PhD Scientific Days 2017

Oral Presentations: Neurosciences

Involvement of D1 dopamine receptor in accumbens nucleus in hedonic food intake

Előadó neve

Durst, Máté

Előadó munkahelye

Department of Anatomy, Histology and Embriology, Semmelweis University

Előadó telefonszáma

+3630-3936706

Előadó e-mail címe

durstmate@yahoo.com

Az előadás címe

Involvement of D1 dopamine receptor in accumbens nucleus in hedonic food intake

Szerző(k) neve és munkahelye

Máté Durst, Katalin Könczöl, Zsuzsanna E. Tóth
Laboratory of Neuroendocrinology and In Situ Hybridization; Department of Anatomy, Histology and Embryology, Semmelweis University; Budapest, Hungary

Témacsoport

neurosciences

Szekció

Oral Presentations: Neurosciences

Data of the presenter

Doctoral School: János Szentágothai Doctoral School of Neurosciences
Program: Neuromorphology and Cell Biology
Supervisor: Zsuzsanna E. Tóth
E-mail address: durstmate@yahoo.com

Text of the abstract

Introduction
Alterations in feeding reward were recognised in obesity but primary reasons of overeating should start before fat depos build up. The cascade of events leading to hyperphagia is not known, malfunction of the accumbens nucleus (Nac), a key reward centre is emphasised.
Aims
We investigated the function of Nac in feeding reward in healthy and obesity-prone rats before the obese phenotype manifested.
Methods
Obesity prone-rats were produced by intrauterine protein restriction (PR). Sweetened condensed milk (SCM) was provided to rats to provoke reward related feeding. Consummatory behaviour and SCM-elicited Fos-reaction within the Nac were analysed. In situ hybridisation was used to detect molecular changes in the mesolimbic dopaminergic system. A pharmacological approach was applied to connect molecular-biological and behavioural data.
Results
Young adult PR animals were slightly hyperphagic, but weight-matched with controls. They produced heightened SCM consumption, and dysfunction in “wanting”, not in “liking” component of food reward. SCM-evoked Fos in Nac medial shell (associated more with “liking”) was proportional to the consumed quantity within both groups. Only PRs exhibited similar relationship in Nac core, related purely to “wanting”. The average Fos-count however was comparable between the groups, indicating neurons in PRs had a higher activation threshold. This was associated with reduced D1R mRNA expressions in the medial shell. Most of the SCM-evoked Fos-positive cells actually expressed D1R mRNA here in controls. Selective D1R agonist SKF82958 injected into the medial shell attenuated SCM intake and diminished “wanting”.
Conclusion
D1R signalling has robust impact on inhibitory control over feeding. Dopamine through D1R seems to build up a stop-signal during SCM intake gradually in the Nac medial shell and Fos-activation may be a morphological manifestation of this. Altered neuronal sensitivity related to D1R malfunction develops before obesity, and may lead to overconsumption through impairing the building up of the stop level.

Kind

Szabad

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

1247

Authors (legacy)

Máté Durst, Katalin Könczöl, Zsuzsanna E. Tóth
Laboratory of Neuroendocrinology and In Situ Hybridization; Department of Anatomy, Histology and Embryology, Semmelweis University; Budapest, Hungary