Source 1primary paper2014PLoS ONE
Toolkit/light-dark masking paradigm
light-dark masking paradigm
Taxonomy: Technique Branch / Method. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
The light-dark masking paradigm is a functional assay used in MPTP-treated non-human primates to test how environmental light and darkness acutely shape daily rest-wake and locomotor activity expression. In the cited study, it showed that expression of daily rest-wake activity in dopamine-depleted monkeys requires the stimulatory and inhibitory effects of light and darkness.
Usefulness & Problems
Why this is useful
This assay is useful for separating light-driven masking effects on behavior from endogenous rhythmic outputs in a dopamine-depleted primate model. The cited work used light-dark versus constant-light conditions to reveal that locomotor/rest-wake expression is strongly dependent on environmental photic context even when hormonal rhythmicity remains preserved.
Problem solved
It addresses the problem of determining whether altered daily activity patterns after dopamine depletion reflect defective behavioral expression under photic conditions rather than a global loss of rhythmic physiology. In the cited MPTP non-human primate study, constant light exposed severe disruption or abolition of locomotor rhythms, whereas hormonal rhythms retained amplitude and phase relationships.
Problem links
Need conditional recombination or state switching
DerivedThe light-dark masking paradigm is a functional assay method used in MPTP-treated non-human primates to test how environmental light and darkness shape daily rest-wake and locomotor activity expression. In the cited study, it showed that expression of daily rest-wake activity in dopamine-depleted monkeys requires the stimulatory and inhibitory effects of light and darkness.
Need precise spatiotemporal control with light input
DerivedThe light-dark masking paradigm is a functional assay method used in MPTP-treated non-human primates to test how environmental light and darkness shape daily rest-wake and locomotor activity expression. In the cited study, it showed that expression of daily rest-wake activity in dopamine-depleted monkeys requires the stimulatory and inhibitory effects of light and darkness.
Taxonomy & Function
Primary hierarchy
Technique Branch
Method: A concrete measurement method used to characterize an engineered system.
Mechanisms
environmental entrainment/challenge with light versus constant lightenvironmental light challenge under constant lightphotic masking of locomotor and rest-wake behaviorphotic masking of locomotor/rest-wake behaviorTechniques
Functional AssayTarget processes
recombinationInput: Light
Implementation Constraints
cofactor dependency: cofactor requirement unknownencoding mode: genetically encodedimplementation constraint: context specific validationimplementation constraint: spectral hardware requirementoperating role: sensor
Implementation in the cited work involves environmental manipulation with light-dark conditions and constant light to assess locomotor/rest-wake and hormonal rhythmic outputs in MPTP-treated non-human primates. Dopamine degeneration in that study was characterized independently by in vivo PET with [(11)C]-PE2I and post-mortem tyrosine hydroxylase and dopamine transporter quantification.
The available evidence is limited to a single study in MPTP-treated non-human primates, so generalizability beyond this model is not established. The supplied evidence does not provide detailed assay parameters such as light intensity, spectral composition, timing schedule, or quantitative performance metrics.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Supporting Sources
Ranked Claims
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
Approval Evidence
1 source4 linked approval claimsfirst-pass slug light-dark-masking-paradigm
Use of a light-dark masking paradigm shows that expression of daily rest-wake activity in MPTP monkeys requires the stimulatory and inhibitory effects of light and darkness.
Source:
circadian challenge responsesupports
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Source:
hormonal rhythm observationsupports
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Source:
mechanistic interpretationsupports
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Source:
phenotype differencesupports
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
Source:
Comparisons
Source-backed strengths
The paradigm functionally challenges the rest-wake/locomotor system with defined lighting environments and can reveal dissociation between behavioral and hormonal rhythmic outputs. In the cited study, it detected severe locomotor rhythm disruption under constant light in dopamine-depleted primates while controls retained free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
Compared with Cas12aVIP
light-dark masking paradigm and Cas12aVIP address a similar problem space because they share recombination.
Shared frame: same top-level item type; shared target processes: recombination; same primary input modality: light
Compared with droplet microfluidic platform
light-dark masking paradigm and droplet microfluidic platform address a similar problem space because they share recombination.
Shared frame: same top-level item type; shared target processes: recombination; same primary input modality: light
Compared with open-source microplate reader
light-dark masking paradigm and open-source microplate reader address a similar problem space because they share recombination.
Shared frame: same top-level item type; shared target processes: recombination; same primary input modality: light
Ranked Citations
- 1.