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(BBSRC DTP) Brain integration and processing of ingestive signals

Project Description

After meal consumption, the brain evaluates the value of its contents and relays this information via neuronal circuits connecting the periphery with the brain (1,2). Although the brain is now recognised as the master regulator of appetite and energy homeostasis, our understanding of how and which circuits decode the post-ingestive nutritional and hedonic value of food from the periphery to the brain remain largely unknown. The advent of new genetic technologies now provide a powerful means by which to unravel the contribution of discrete neurons to appetitive behaviour and systemic energy balance with unprecedented spatial and temporal resolution (2,3).
The host laboratories have started to phenotype the neurones in the caudal brainstem, an important brain region that serves as a first relay station for peripherally generated signals entering the brain (4,5). Published (2,4) and unpublished data suggest that segregated brainstem circuits selectively respond to distinct nutritional and non-nutritional signals and transmit this information to multiple second order brain regions so that the brain can compute and attribute motivational valence. The overarching aim of this project is to resolve these circuits and characterise them at the genetic, structural and functional level.
To this end, the student will receive training in using the latest genetic technologies available that will allow him/her to genetically tag distinct brainstem neurons after they have responded to the nutritional and non-nutritional signals. This permanent genetic tagging will then allow the student to identify the neurons and their connections, record their activity during normal behaviour and selectively activate/inhibit them to interrogate their significance to behaviour.
Resolving these circuits will not only expand our understanding of how ingestive behaviour is regulated, but it will also inform design of novel medications with improved efficacy and patient compliance.

Entry Requirements:
Applications are invited from UK/EU nationals only. Applicants must have obtained, or be about to obtain, at least an upper second class honours degree (or equivalent) in a relevant subject.

Funding Notes

This project is to be funded under the BBSRC Doctoral Training Partnership. If you are interested in this project, please make direct contact with the Principal Supervisor to arrange to discuss the project further as soon as possible. You MUST also submit an online application form - full details on how to apply can be found on the BBSRC DTP website View Website

As an equal opportunities institution we welcome applicants from all sections of the community regardless of gender, ethnicity, disability, sexual orientation and transgender status. All appointments are made on merit.


1: Andermann ML, Lowell BB. Toward a Wiring Diagram Understanding of Appetite Control. Neuron. 2017 Aug 16;95(4):757-778. doi: 10.1016/j.neuron.2017.06.014.
2: Han W, Tellez LA, Perkins MH, Perez IO, Qu T, Ferreira J, Ferreira TL, Quinn D, Liu ZW, Gao XB, Kaelberer MM, Bohórquez DV, Shammah-Lagnado SJ, de Lartigue G, de Araujo IE. A Neural Circuit for Gut-Induced Reward. Cell. 2018 Oct 18;175(3):887-888. doi: 10.1016/j.cell.2018.10.018.
3: Resendez SL, Jennings JH, Ung RL, Namboodiri VM, Zhou ZC, Otis JM, Nomura H, McHenry JA, Kosyk O, Stuber GD. Visualization of cortical, subcortical and deep brain neural circuit dynamics during naturalistic mammalian behavior with head-mounted microscopes and chronically implanted lenses. Nat Protoc. 2016 Mar;11(3):566-97. doi: 10.1038/nprot.2016.021.
4: D'Agostino G, Lyons DJ, Cristiano C, Burke LK, Madara JC, Campbell JN, Garcia AP, Land BB, Lowell BB, Dileone RJ, Heisler LK. Appetite controlled by a cholecystokinin nucleus of the solitary tract to hypothalamus neurocircuit. Elife. 2016 Mar 14;5. pii: e12225. doi: 10.7554/eLife.12225
5: Dodd GT, Worth AA, Nunn N, Korpal AK, Bechtold DA, Allison MB, Myers MG Jr, Statnick MA, Luckman SM. The thermogenic effect of leptin is dependent on a distinct population of prolactin-releasing peptide neurons in the dorsomedial hypothalamus. Cell Metab. 2014 Oct 7;20(4):639-49. doi: 10.1016/j.cmet.2014.07.022.

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