Influence of the mesocortical dopaminergic system on activity, food hoarding, social-agonistic behavior, and spatial delayed alternation in male rats.

Abstract

In order to assess the behavioral role of the dopaminergic mesocortical input to the prefrontal cortex, bilateral lesions were made in the ventral tegmental area (VTA). The possibility of a functional recovery by the administration of a dopamine agonist was examined. General activity, food hoarding, social-agonistic behavior, and spatial delayed alternation performance were recorded in rats with VTA lesions and in sham-operated animals. In the open field animals with VTA lesions were more active but showed less anxiety. Food hoarding was impaired. In dyadic interactions with sham-operated opponents, VTA rats were socially more active, whereas sham operates performed more keeping down and aggressive grooming. This behavioral deficit was partially recovered when apomorphine was administered prior to testing. VTA animals were impaired in the performance of a spatial delayed alternation task with an intertrial interval of 15 s, whereas no impairment was found with a 0-s intertrial interval. The theoretical implications of these findings are discussed.

Effects of gonadectomy and hormone replacement on a spontaneous novel object recognition task in adult male rats

“…Like effects on the spatial working memory processes of the medial prefrontal cortex demonstrated previously (Daniel et al, 2003;Kritzer et al, 2007;Kritzer et al, 2001), the adverse effects of GDX on the NOR task observed here were attenuated by supplementing GDX animals with TP but not E, and were significantly correlated with a bioassay of circulating androgens--BSM weight. Although not examined in this study, there are several reasons to suspect that correlations previously found between the effects of GDX on medial prefrontal working memory function and on the density of its functionally critical dopamine (DA) innervation (Kritzer et al, 2007) may also extend to the perirhinal-dependent processes of the NOR task, since the effects of GDX on DA innervation in perirhinal prefrontal fields are qualitatively and quantitatively similar to those observed in medial prefrontal areas and are likewise androgen dependent (Kritzer et al, 2003), and because performance on NOR tasks, like that of the medial prefrontal cortical-mediated spatial working memory (Stam et al, 1989;Zahrt et al, 1997) is also impaired by selective perturbations of the prefrontal dopamine system (Morrow et al, 2000). Accordingly, as the study of gonadal hormone influence in males over the executive and mnemonic functions of the prefrontal cortex in rats continues to expand, it may be increasingly important to explore the DAergic endpoints in parallel with behavior.…”

An animal model of early-treated PKU

“…On the contrary, depletion of dopamine or inhibition of dopamine receptors in prefrontal cortex produces behavioral impairments comparable to those produced by destruction or removal of prefrontal cortex (Brozoski et al, 1979;Simon et al, 1980;Stam et al, 1989;Sawaguchi and Goldman-Rakic, 199 1). In one study with nonhuman primates, depletion of nearly 90% of the dopamine in prefrontal cortex was required to achieve this effect (Brozoski et al, 1979), but when this has been studied in the rat, the deficit in delayed alternation performance has been found with dopamine reductions more comparable to those reported here (32% of controls, Simon et al, 1980;29% of controls, Stam et al, 1989).…”

Regulation of Working Memory by Dopamine D4 Receptor in Rats

“…Lesioning the mesocortical dopamine pathway from the ventral tegmental area to PFC results in impaired working memory in both primates (Brozoski et al, 1979) and rats (Bubser and Schmidt, 1990;Simon, 1981). Deficits induced as such can be rescued with the dopamine precursor L-DOPA, or the dopamine agonist apomorphine, to directly implicate dopaminergic mechanisms (Brozoski et al, 1979;Stam et al, 1989). Recent studies in human subjects have also provided evidence indicating that working memory is modulated by dopaminergic transmission (Mattay et al, 2000).…”