HHS Recovery Act Recipient Reporting Readiness Tool

Step 4. Review and Copy the Grant Awards Data

TAGGS provides some – but not all – of the data needed for the Recipient Report. Recipients are responsible for directly collecting and reporting all required data to FederalReporting.gov. Data that HHS does not currently collect are highlighted in yellow. Do not copy this highlighted information. Please enter the appropriate data for your organization in these required fields. For assistance with entering these data please contact FederalReporting.gov.

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Prime Recipient Report

Award Detail for: NEURONAL EXCITABILITY AND MOTILITY IN COLITIS
Recipient Name:UNIVERSITY OF VERMONT
DUNS Number: 066811191
223 WATERMAN BUILDING
BURLINGTON, VT 05405

Reporting Information

Award Type*: Grant

Award Number*: 3R01DK062267-06S1

Final Report*: Recipient responsible for this data

Award Recipient Information

Recipient DUNS Number*: 066811191

Recipient Account Number: Recipient responsible for this data

Recipient Congressional District*: Not Available

Award Information

Funding Agency Code*: 7529

Awarding Agency Code*:7529

Award Date*: 09-07-2009

Amount of Award*: $ 75,706

Program Source (TAS)*: 750883

CFDA Number*: 93.701

Sub Account Number for Program Source (TAS)*: Recipient responsible for this data

Total Number of Sub Awards to Individuals*: Recipient responsible for this data

Total Amount of Sub Awards to Individuals*: Recipient responsible for this data

Total Number of Payments to Vendors less than $25,000/award*: Recipient responsible for this data

Total Amount of Payments to Vendors less than $25,000/award*: Recipient responsible for this data

Total Number of Sub Awards less than $25,000/award*: Recipient responsible for this data

Total Amount of Sub Awards less than $25,000/award*: Recipient responsible for this data

Award Description* DESCRIPTION (provided by applicant): Intestinal inflammation leads to changes in a variety of functions, including motility, secretion and sensitivity. Neural circuits of the bowel regulate ll of these functions, and it is likely that changes in these reflex circuits contribute to the symptos suffered by afflicted individuals. In the past 8 years, we have evaluated inflammation-induced changes along the circuitry of the colon in a step-wise fashion, and we have identified fundamental changes at several sites, including: (1) increased serotonin availability in the mucosal layer; (2) intrinsic sensory neuron hyperexcitability; (3) facilitation of synaptic signals between neurons; and (4) attenuated inhibitory purinergic neuromuscular transmission. Furthermore, we have elucidated the mechanisms that underlie many of these changes, determined what changes persist following recovery from inflammation, and linked changed in neural function to altered motility patterns. In this grant application, we are proposing to build upon our findings and those of others to examine novel mechanisms by which gut functions and bone density can be affected by inflammation, and explore innovative approaches to prevent or reverse these changes and to minimize mucosal damage during the inflammatory response. The first aim of this grant application is designed to test the hypothesis that the inflammation- induced decrease in purinergic neuromuscular transmission involves a decrease in purine synthesis and release as the result of oxidative stress damage to mitochondria in the muscular is of the inflamed colon. Experiments proposed in the second aim is based on our recent discovery that 5-HT4 receptors (5HT4Rs) are highly expressed in the colonic epithelium, and that activation of these receptors induces 5-HT, mucus, and Cl- secretion, and promotes propulsive motility. We will test the hypothesis that activation of 5-HT4Rs on cells in the epithelial lining has a protective effect, attenuating the severity of colitis and protecting colonc motor function. Specific aim 3 is based on the knowledge that various forms of intestinal inflammation are associated with decreased bone density, and the recent discovery that circulating gut-derived serotonin has a negative impact on bone formation. We will test the hypothesis that the inflammation-induced increase in mucosal serotonin availability contributes to the decrease in bone density, and that these effects can be reduced by modulating mucosal serotonin signaling or by inhibiting the 5-HT1B receptor, which is expressed by pro-osteoblasts. This proposal involves an integrated approach, using state-of-the-art techniques, to investigate novel concepts related to the neuromuscular and serotonin signaling in the gut, and to examine a potential damaging relationship between mucosal serotonin and bone integrity. The findings of these studies will greatly improve our understanding of purinergic neuromuscular transmission and mucosal serotonin signaling in the gut. PUBLIC HEALTH RELEVANCE: Gastrointestinal (GI) disorders, including Crohn's Disease and ulcerative colitis, are extremely common. They cause a great deal of suffering and are very costly to the healthcare system and society. There is a pressing need to gain a better understanding of how and why gut functions and sensation change in response to inflammation, and how to prevent these changes from occurring. The proposed studies will involve the use of animal models and human tissues to investigate the mechanisms of changes in intestinal serotonin signaling and neuromuscular transmission that occur in the inflamed colon. Our studies will test the hypothesis that treatment strategies targeting free radicals and specific serotonin receptors could dampen the extent of the inflammatory response, and prevent associated damage to gut functions and bone density.

Project Information

Project Name or Project/Program Title*: NEURONAL EXCITABILITY AND MOTILITY IN COLITIS

Project Status*: Recipient responsible for this data

Total Federal Amount of ARRA Funds Received/Invoiced*: Recipient responsible for this data

Number of Jobs*: Recipient responsible for this data

Description of Jobs Created*: Recipient responsible for this data

Quarterly Activities/Project Description*: Recipient responsible for this data

Activity Code (NAICS or NTEE-NPC)*: Recipient responsible for this data

Total Federal Amount of ARRA Expenditure* (Enter the cumulative total amount of Recovery Funds received that were expended to projects or activities. Refer to the Data Model for details on how to calculate this amount.): Recipient responsible for this data

Total Federal ARRA Infrastructure Expenditure Recipient responsible for this data

Infrastructure Contact Name: Recipient responsible for this data

Infrastructure Contact Email: Recipient responsible for this data

Infrastructure Contact Phone: Recipient responsible for this data

Infrastructure Contact Phone Ext: Recipient responsible for this data

Infrastructure Contact Street Address 1: 223 WATERMAN BUILDING

Infrastructure Contact Street Address 2: Not Available

Infrastructure Contact Street Address 3: Recipient responsible for this data

Infrastructure City: BURLINGTON

Infrastructure State: VT

Infrastructure ZIP Code+4: 05405

Infrastructure Purpose and Rationale (If applicable, enter an explanation about how the infrastructure investment will contribute to one or more purposes of the Recovery Act. Refer to the Data Model for details on what to report. 4000 characters or less.): Recipient responsible for this data

Primary Place of Performance

Street Address 1: 85 SOUTH PROSPECT STREET340 WATERMAN BUILDING

Street Address 2: BURLINGTON

City*: BURLINGTON

State*: VT

ZIP Code+4*: 054050160

Congressional District*: 1

Country*: US

Recipient Highly Compensated Officers

Prime Recipient Indication of Reporting Applicability*: Recipient responsible for this data

1. Officer Name and Compensation: Recipient responsible for this data
2. Officer Name and Compensation: Recipient responsible for this data
3. Officer Name and Compensation: Recipient responsible for this data
4. Officer Name and Compensation: Recipient responsible for this data
5. Officer Name and Compensation: Recipient responsible for this data

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