Biological Session VII

HYPOTHALAMIC CONTROL OF BEHAVIOR

Understanding the neural circuits of stress eating

Frank Julius Meye

Translational Neuroscience Department, University Medical Center Utrecht, Netherlands  

Abstract: Stress can enhance cravings for palatable food (e.g. fat and sugar) and can also increase impulsive behavior. In vulnerable individuals these effects contribute to binge eating and obesity. The neurobiology underlying stress eating remains largely unclear, however our lab seeks to understand how stress alters neural circuit function to increase the pursuit of palatable foods. In particular we focus on how stress alters communication within cortical-hypothalamic-(meso)limbic networks. We assess the stress-altered functioning of such circuitry using a combination of ex vivo techniques (in particular patch-clamp slice electrophysiology) combined with various in vivo approaches (behavioral assays during neural circuit monitoring/manipulation techniques). With these approaches we strive to provide multi-level insight in the neurobiological mechanisms of stress eating responses.

Role of AgRP / NPY neurons in development of the obesity phenotype  on the mouse model with induced deletion of the Dicer1 gene

Karolina Hajdukiewicz1,Urszula Wojda2, Witold Konopka3

1 Braincity/ Laboratory of Neuronal Plasticity, Nencki Institute of Experimental Biology PAS, Warsaw, Poland 
2 Laboratory of Preclinical Testing of Higher Standard, Nencki Institute of Experimental Biology PAS, Warsaw, Poland
3 Life Sciences and Biotechnology/Laboratory of Neuroplasticity and Metabolism, PORT-Polish Center for Biotechnology Development, Wroclaw, Poland

Abstract: 

Food is the foundation of the survival pyramid while hunger is the primary motivator of the search for and acquisition of nourishment. The brain is the locus of superior centers involved in hunger and satiety regulation. The arcuate nucleus located in the hypothalamus is the primary first-order center processing the body’s energy status information. Said structure’s functional division includes two populations of opposing neurons: AgRP/NPY, which stimulates food intake, and POMC/CART, responsible for promoting satiety and appetite suppression. Any disturbances within the arcuate nucleus may lead to changes in eating behavior and development of metabolic diseases such as obesity.  
Neurospecific deletion of the Dicer1 gene, which leads to massive microRNA loss, is an example of such impairment. This mutation promotes obesity development linked to increased food intake. Here, this phenomenon is described in relation to orexigenic AgRP/NPY neurons. The microRNA-loss-dependent obesity is established through study of selected transgenic animal models and use of sophisticated genome editing tools.         

Changes in the Dorsomedial Hypothalamic hormonal responses and basal activity in high-fat diet fed rats under feeding restriction

Gawron E. , Sanetra A. M. , Palus-Chramiec K. , Lewandowski M. H. 

Department of Neurophysiology and Chronobiology, Jagiellonian University in Kraków, Poland 

Abstract: The dorsomedial hypothalamus (DMH) is a part of the food-entrainable oscillator regulating circadian periods of feeding and drinking, as well as energy expenditure. Our previous research presented differences in the DMH activity between rats under control (CD) and high-fat diet (HFD). HFD group characterised by additional feeding during daytime, therefore their non-active phase. Following that study, we decided to use a similar protocol modified by applying a feeding restriction, allowing the animals to feed only during their physiological period of behavioural activity. This allowed us to observe whether the disruption seen in the DMH activity in HFD group is purely the result of a modified diet or if it originates from animals’ feeding behaviour instead. Using data obtained with immunohistochemical and electrophysiological methods we analysed if aforementioned changes in the DMH activity also occur after night-feeding only. Ex-vivo multi-electrode array recordings (MEA) also allowed us to compare the DMH neuronal activity after applying 3 pivotal satiety hormones: oxyntomodulin (OXM), glucagon-like peptide 2 (Glp2) and exendin-4 (Exn4). We compared its responses not only between the CD and HFD groups but also between day and night. This research proposes restricted feeding to prevent HFD induced disruptions in the DMH activity and presents its responses to satiety hormones. 

Oxytocin signalling in the brainstem nucleus incertus modulates arousal related behaviours

Alan Kania1-3, Kamil Pradel2, Anna Gugula2, Lukasz Chrobok2, Arthur Lefevre1, Konstantinos Afordakos1, Quirin Krabichler1, Sherie Ma4, Carlo Cifani3, Andrew L. Gundlach4, Valery Grinevich1, Anna Blasiak2

1Department of Neuropeptide Research in Psychiatry, Central Institute of Mental Health, University of Heidelberg, Mannheim, Germany 
2Department of Neurophysiology and Chronobiology, Institute of Zoology and Biomedical Research, Faculty of Biology, Jagiellonian University, Krakow, Poland 
3School of Pharmacy, Pharmacology Unit, University of Camerino, Camerino, Italy 
4The Florey Institute of Neuroscience and Mental Health, and Florey Department of Neuroscience and Mental Health, The University of Melbourne, Victoria, Australia 

Abstract: Oxytocin (OT)/oxytocin receptor (OTR) signalling modulates food/water intake, reproduction, memory, emotional processing, and social interaction among others. A possible effector of these actions are the OTR-expressing neurons in the nucleus incertus (NI) that modulate arousal and other processes that overlap with known OT functions. Therefore, our aim was to characterise the anatomy, neuronal and behavioural effects of OT/OTR signalling in the rat NI. 
In these studies, we employed situ hybridisation, immunostaining, viral tract-tracing, and electrophysiological ex vivo. Finally, using a newly generated OTR-IRES-Cre knock-in rat, we chemogenetically activated NI OTR-expressing neurons and examined the effects on behaviour. 
A majority of OTR mRNA-positive NI neurons are GABAergic. OT dose- and OTR-dependently excited 70% of NI neurons. The NI lacks a substantial OT innervation, but the juxtaposition to the fourth ventricle suggests endogenous OT may reach the NI via the cerebrospinal fluid. Chemogenetic activation of OTR NI neurons promoted locomotor activity, reduced anxiety, altered social interaction, and improved social recognition. 
These studies identify the brainstem nucleus incertus as a site of action of OT/OTR signalling. Notably, our results reveal a possible neuronal mechanism underlying OT-mediated modulation of arousal, and provide evidence for a key role of extrahypothalamic OT actions in governing behaviour.

Funding: Alexander von Humboldt Foundation, Germany: Humboldt Research Fellowship; NSC, Poland: UMO-2018/30/E/NZ4/00687. 

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