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Characterization of the signaling pathways that produce nociceptor sensitization in Drosophila

Award Number: R15NS095195
ORGANIZATION: NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 09/30/2015
PERIOD OF PERFORMANCE END DATE: 06/30/2023

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Characterization of the signaling pathways that produce nociceptor sensitization in Drosophila - Normal pain promotes health by warning us of potential tissue damage, but abnormal pain reduces the quality of life for millions around the world. Pain sensitization after injury also promotes health by reducing re-injury during healing. Some types of abnormal pain, including chronic pain, result from dysregulation of the pain sensitization system. Available treatment for chronic pain is inadequate, in part because the deleterious side effects of our best analgesics, the opioids, are made more hazardous by longer use. Better treatments for abnormal pain are badly needed. We propose to reveal novel targets for pain medications by exploiting the powerful genetic toolkit of the Drosophila model. When the fruit fly larva is injured by a controlled dose of ultraviolet (UV) radiation, the animal exhibits allodynia, a manifestation of nociceptive sensitization. This means that the injured animal will react with a nocifensive avoidance behavior in the form of an unmistakable corkscrew roll, in response to a thermal stimulus that most uninjured animals find innocuous. This injury induced sensitization paradigm has previously been used to demonstrate that the nociceptor neuron requires signaling by the Bone Morphogenetic Proteins (BMP) pathway to produce allodynia. BMP signaling components in the fly are very similar to their mammalian orthologs. Preliminary results indicate that a transcriptional and translational response is necessary in the nociceptor neurons in order to produce allodynia following injury. Aim 1 will examine the necessity of a set of BMP related transcriptional regulators like brinker, yorkie and bantam. This will be accomplished by targeting an RNAi silencing construct of each gene specifically to the nociceptor neurons using the Gal4/UAS system. Aim 2 will bring additional BMP pathway and other components to light by identifying transcriptional and translationally regulated genes, again using Gal4/UAS gene targeting, ribosome-tagging and immunopurification tools, RNA sequencing and bioinformatics. Aim 3 will begin to translate the discoveries made in Drosophila into mammalian systems by testing BMP pathway inhibiting drugs for efficacy in providing relief from injury-induced pain sensitization. The proposed studies have the potential to identify all components regulated by transcription and translation in the signaling pathways required for allodynia. Because of the high degree of functional conservation between fly and mammalian BMPs, components identified by these experiments may represent targets for novel medications for the treatment of abnormal pain in humans.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2024 ( Subtotal = -$4,076 )
2024	2020	UNIVERSITY OF NEW ENGLAND	11 HILLS BEACH RD	BIDDEFORD	ME	04005	YORK	USA	Extramural Research Programs in the Neurosciences and Neurological Disorders	000	2	2/27/2024	COMPETING CONTINUATION	-$4,076
														Subtotal = -$4,076

Issue Date FY: 2021 ( Subtotal = $0 )
2021	2015	UNIVERSITY OF NEW ENGLAND	11 HILLS BEACH RD	BIDDEFORD	ME	04005	YORK	USA	Extramural Research Programs in the Neurosciences and Neurological Disorders	000	1	10/1/2020	NEW	$0
2021	2015	UNIVERSITY OF NEW ENGLAND	11 HILLS BEACH RD	BIDDEFORD	ME	04005	YORK	USA	Extramural Research Programs in the Neurosciences and Neurological Disorders	001	1	10/3/2020	NEW	$0
2021	2015	UNIVERSITY OF NEW ENGLAND	11 HILLS BEACH RD	BIDDEFORD	ME	04005	YORK	USA	Extramural Research Programs in the Neurosciences and Neurological Disorders	002	1	10/3/2020	NEW	$0
														Subtotal = $0

Issue Date FY: 2020 ( Subtotal = $423,926 )
2020	2020	UNIVERSITY OF NEW ENGLAND	11 HILLS BEACH RD	BIDDEFORD	ME	04005	YORK	USA	Extramural Research Programs in the Neurosciences and Neurological Disorders	001	2	6/5/2020	COMPETING CONTINUATION	$437,164
2020	2020	UNIVERSITY OF NEW ENGLAND	11 HILLS BEACH RD	BIDDEFORD	ME	04005	YORK	USA	Extramural Research Programs in the Neurosciences and Neurological Disorders	002	2	6/10/2020	COMPETING CONTINUATION	-$11,164
2020	2015	UNIVERSITY OF NEW ENGLAND	11 HILLS BEACH RD	BIDDEFORD	ME	04005	YORK	USA	Extramural Research Programs in the Neurosciences and Neurological Disorders	000	1	3/25/2020	NEW	-$2,074
														Subtotal = $423,926

Issue Date FY: 2015 ( Subtotal = $443,490 )
2015	2015	UNIVERSITY OF NEW ENGLAND	11 HILLS BEACH ROAD	BIDDEFORD	ME	04005	YORK	USA	Extramural Research Programs in the Neurosciences and Neurological Disorders	000	1	9/18/2015	NEW	$443,490
														Subtotal = $443,490

Grand Total All Awards = $863,340

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Characterization of the signaling pathways that produce nociceptor sensitization in Drosophila

Award Number: R15NS095195

ORGANIZATION: NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 09/30/2015

PERIOD OF PERFORMANCE END DATE: 06/30/2023

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