Neuroscience 2004 Abstract
| Presentation Number: | 380.9 |
|---|---|
| Abstract Title: | Neurotrophin-4 knock-in mice with increased intraganglionic laminar endings and enhanced short-term satiety exhibit an increased sensitivity to CCK. |
| Authors: |
Fox, E. A.*1
; Chi, M. M.1
; Silva, D.2
; Fan, G.2
1Dept Psycholog Sci, Purdue Univ, West Lafayette, IN 2CA, 703 Third Street, 47907-2004, |
| Primary Theme and Topics |
Homeostatic and Neuroendocrine Systems - Regulation of Food Intake and Body Weight -- Integration of peripheral signals |
| Secondary Theme and Topics | Homeostatic and Neuroendocrine Systems<br />- Gastrointestinal and urogenital regulation |
| Session: |
380. Signaling, Development, and Anatomy Slide |
| Presentation Time: | Monday, October 25, 2004 10:00 AM-10:15 AM |
| Location: | San Diego Convention Center - Room 32B |
| Keywords: | vagal afferents, small intestine, meal patterns, food intake |
Neurotrophin-4 knockout (NT4KO) mice have impaired short-term satiety associated with a loss of intestinal vagal intraganglionic laminar endings (IGLEs; Fox, J Neurosci, 21:8602, 2001). In contrast, mice overexpressing NT4 (NT4 knock-in mice, NT4KI; Fan, Nat Neurosci, 3:350, 2000) have an enhancement of some components of short-term satiety and preliminary results suggest they have increased IGLEs restricted to the intestine (Fox, 2003, SFN mtg). These different changes in satiety in NT4KO and NT4KI mice imply that altered vagal afferent signaling, rather than general disruption of intestinal function may have caused these perturbations of satiety. To further investigate this relationship, the effect of exogenous CCK-8 on short-term food intake, which is largely mediated by vagal gastrointestinal afferents, was examined in NT4KI mice (n=12) and wild types (n=9). Mice maintained on pelleted chow and water ad libitum were adapted to precision pellets (BioServ, 20mg). On test days sulfated CCK-8 (0.5, 1, 2, or 4 µg/kg) or saline was injected i.p. 5 min prior to pellet access. NT4KI mice were more sensitive than wild types to CCK, exhibiting suppression at a lower dose than controls and larger suppressions of intake at a given dose (e.g., increases at 2 µg/kg dose: females 77%, males 142%; p<0.05). The role of CCK-A receptors in increased suppression was examined by pretreating with devazepide (300 µg/kg in saline, 1% DMSO) 15 min prior to 4 µg/kg CCK-8 injection. This devazapide treatment prevented CCK-8 suppression of food intake. The present findings suggest NT4KI mice have increased CCK sensitivity through activation of CCK-A receptors and thus strengthen the association of increased intestinal IGLEs with enhanced short-term satiety.
Supported by School of Liberal Arts Grant, Purdue University
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2004 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2004. Online.
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