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NTS Catecholamine Neurons Mediate Hypoglycemic Hunger

Glucose was the main energy source for the brain. The decrease in blood glucose was incompatible with the continuity of life. For this, maintaining the blood sugar level was secured by many alternative systems. Increased appetite was one of the main protection mechanisms against hypoglycemia.

MCH Dependent Reward and Feeding

Medipol Üniversitesi Rejeneratif ve Restoratif Tıp Araştırmaları Merkezi bünyesinde faaliyet gösteren Elektrofizyoloji ve Davranış Laboratuvarımızda vücudumuzda meydana gelen olayların arkasında yatan sinir ağları inceleniyor.

Metabolism Research Laboratory has been activated

Changing nutrition and living habits with the industrial revolution made metabolic diseases an important global public health problem. Now, compared to a hundred years ago, we provide food more easily, consume more and act less to obtain food.

Q-Lab Social Meeting

Q-lab team got together for dinner. The intensity of new projects and the reward for long work. The team are excited and happy.

Selected Works

Poster/ The Hypotalamic Glutamaterjic Neurons Modulate the Effects of High Fat Diet on Cognition

Isıldar H.K., Atayolu R., Dilsiz P., Oz Ates E., Alp M.I.

Turkish Neuroscience 2020

2020 November

Certain groups of neurons in the hypothalamus are responsible for regulate food intake. It is known that eating high-fat, causes disruptions in this signaling in the hypothalamus. Glutamate is the most common neurotransmitter in brain and plays a key role in LTP formation and learning. In this study, it is hypothesized that the negative effects of eating high-fat on cognition occur through hypothalamic glutamatergic neurons. The role of glutametergic neurons has been investigated in the effect of high-fat diet on food intake and memory in the hypothalamus for a long time.

Paper/ NTS Catecholamine Neurons Mediate Hypoglycemic Hunger via Medial Hypothalamic Feeding Pathways

Aklan I, Sayar Atasoy N, Yavuz Y, Ates T, Coban I, Koksalar F, Filiz G, Topcu IC, Oncul M, Dilsiz P, Cebecioglu U, Alp MI, Yilmaz B, Davis DR, Hajdukiewicz K, Saito K, Konopka W, Cui H, Atasoy D.

Cell Metabolism

2019 December

Glucose is the essential energy source for the brain, whose deficit, triggered by energy deprivation or therapeutic agents, can be fatal. Increased appetite is the key behavioral defense against hypoglycemia; however, the central pathways involved are not well understood. Here, we describe a glucoprivic feeding pathway by tyrosine hydroxylase (TH)-expressing neurons from nucleus of solitary tract (NTS), which project densely to the hypothalamus and elicit feeding through bidirectional adrenergic modulation of agouti-related peptide (AgRP)- and proopiomelanocortin (POMC)-expressing neurons. Acute chemogenetic inhibition of arcuate nucleus (ARC)-projecting NTSTH neurons or their target, AgRP neurons, impaired glucoprivic feeding induced by 2-Deoxy-D-glucose (2DG) injection. Neuroanatomical tracing results suggested that ARC-projecting orexigenic NTSTH neurons are largely distinct from neighboring catecholamine neurons projecting to parabrachial nucleus (PBN) that promotes satiety. Collectively, we describe a circuit organization in which an ascending pathway from brainstem stimulates appetite through key hunger neurons in the hypothalamus in response to hypoglycemia.

Paper/ MCH Neuron Activity Is Sufficient for Reward and Reinforces Feeding

Dilsiz P, Aklan I, Sayar Atasoy N, Yavuz Y, Filiz G, Koksalar F, Ates T, Oncul M, Coban I, Ates Oz E, Cebecioglu U, Alp MI, Yilmaz B, Atasoy D

Neuroendocrinology

2019 June

Melanin-concentrating hormone (MCH)-expressing neurons have been implicated in regulation of energy homeostasis and reward, yet the role of their electrical activity in short-term appetite and reward modulation has not been fully understood.

Paper/ Inactivation of Magel2 Suppresses Oxytocin Neurons Through Synaptic Excitation-Inhibition Imbalance

Ates T., Oncul M., Dilsiz P., Topcu I.C., Civas C.C., Alp M.I., Aklan I., Ates Oz E., Yavuz Y., Yilmaz B., Sayar Atasoy N., Atasoy D.

Neurobiology of Disease

2018 September

Prader-Willi and the related Schaaf-Yang Syndromes (PWS/SYS) are rare neurodevelopmental disorders characterized by overlapping phenotypes of high incidence of autism spectrum disorders (ASD) and neonatal feeding difficulties. Based on clinical and basic studies, oxytocin pathway defects are suggested to contribute disease pathogenesis but the mechanism has been poorly understood. Specifically, whether the impairment in oxytocin system is limited to neuropeptide levels and how the functional properties of broader oxytocin neuron circuits affected in PWS/SYS have not been addressed. Using cell type specific electrophysiology, we investigated basic synaptic and cell autonomous properties of oxytocin neurons in the absence of MAGEL2; a hypothalamus enriched ubiquitin ligase regulator that is inactivated in both syndromes. We observed significant suppression of overall ex vivo oxytocin neuron activity, which was largely contributed by altered synaptic input profile; with reduced excitatory and increased inhibitory currents. Our results suggest that dysregulation of oxytocin system goes beyond altered neuropeptide expression and synaptic excitation inhibition imbalance impairs overall oxytocin pathway function.