Nalazite se na CroRIS probnoj okolini. Ovdje evidentirani podaci neće biti pohranjeni u Informacijskom sustavu znanosti RH. Ako je ovo greška, CroRIS produkcijskoj okolini moguće je pristupi putem poveznice www.croris.hr
izvor podataka: crosbi

Emotional response in dopamine D2L receptor-deficient mice (CROSBI ID 144779)

Prilog u časopisu | izvorni znanstveni rad | međunarodna recenzija

Hranilović, Dubravka ; Bućan, Maja ; Wang, Yanyan Emotional response in dopamine D2L receptor-deficient mice // Behavioural brain research, 195 (2008), 2; 246-250

Podaci o odgovornosti

Hranilović, Dubravka ; Bućan, Maja ; Wang, Yanyan

engleski

Emotional response in dopamine D2L receptor-deficient mice

The dopamine D2 receptor (D2R) system has been implicated in emotional processing which is often impaired in dopamine related disorders. The long (D2L) and the short (D2S) isoforms of D2R are generated by alternative splicing of the same gene. To study differential roles of the two D2R isoforms, D2L-deficient mice (D2L-/-) expressing functional D2S were previously generated. In this study contribution of D2L isoform to emotional response was investigated by examining behaviors that reflect emotionallity (exploratory behavior, anxiety level and learned helplessness) in D2L-/- and WT mice. While the thigmotactic, locomotor and general components of anxiety in zero maze did not differ among the genotipes, D2L-/- mice displayed significantly lower level of exploration in a hole board and zero maze, and significantly higher increase in latency to escape from a foot shock after the learned helplessness training, compared with WT mice. These results suggest that D2L may play a more prominent role than D2S in mediating emotional response, such as behavioral reactions to novelty and inescapable stress. Our findings provide a better understanding of the molecular and cellular mechanisms underlying emotional responses.

dopamine; D2L isoform; knockout mice; exploration; anxiety; learned helplessness

nije evidentirano

nije evidentirano

nije evidentirano

nije evidentirano

nije evidentirano

nije evidentirano

Podaci o izdanju

195 (2)

2008.

246-250

objavljeno

0166-4328

Povezanost rada

Temeljne medicinske znanosti, Biologija

Indeksiranost