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Mitochondrial Regulation of Nociceptor Function

Award Number: R01NS131571
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: 02/15/2023
PERIOD OF PERFORMANCE END DATE: 01/31/2028

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Mitochondrial Regulation of Nociceptor Function - Chronic pain affects more than 50 million Americans per year, resulting in extraordinary personal and societal costs. Adding to the dilemma, deaths involving prescription opiate analgesics have almost quadrupled in the last ten years. The clinical challenge of pain management is underscored by evidence that chronic pain is mechanistically distinct from acute pain, therefore a thorough understanding of the molecular and cellular mechanisms underlying the transition to chronic pain is fundamental to improving and expanding treatment options. Hyperalgesic priming is a compelling model of the transition to chronic pain in which an initial injury resolves, but leaves the animal in a primed state in which a second insult induces a greatly prolonged pain response. Experiments proposed here will examine the impact of mitochondrial dynamics on the development of acute and chronic inflammatory pain compared to a nerve injury model of neuropathic pain, and will explore molecular mechanisms mediating proposed anti-nociceptive actions of endogenous uncoupling mechanisms and mitochondrial uncoupling drugs. Specific Aim 1 will examine the how mitochondrial function changes in response to noxious insult and the impact of mitochondrial regulation on acute hyperalgesia in sensory ganglia. Specific Aim 2 will use patch clamp electrophysiology to demonstrate changes in electrical properties of sensory neurons in response to manipulation of mitochondrial function, and will identify cell signaling pathways that mediate mitochondrial effects on neuronal excitability. Specific Aim 3 will characterize changes in mitochondrial function unique to the transition to chronic pain, and will elucidate cell signaling pathways modulating the impact of mitochondrial function on inflammatory and neuropathic pain chronification. This proposal will use innovative approaches to explore novel mechanisms by which mitochondria influence the manifestation of acute and chronic pain, and test the therapeutic potential of targeting these mechanisms for pain relief.


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: 2025 ( Subtotal = $361,250 )
2025	2025	UNIVERSITY OF NEW ENGLAND	11 HILLS BEACH RD	BIDDEFORD	ME	04005	YORK	USA	Extramural Research Programs in the Neurosciences and Neurological Disorders	000	3	1/17/2025	NON-COMPETING CONTINUATION	$361,250
														Subtotal = $361,250

Issue Date FY: 2024 ( Subtotal = $389,347 )
2024	2024	UNIVERSITY OF NEW ENGLAND	11 HILLS BEACH RD	BIDDEFORD	ME	04005	YORK	USA	Extramural Research Programs in the Neurosciences and Neurological Disorders	001	2	4/9/2024	NON-COMPETING CONTINUATION	$28,097
2024	2024	UNIVERSITY OF NEW ENGLAND	11 HILLS BEACH RD	BIDDEFORD	ME	04005	YORK	USA	Extramural Research Programs in the Neurosciences and Neurological Disorders	000	2	1/25/2024	NON-COMPETING CONTINUATION	$361,250
														Subtotal = $389,347

Issue Date FY: 2023 ( Subtotal = $437,341 )
2023	2023	UNIVERSITY OF NEW ENGLAND	11 HILLS BEACH RD	BIDDEFORD	ME	04005	YORK	USA	Extramural Research Programs in the Neurosciences and Neurological Disorders	000	1	2/9/2023	NEW	$437,341
														Subtotal = $437,341

Grand Total All Awards = $1,187,938

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Mitochondrial Regulation of Nociceptor Function

Award Number: R01NS131571

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: 02/15/2023

PERIOD OF PERFORMANCE END DATE: 01/31/2028

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