As well, it would probably be valuable to explore whether such neurofunctional reorganization also occurs in aging animal models. Such studies would be important in order to distinguish between the engagements of such normal age-related phenomena and those phenomena linked to a neurodegenerative process. Abbreviations BA selleckchem Brodmann area CRUNCH compensation-related utilization of neural circuits hypothesis fMRI functional magnetic resonance imaging HAROL Dhemispheric asymmetry reduction in older adults PASA posterior–anterior shift in aging STAC scaffolding theory of aging and cognition VF verbal fluency “
“Using a transgenic mouse (Mus musculus) in which nestin-expressing progenitors

are labeled with enhanced green fluorescent protein, we previously characterized the expression of excitatory amino acid transporter 2 (GltI) and excitatory amino acid transporter 1 (Glast) on early neural progenitors in vivo. To address their functional role in this cell population, we manipulated their expression in P7 neurospheres isolated from the dentate gyrus. We observed that knockdown

of GltI or Glast was associated with decreased bromodeoxyuridine incorporation and neurosphere formation. Moreover, we determined that both glutamate transporters regulated progenitor proliferation in a calcium-dependent and metabotropic glutamate receptor-dependent manner. To address the relevance of this in vivo, we utilized models mafosfamide of acquired brain selleck inhibitor injury, which are known to induce hippocampal neurogenesis. We observed that GltI and Glast were specifically upregulated in progenitors following brain injury, and that this increased expression was maintained for many weeks. Additionally, we found that recurrently injured animals with increased

expression of glutamate transporters within the progenitor population were resistant to subsequent injury-induced proliferation. These findings demonstrate that GltI and Glast negatively regulate calcium-dependent proliferation in vitro and that their upregulation after injury is associated with decreased proliferation after brain trauma. “
“Reward sensitivity, or the tendency to engage in motivated approach behavior in the presence of rewarding stimuli, may be a contributory factor for vulnerability to disinhibitory behaviors. Although evidence exists for a reward sensitivity-related increased response in reward brain areas (i.e. nucleus accumbens or midbrain) during the processing of reward cues, it is unknown how this trait modulates brain connectivity, specifically the crucial coupling between the nucleus accumbens, the midbrain, and other reward-related brain areas, including the medial orbitofrontal cortex and the amygdala. Here, we analysed the relationship between effective connectivity and personality in response to anticipatory reward cues.