Quinpirole in the ventral pallidum evokes food-related motivational learning deficit
01/30/2020
Gabriella Kékesi1, László Péczely2, Veronika Kállai2, Tamás Ollmann2, Kristóf László2, Alexandra Büki1, László Lénárd2, Gyöngyi Horváth1
1 Department of Physiology, Faculty of Medicine, University of Szeged, Szeged; 2Institute of Physiology, Faculty of Medicine, University of Pécs, Pécs
Earlier data indicated that the overactivation of dopamine D2 receptors (D2Rs) in the nucleus accumbens can lead to positive symptoms of schizophrenia and cognitive disturbances, as well. The ventral pallidum (VP) is one of the key structures of the basal forebrain limbic circuitry. While its GABAergic input originates in the nucleus accumbens, its dopaminergic innervation comes mainly from the ventral tegmental area. D2Rs of the VP take part in motivational and learning processes in healthy rats, however, their potential role in triggering schizophrenia-like symptoms has not yet been investigated. In the present study the D2R agonist, quinpirole (QP), was applied into the VP to reveal its effect on food-related motivational-learning process. The delayed (3, 21 and 24 hours) effects of QP microinjection (1 µg/0.4 µl) were investigated in the AMBITUS, that is a combination of the hole-board and corridor tests. Saline and QP treated control Wistar and Wisket groups were compared (n=5-7/group).Wisket group showed significantly lower exploratory activity and learning capacity before QP administration compared to Wistar one. Regarding the locomotor activity, no effect of treatment was detected in either groups at any investigated time points. QP resulted in decreased exploratory and food-collecting activities in Wistar rats with 21 and 24 hours’ delay, while this treatment did not influence these behaviors in Wisket rats.In summary, our results revealed that the VP D2R activation induces schizophrenia-like motivational learning deficit in control animals, but it does not worsen this symptom domain in schizophrenia model rats. Supports: GINOP 2.3.3-15-2016-00031 and ÚNKP-18-3-III-PTE-374.