Dr Trapp is a Senior Lecturer in Medicine and heads the Autonomic Lab. He trained as a biologist at the Carl von Ossietzky University in Oldenburg, Germany. He obtained his PhD at the Georg August University in Goettingen, Germany, with studies on the cellular physiology of vagal neurons and the first description of ATP-sensitive potassium channels in autonomic neurons. Dr Trapp then relocated as a DFG-Fellow to Oxford in order to study the molecular properties of these channels in detail with Prof Frances Ashcroft, FRS. Subsequently, he obtained a Career Development Award from the MRC and established the Autonomic Lab, first at University College London, and then at Imperial where he became a Lecturer in 2006 and Senior Lecturer in 2008. 

The Autonomic Lab 

located in: Cell Biology Section, Sir Alexander Fleming Building, South Kensington Campus

Work in our lab focuses on the autonomic nervous system and more specifically on the parasympathetic vagal system. The efferent vagal nerve is responsible for the parasympathetic innervations of all mayor organs. It plays a pivotal role in homeostatic processes. For example, it is important for cardiovascular control, modulating heart rate and blood pressure, for gastrointestinal motility, and it is involved in glucose homeostasis; for example it controls the anticipatory insulin release preceding ingestion of food and other cephalic phase responses. The afferent vagal nerve is the main source of visceral sensory information for the brain and terminates in the nucleus tractus solitarius. Amongst other information it provides satiety-related signals from chemo- and mechanosensors in the digestive system.

We are mainly interested in the role of the vagal system in the control of energy metabolism, because Type 2 diabetes and severe obesity are becoming increasingly prevalent in our society and impose a growing financial burden on the health service. In order to develop an effective cure for these metabolic disorders, it is essential to understand how our body regulates its energy balance. This specifically includes understanding which signals elicit (or suppress) feeding. Prime candidates for such signals are the blood glucose level and the amount of fat stored by the body. The primary aim of our research is to elucidate the molecular and electrical pathways the brain employs to monitor and regulate glucose levels.

Current Projects (Enquiries by prospective PhD or Project Students are always welcome)

Molecular and electrical properties of glucose-sensing cells in the dorsal vagal complex

Our brain requires a constant regulated supply of glucose for its survival. Mechanisms exist to measure brain glucose levels and to mount an appropriate regulatory response on blood glucose levels and food intake. The molecular and electrical pathways involved are currently under intense investigation by many laboratories. We are investigating the mechanisms involved in sensing/measuring glucose levels within the lower brainstem.  We use a combination of molecular, histochemical and electrophysiological techniques to achieve this goal.

Balfour et al., (2006) J.Physiol 570:469.

Balfour & Trapp, (2007) J.Physiol 579:691.

Regulation of the activity of glucagon-like-peptide 1 releasing neurones of the vagal complex

Glucagon-like peptide 1 (GLP-1) is released as a satiety hormone from the gut. Injection of GLP-1 into the brain suppresses feeding. A small population of centrally-projecting neurones in the vagal complex also expresses GLP-1 (green fluorescence in Fig). Release of GLP-1 from these cells might be responsible for central GLP-1 effects. We investigate which factors govern the activity of this cell population.

Hisadome et al., (2010) Diabetes 59:1890

Llewellyn-Smith et al., (2011) Neuroscience 180:111

Trapp & Hisadome (2011) Aut Neurosci: Basic and Clinical 161:14

Hisadome et al., (2011) Diabetes 60:2701

 Confocal stack of GLP-1 cells and catecholaminergic cells

Role of 'background' 2-pore domain K⁺ channels in the autonomic nervous system

2-pore domain K⁺channels have been identified as contributors to the resting K⁺ conductance of neurones and were originally thought of as 'background' conductance that shifts the membrane potential towards the potassium equilibrium potential. Research over the past few years however has demonstrated that these channels are highly regulated a various factors, including extracellular pH, neurotransmitters, volatile anaesthetics and mechanical stress, and that they fine-tune neuronal excitability. They feature prominently in the research of several groups in Biophysics and we are interested in their expression pattern and functional significance in the regulation of neuronal excitability.

Hopwood & Trapp,(2005) J.Physiol. 568:145.

Trapp et al.,(2008) J.Neurosci. 28:8844.

Veale et al., (2010) JBC 285:29295.

Molecular mechanisms of xenon preconditioning

The noble gas xenon is an anaesthetic with neuroprotective properties. We have recently identified ATP-sensitive K⁺ channels as an important molecular target for xenon. We are now in the process of elucidating the exact details of how xenon achieves activation of these channels. 

Bantel et al., (2009) Anesthesiol. 110: 986. 

Bantel et al., (2010) Anesthesiol. 112:623.  

Autonomic Lab - After Hours