Cognition (i.e. how individuals perceive, process and react to environmental cues) is fundamental to all animals’ life. Despite this, what explains variation in cognitive abilities is still mainly unclear. Environment is assumed to influences cognitive variation, but the mechanisms for this are still unknown. According to the social intelligence hypothesis, living in a group with a rich social environment, generate challenges that can enhance cognitive abilities. Impulsivity (to not be able to inhibit impulses), one aspect of cognition, may be influenced by the social environment, however this has not yet been experimentally tested. Impulsivity can complicate life, both for humans and animals. In humans, high levels of impulsivity and lack of self-control are associated with addictions and psychiatric disorders, thus is considered to be maladaptive. In animals, impulsivity correlates with stereotypies. To improve our understanding of impulsivity, I experimentally investigated how early social environment affects individual variation in impulsivity. To test this, red junglefowl chicks were used because their group living nature, and our accumulated knowledge on their cognition and behaviour. To manipulate the social environment, chicks either grew up in larger groups (with 17 individuals) or smaller groups (with 7 individuals). During the chicks’ first five weeks of life, three aspects of impulsivity were tested; impulsive action, persistence (in a detour reaching test) and routine formation (in a reversal learning test). Chicks that grew up in larger groups tended to perform less impulsive actions, while social environment did not explain variation in persistence. Chicks from larger groups had less strong routine formation compared to chicks raised in smaller groups. This partially supports the social intelligence hypothesis, and suggest that early social life can affect cognitive traits and explain individual variation in such.

Global cerebral ischemia (GCI) in rats has been shown to promote exploration of anxiogenic zones of the Elevated-Plus Maze (EPM) and Open Field Test (OFT). This study investigated changes in impulsive choice and/or defensive responses as possible contributors of heightened anxiogenic exploration observed after ischemia. Impulsivity was assessed using delay discounting (DD) paradigms, while the Predator Odour Test (PO) served to assess changes in defensive responses towards a naturally aversive stimulus. Male Long Evans rats underwent 9 days of autoshaping training and 24 days of DD training prior to GCI or sham surgery (n= 9/group). Post-surgery, rats completed the OFT, EPM, and PO, followed by 6 days of DD sessions. Blood droplets served to evaluate corticosterone secretion associated with PO exposure. With impulsivity being regulated through mesocorticolimbic monoaminergic pathways, we also characterized post-ischemic changes in the expression of dopamine D2 receptors (DRD2), dopamine transporters (DAT), and ΔFosB in the basolateral amygdala (BLA), nucleus accumbens core (NAcC) and shell (NAcS), and ventromedial prefrontal cortex (vmPFC) using immunohistofluorescence. Our findings revealed no impact of GCI on delay discounting rates, while PO approach behaviours were minimally affected. Nonetheless, GCI significantly reduced DRD2 and ΔFosB-ir in the NAcS and NAcC, respectively, while DAT-ir was diminished in both NAc subregions. Collectively, our findings refine the understanding of cognitive-behavioural and biochemical responses following stroke or cardiac arrest. They support significant alterations to the dopaminergic mesocorticolimbic pathway after ischemia, which are not associated with altered impulsive choice in a DD task but may influence locomotor exploration of the OFT and EPM.