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Article ; Online: Caffeine Delays Ethanol-Induced Sedation in Drosophila

Tremblay, Sonia / Zeng, Yanqiqi / Yue, Aixin / Chabot, Kiana / Mynahan, Abigail / Desrochers, Stephanie / Bridges, Sarra / Ahmad, S. Tariq

Biology (Basel). 2022 Dec. 30, v. 12, no. 1

2022

Abstract: Caffeine and ethanol are among the most widely available and commonly consumed psychoactive substances. Both interact with adenosine receptor-mediated signaling which regulates numerous neurological processes including sleep and waking behaviors. In ... ...

Abstract	Caffeine and ethanol are among the most widely available and commonly consumed psychoactive substances. Both interact with adenosine receptor-mediated signaling which regulates numerous neurological processes including sleep and waking behaviors. In mammals, caffeine is an adenosine receptor antagonist and thus acts as a stimulant. Conversely, ethanol is a sedative because it promotes GABAergic neurotransmission, inhibits glutamatergic neurotransmission, and increases the amount of adenosine in the brain. Despite seemingly overlapping interactions, not much is known about the effect of caffeine on ethanol-induced sedation in Drosophila. In this study, using Drosophila melanogaster as a model, we show that caffeine supplementation in food delays the onset of ethanol-induced sedation in males and females of different strains. The resistance to sedation reverses upon caffeine withdrawal. Heterozygous adenosine receptor mutant flies are resistant to sedation. These findings suggest that caffeine and adenosine receptors modulate the sedative effects of ethanol in Drosophila.
Keywords	Drosophila melanogaster ; adenosine ; antagonists ; brain ; caffeine ; ethanol ; heterozygosity ; models ; mutants ; purinergic receptors ; sedation ; sedatives ; sleep ; synaptic transmission
Language	English
Dates of publication	2022-1230
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article ; Online
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology12010063
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: The role of CHMP2B

Krasniak, Christopher S / Ahmad, S Tariq

Brain research

2016 Volume 1649, Issue Pt B, Page(s) 151–157

Abstract: Charged multivesicular body protein 2B (CHMP2B) - a component of the endosomal complex required for transport-III (ESCRT-III) - is responsible for the vital membrane deformation functions in autophagy and endolysosomal trafficking. A dominant mutation in ...

Abstract	Charged multivesicular body protein 2B (CHMP2B) - a component of the endosomal complex required for transport-III (ESCRT-III) - is responsible for the vital membrane deformation functions in autophagy and endolysosomal trafficking. A dominant mutation in CHMP2B (CHMP2B
MeSH term(s)	Animals ; Autophagy/genetics ; Endosomal Sorting Complexes Required for Transport/chemistry ; Endosomal Sorting Complexes Required for Transport/genetics ; Endosomal Sorting Complexes Required for Transport/physiology ; Frontotemporal Dementia/genetics ; Frontotemporal Dementia/physiopathology ; Humans ; Mice ; Mutation ; Neurons/physiology
Chemical Substances	CHMP2B protein, human ; Endosomal Sorting Complexes Required for Transport
Language	English
Publishing date	2016-10-15
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	1200-2
ISSN	1872-6240 ; 0006-8993
ISSN (online)	1872-6240
ISSN	0006-8993
DOI	10.1016/j.brainres.2016.02.051
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Article ; Online: Molecular Genetics of Frontotemporal Dementia Elucidated by

Vandal, Sarah E / Zheng, Xiaoyue / Ahmad, S Tariq

International journal of molecular sciences

2018 Volume 19, Issue 6

Abstract: Frontotemporal dementia (FTD) is the second most common senile neurodegenerative disease. FTD is a heterogeneous disease that can be classified into several subtypes. A mutation ... ...

Abstract	Frontotemporal dementia (FTD) is the second most common senile neurodegenerative disease. FTD is a heterogeneous disease that can be classified into several subtypes. A mutation in
MeSH term(s)	Animals ; Disease Models, Animal ; Drosophila melanogaster/genetics ; Endosomes/metabolism ; Frontotemporal Dementia/genetics ; Humans ; Lysosomes/metabolism ; Mutation/genetics
Language	English
Publishing date	2018-06-09
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms19061714
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Article: Caffeine Delays Ethanol-Induced Sedation in

Tremblay, Sonia / Zeng, Yanqiqi / Yue, Aixin / Chabot, Kiana / Mynahan, Abigail / Desrochers, Stephanie / Bridges, Sarra / Ahmad, S Tariq

Biology

2022 Volume 12, Issue 1

Abstract	Caffeine and ethanol are among the most widely available and commonly consumed psychoactive substances. Both interact with adenosine receptor-mediated signaling which regulates numerous neurological processes including sleep and waking behaviors. In mammals, caffeine is an adenosine receptor antagonist and thus acts as a stimulant. Conversely, ethanol is a sedative because it promotes GABAergic neurotransmission, inhibits glutamatergic neurotransmission, and increases the amount of adenosine in the brain. Despite seemingly overlapping interactions, not much is known about the effect of caffeine on ethanol-induced sedation in
Language	English
Publishing date	2022-12-30
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology12010063
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Mutations in the circadian gene period alter behavioral and biochemical responses to ethanol in Drosophila.

Liao, Jennifer / Seggio, Joseph A / Ahmad, S Tariq

Behavioural brain research

2016 Volume 302, Page(s) 213–219

Abstract: Clock genes, such as period, which maintain an organism's circadian rhythm, can have profound effects on metabolic activity, including ethanol metabolism. In turn, ethanol exposure has been shown in Drosophila and mammals to cause disruptions of the ... ...

Abstract	Clock genes, such as period, which maintain an organism's circadian rhythm, can have profound effects on metabolic activity, including ethanol metabolism. In turn, ethanol exposure has been shown in Drosophila and mammals to cause disruptions of the circadian rhythm. Previous studies from our labs have shown that larval ethanol exposure disrupted the free-running period and period expression of Drosophila. In addition, a recent study has shown that arrhythmic flies show no tolerance to ethanol exposure. As such, Drosophila period mutants, which have either a shorter than wild-type free-running period (perS) or a longer one (perL), may also exhibit altered responses to ethanol due to their intrinsic circadian differences. In this study, we tested the initial sensitivity and tolerance of ethanol exposure on Canton-S, perS, and perL, and then measured their Alcohol Dehydrogenase (ADH) and body ethanol levels. We showed that perL flies had slower sedation rate, longer recovery from ethanol sedation, and generated higher tolerance for sedation upon repeated ethanol exposure compared to Canton-S wild-type flies. Furthermore, perL flies had lower ADH activity and had a slower ethanol clearance compared to wild-type flies. The findings of this study suggest that period mutations influence ethanol induced behavior and ethanol metabolism in Drosophila and that flies with longer circadian periods are more sensitive to ethanol exposure.
MeSH term(s)	Age Factors ; Alcohol Dehydrogenase/metabolism ; Analysis of Variance ; Animals ; Animals, Genetically Modified ; Central Nervous System Depressants/pharmacology ; Circadian Rhythm/drug effects ; Circadian Rhythm/physiology ; Drosophila ; Drosophila Proteins/genetics ; Drug Tolerance ; Ethanol/pharmacology ; Male ; Period Circadian Proteins/genetics ; Period Circadian Proteins/metabolism ; Reaction Time/drug effects ; Reaction Time/genetics
Chemical Substances	Central Nervous System Depressants ; Drosophila Proteins ; Period Circadian Proteins ; Ethanol (3K9958V90M) ; Alcohol Dehydrogenase (EC 1.1.1.1)
Language	English
Publishing date	2016-04-01
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	449927-x
ISSN	1872-7549 ; 0166-4328
ISSN (online)	1872-7549
ISSN	0166-4328
DOI	10.1016/j.bbr.2016.01.041
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Article: The Drosophila apterous56f mutation impairs circadian locomotor activity

Kohiyama, Mayumi / Bonser, Danielle / Leung, Lisa / Fall, Alexandra / Canada, Nathan / Qu, Boyang / Ahmad, S. Tariq / Possidente, Bernard

Biological rhythm research. 2019 May 4, v. 50, no. 3

2019

Abstract: We investigated effects of apterous mutation ap56f on circadian locomotor activity, eclosion rhythms, and transcript levels of period and timeless in Drosophila. We investigated circadian locomotor activity and eclosion rhythms in ap56f and wild-type ... ...

Abstract	We investigated effects of apterous mutation ap56f on circadian locomotor activity, eclosion rhythms, and transcript levels of period and timeless in Drosophila. We investigated circadian locomotor activity and eclosion rhythms in ap56f and wild-type flies, their F1 and F2 offspring, and wingless vestigial mutants and show that ap56f disrupts circadian locomotor rhythms in a genetically recessive manner, that is not caused by the absence of wings. The apblt strain also showed impaired circadian activity rhythms, providing independent evidence for a significant role of apterous in circadian locomotor rhythm expression. The ap56f mutation did not disrupt a circadian eclosion rhythm or rhythmic expression of the period and timeless clock genes, indicating that apterous is not essential for circadian clock function, but is necessary for coupling locomotor activity to a circadian clock. Timeless transcription was reduced in ap56f flies in 12:12 LD, suggesting that apterous may modulate core clock gene expression.
Keywords	Drosophila ; circadian clocks ; eclosion ; gene expression ; genes ; locomotion ; messenger RNA ; mutants ; mutation ; progeny ; transcription (genetics) ; wings
Language	English
Dates of publication	2019-0504
Size	p. 375-388.
Publishing place	Taylor & Francis
Document type	Article
ZDB-ID	1185065-6
ISSN	1744-4179 ; 0929-1016
ISSN (online)	1744-4179
ISSN	0929-1016
DOI	10.1080/09291016.2018.1447353
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Methods to characterize spontaneous and startle-induced locomotion in a rotenone-induced Parkinson's disease model of Drosophila.

Liao, Jennifer / Morin, Laura W / Ahmad, S Tariq

Journal of visualized experiments : JoVE

2014 , Issue 90

Abstract: Parkinson's disease is a neurodegenerative disorder that results from the degeneration of dopaminergic neurons in the central nervous system, primarily in the substantia nigra. The disease causes motor deficiencies, which present as rigidity, tremors and ...

Abstract	Parkinson's disease is a neurodegenerative disorder that results from the degeneration of dopaminergic neurons in the central nervous system, primarily in the substantia nigra. The disease causes motor deficiencies, which present as rigidity, tremors and dementia in humans. Rotenone is an insecticide that causes oxidative damage by inhibiting the function of the electron transport chain in mitochondria. It is also used to model Parkinson's disease in the Drosophila. Flies have an inherent negative geotactic response, which compels them to climb upwards upon being startled. It has been established that rotenone causes early mortality and locomotion defects that disrupt the flies' ability to climb after they have been tapped downwards. However, the effect of rotenone on spontaneous movement is not well documented. This study outlines two sensitive, reproducible, and high throughput assays to characterize rotenone-induced deficiencies in short-term startle-induced locomotion and long-term spontaneous locomotion in Drosophila. These assays can be conveniently adapted to characterize other Drosophila models of locomotion defects and efficacy of therapeutic agents.
MeSH term(s)	Animals ; Disease Models, Animal ; Drosophila ; Locomotion/physiology ; Male ; Parkinson Disease/physiopathology ; Reflex, Startle/physiology ; Rotenone
Chemical Substances	Rotenone (03L9OT429T)
Language	English
Publishing date	2014-08-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Video-Audio Media
ZDB-ID	2259946-0
ISSN	1940-087X ; 1940-087X
ISSN (online)	1940-087X
ISSN	1940-087X
DOI	10.3791/51625
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Article: Methods to characterize spontaneous and startle-induced locomotion in a rotenone-induced parkinson's disease model of Drosophila

Liao, Jennifer / Morin, Laura W / Ahmad, S. Tariq

Journal of visualized experiments. 2014 Aug. 17, , no. 90

2014

Abstract: Parkinson’s disease is a neurodegenerative disorder that results from the degeneration of dopaminergic neurons in the central nervous system, primarily in the substantia nigra. The disease causes motor deficiencies, which present as rigidity, tremors and ...

Abstract	Parkinson’s disease is a neurodegenerative disorder that results from the degeneration of dopaminergic neurons in the central nervous system, primarily in the substantia nigra. The disease causes motor deficiencies, which present as rigidity, tremors and dementia in humans. Rotenone is an insecticide that causes oxidative damage by inhibiting the function of the electron transport chain in mitochondria. It is also used to model Parkinson’s disease in the Drosophila. Flies have an inherent negative geotactic response, which compels them to climb upwards upon being startled. It has been established that rotenone causes early mortality and locomotion defects that disrupt the flies’ ability to climb after they have been tapped downwards. However, the effect of rotenone on spontaneous movement is not well documented. This study outlines two sensitive, reproducible, and high throughput assays to characterize rotenone-induced deficiencies in short-term startle-induced locomotion and long-term spontaneous locomotion in Drosophila. These assays can be conveniently adapted to characterize other Drosophila models of locomotion defects and efficacy of therapeutic agents.
Keywords	Drosophila ; Parkinson disease ; central nervous system ; dementia ; disease models ; electron transport chain ; geotaxis ; humans ; insecticides ; locomotion ; mitochondria ; mortality ; neurons ; rotenone ; therapeutics
Language	English
Dates of publication	2014-0817
Size	p. e51625.
Publishing place	Journal of Visualized Experiments
Document type	Article
ZDB-ID	2259946-0
ISSN	1940-087X
ISSN	1940-087X
DOI	10.3791/51625
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Expression of mutant CHMP2B linked to neurodegeneration in humans disrupts circadian rhythms in

Lee, DaWon / Zheng, Xiaoyue / Shigemori, Kay / Krasniak, Christopher / Bin Liu, Jie / Tang, Chao / Kavaler, Joshua / Ahmad, S Tariq

FASEB bioAdvances

2019 Volume 1, Issue 8, Page(s) 511–520

Abstract: Mutations in CHMP2B, an ESCRT-III (endosomal sorting complexes required for transport) component, are associated with frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS). Neurodegenerative disorders including FTD are also associated ... ...

Abstract	Mutations in CHMP2B, an ESCRT-III (endosomal sorting complexes required for transport) component, are associated with frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS). Neurodegenerative disorders including FTD are also associated with a disruption in circadian rhythms, but the mechanism underlying this defect is not well understood. Here, we ectopically expressed the human CHMP2B variant associated with FTD (CHMP2B
Language	English
Publishing date	2019-07-11
Publishing country	United States
Document type	Journal Article
ISSN	2573-9832
ISSN (online)	2573-9832
DOI	10.1096/fba.2019-00042
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Article ; Online: Larval ethanol exposure alters adult circadian free-running locomotor activity rhythm in Drosophila melanogaster.

Seggio, Joseph A / Possidente, Bernard / Ahmad, S Tariq

Chronobiology international

2012 Volume 29, Issue 1, Page(s) 75–81

Abstract: Alcohol consumption causes disruptions in a variety of daily rhythms, including the sleep-wake cycle. Few studies have explored the effect of alcohol exposure only during developmental stages preceding maturation of the adult circadian clock, and none ... ...

Abstract	Alcohol consumption causes disruptions in a variety of daily rhythms, including the sleep-wake cycle. Few studies have explored the effect of alcohol exposure only during developmental stages preceding maturation of the adult circadian clock, and none have examined the effects of alcohol on clock function in Drosophila. This study investigates developmental and behavioral correlates between larval ethanol exposure and the adult circadian clock in Drosophila melanogaster, a well-established model for studying circadian rhythms and effects of ethanol exposure. We reared Drosophila larvae on 0%, 10%, or 20% ethanol-supplemented food and assessed effects upon eclosion and the free-running period of the circadian rhythm of locomotor activity. We observed a dose-dependent effect of ethanol on period, with higher doses resulting in shorter periods. We also identified the third larval instar stage as a critical time for the developmental effects of 10% ethanol on circadian period. These results demonstrate that developmental ethanol exposure causes sustainable shortening of the adult free-running period in Drosophila melanogaster, even after adult exposure to ethanol is terminated, and suggests that the third instar is a sensitive time for this effect.
MeSH term(s)	Alcohol Drinking/adverse effects ; Animals ; Biological Clocks/drug effects ; Central Nervous System Depressants/pharmacology ; Circadian Rhythm/drug effects ; Darkness ; Dose-Response Relationship, Drug ; Drosophila melanogaster/drug effects ; Drosophila melanogaster/embryology ; Ethanol/pharmacology ; Gene Expression Regulation, Developmental ; Larva/drug effects ; Light ; Models, Biological ; Movement ; Running ; Time Factors
Chemical Substances	Central Nervous System Depressants ; Ethanol (3K9958V90M)
Language	English
Publishing date	2012-02
Publishing country	England
Document type	Journal Article
ZDB-ID	998996-1
ISSN	1525-6073 ; 0742-0528
ISSN (online)	1525-6073
ISSN	0742-0528
DOI	10.3109/07420528.2011.635236
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