tracking for Long-Term Analysis of Drosophila Sleep and Locomotion Using the “Tracker” Program
Drosophila melanogaster has been used for decades in the study of circadian behavior, and more recently has become a popular model for the study of sleep. The classic method for monitoring fly activity involves counting the number of infrared beam crosses in individual small glass tubes. Incident recording methods such as this can measure gross locomotor activity, but they are unable to provide details about where the fly is located in space and do not detect small movements (i.e. anything less than half the enclosure size), which could lead to an overestimation of sleep and an inaccurate report of the behavior of the fly. This is especially problematic if the fly is awake, but is not moving distances that span the enclosure. Similarly, locomotor deficiencies could be incorrectly classified as sleep phenotypes. To address these issues, we have developed a locomotor tracking technique (the \"Tracker\" program) that records the exact location of a fly in real time. This allows for the detection of very small movements at any location within the tube. In addition to circadian locomotor activity, we are able to collect other information, such as distance, speed, food proximity, place preference, and multiple additional parameters that relate to sleep structure. Direct comparisons of incident recording and our motion tracking application using wild type and locomotor-deficient (CASK-β null) flies show that the increased temporal resolution in the data from the Tracker program can greatly affect the interpretation of the state of the fly. This is especially evident when a particular condition or genotype has strong effects on the behavior, and can provide a wealth of information previously unavailable to the investigator. The interaction of sleep with other behaviors can also be assessed directly in many cases with this method.
Journal Article
Sleep deprivation impairs cAMP signalling in the hippocampus
Lost sleep, found memories
It is well known that sleep deprivation can have cognitive consequences, including learning and memory deficits, but the mechanisms by which sleep deprivation affects brain function remain unknown. New experiments identify the cyclic AMP pathway as a functional target of sleep deprivation, specifically the impairment of cAMP/PKA-based plasticity in the hippocampus. Rescuing cAMP signalling using phosphodiesterase inhibitors also rescues the memory deficits, pointing to cAMP/PKA signalling enhancers as a possible therapeutic approach to counteract the cognitive effects of lost sleep.
Sleep deprivation can have adverse cognitive effects, with one of the major consequences on the brain being memory deficits in learning models that are dependent on the hippocampus. A molecular mechanism by which brief sleep deprivation alters hippocampal function is now identified in mice; it involves the impairment of cyclic-AMP- and protein-kinase-A-dependent forms of synaptic plasticity.
Millions of people regularly obtain insufficient sleep
1
. Given the effect of sleep deprivation on our lives, understanding the cellular and molecular pathways affected by sleep deprivation is clearly of social and clinical importance. One of the major effects of sleep deprivation on the brain is to produce memory deficits in learning models that are dependent on the hippocampus
2
,
3
,
4
,
5
. Here we have identified a molecular mechanism by which brief sleep deprivation alters hippocampal function. Sleep deprivation selectively impaired 3′, 5′-cyclic AMP (cAMP)- and protein kinase A (PKA)-dependent forms of synaptic plasticity
6
in the mouse hippocampus, reduced cAMP signalling, and increased activity and protein levels of phosphodiesterase 4 (PDE4), an enzyme that degrades cAMP. Treatment of mice with phosphodiesterase inhibitors rescued the sleep-deprivation-induced deficits in cAMP signalling, synaptic plasticity and hippocampus-dependent memory. These findings demonstrate that brief sleep deprivation disrupts hippocampal function by interfering with cAMP signalling through increased PDE4 activity. Thus, drugs that enhance cAMP signalling may provide a new therapeutic approach to counteract the cognitive effects of sleep deprivation.
Journal Article
Differential regulation of sleep by blue, green, and red light in Drosophila melanogaster
Exposure to blue-enriched light from electronic devices is an emergent disruptor of human sleep, especially at particular times of day. Further dissection of this phenomenon necessitates modeling in a tractable model organism.
Thus, we investigated the effects of light color on sleep in
. We measured sleep in red-eyed Canton-S (CS) and white-eyed
flies in baseline 12:12 light/dark conditions and experimental conditions with light-color (blue, red, or green) exposure for all 12 h of daylight or 3 h in the morning or evening.
Blue light reduced daytime and nighttime sleep in CS but not in
, potentially indicating a role for the compound eye in blue light's effects on fruit fly sleep. Red light, especially in the evening, reduced sleep during exposure in both strains. Green light had minimal effects on sleep in CS flies, but evening exposure reduced sleep in
flies, mimicking red light's effects.
In conclusion, light's effects on sleep in
are dependent on wavelength and time-of-day. Future studies will aim to dissect these mechanisms genetically.
Journal Article
The Roles of Discrete Populations of Neurons Expressing Short Neuropeptide F in Sleep Induction in Drosophila melanogaster
ABSTRACT
Sleep is of vital importance in our lives, yet we are far from understanding the neuronal networks that control the amount and timing of sleep. There is substantial conservation of known sleep‐regulating transmitters, allowing for studies in simpler organisms to lead the way in gaining insight into the organization of sleep control circuits. In Drosophila melanogaster, we recently showed that optogenetic activation of neurons that produce the neuropeptide Y (NPY)‐related transmitter short neuropeptide F (sNPF) increases time spent asleep. However, sNPF is expressed in several neuronal populations, and thus it is unknown which of those populations play roles in the sleep‐promoting effect. In this study, we addressed this issue using a genetic approach to limit optogenetic activation to subsets of sNPF‐expressing neurons. We found that sleep promotion was shorter‐lived when cryptochrome (CRY)‐positive neurons were excluded from being activated. Pigment‐dispersing factor (PDF) neurons were not required for sleep promotion, nor were mushroom body (MB) neurons. Acute reactions to a short, 10‐s period of optogenetic activation were largely unchanged by excluding activation of the three neuronal populations mentioned above. Together, these results suggest that clock neurons that are CRY‐positive and PDF‐negative are important contributors to the long‐lasting sleep promotion produced by sNPF neuron activation. However, other neurons targeted by the sNPF‐GAL4 driver appear to mediate the more rapid behavioral responses. Future studies will seek to identify these additional sNPF neuron populations and to determine how sNPF‐expressing clock neurons act in concert with other neuronal circuits to promote sleep.
Graphical
It is critical to understand how sleep is regulated. Short neuropeptide F (sNPF) neurons have been shown to regulate sleep in the fruit fly, Drosophila melanogaster. In this study, we found that a subset of sNPF neurons that express cryptochrome but not pigment dispersing factor play an important role in driving long‐lasting increases in sleep induced when sNPF neurons are activated.
Journal Article
Jews and Judaism in the New York Times
In a recent book, Following 9/11: Religion Coverage in the New York Times, Christopher Vecsey examines journalistic definitions of “religion,” before and (especially) after the terrible events of September 11, 2001. Here he explores Times portrayals of the cumulative religious tradition called Judaism, embodied by peoples who have called themselves Jews—from antiquity to modernity, throughout the world, and especially in the United States, where a plurality of Jews live today and where the Times is published. To understand Judaism today is to fathom its diverse texts, beliefs, rituals, ethics, and institutions, the contemporary concerns of Jews, and the relationships not only among Jews, but also between Jews and gentiles, and the continuing impact of anti-Semitism upon Jewish life. Since the 1940s, Jews and Judaism have been profoundly affected by the horrific course of the Holocaust, and by the formation of Israel as a Jewish nation-state. These have been the major themes in the Times' treatment of Judaism—chronicled in thousands of articles. Like an insider to Jewish tradition, the paper recounts favorite holy day recipes and tales of survival and travail in a multi-national and assimilative world. In so doing, however, the paper probes not only concurrence within Judaism, but more tellingly, a complex, multi-cultural, at-odds-with-itself Jewishness. Rather than thinking of the Times as a mouthpiece for Jewish interests, it is far more accurate to say that the Times has analyzed, like an outsider, the paradoxes, the tensions, and the culture wars in contemporary Jewish existence, in order to define pluralistic Judaism as a political, cultural, religious entity. The Times treats Judaism humanistically, showing that it is the Jewish people who are most important to Judaism, not merely the texts, the theology, or the institutions. The paper works from perspectival Talmudic principles, reporting multiple viewpoints in the circle of Jewish faith, observance, contestation, and disbelief, constantly questioning all sources, as an observant instrument of inquiry into Jewish existence, to expose Judaism's points of conflict as well as its areas of consensus.
eBook
hkb is required for DIP-α expression and target recognition in the Drosophila neuromuscular circuit
Our nervous system contains billions of neurons that form precise connections with each other through interactions between cell surface proteins. In
Drosophila
, the Dpr and DIP immunoglobulin protein subfamilies form homophilic or heterophilic interactions to instruct synaptic connectivity, synaptic growth, and cell survival. However, the upstream regulatory mechanisms of Dprs and DIPs are not clear. On the other hand, while transcription factors have been implicated in target recognition, their downstream cell surface proteins remain mostly unknown. We conduct an F1 dominant modifier genetic screen to identify regulators of Dprs and DIPs. We identify
huckebein
(
hkb
), a transcription factor previously implicated in target recognition of the dorsal Is motor neuron. We show that
hkb
genetically interacts with
DIP-α
and loss of
hkb
leads to complete removal of
DIP-α
expression specifically in dorsal Is motor neurons. We then confirm that this specificity is through the dorsal Is motor neuron specific transcription factor,
even-skipped
(
eve
), which acts downstream of
hkb
. Analysis of the genetic interaction between
hkb
and
eve
reveals that they act in the same pathway to regulate dorsal Is motor neuron connectivity. Our study provides insight into the transcriptional regulation of
DIP-α
and suggests that distinct regulatory mechanisms exist for the same CSP in different neurons.
A dominate modifier screen in
Drosophila
identifies transcriptional regulators that control expression of DIP-α, a cell surface protein, and synaptic target recognition in the neuromuscular system.
Journal Article
