Neuroscience
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The role of the dopamine D2 receptor (D2R) in regulating appetitive behavior continues to be controversial. Earlier literature suggests that reduced D2R signaling diminishes motivated behavior while more recent theories suggest that reduced D2R, as has been putatively observed in obesity, facilitates compulsive appetitive behavior and promotes overeating. Using a homecage foraging paradigm with mice, we revisit classic neuroleptic pharmacological studies from the 1970s that led to the 'extinction mimicry' hypothesis: that dopamine blockade reduces reinforcement leading to an extinction-like reduction in a learned, motivated behavior. ⋯ The selective knockouts exhibit no change in sucrose preference or sucrose reinforcement. These data suggest that striatal D2R regulates effort in response to costs, mediating cost sensitivity and behavioral thrift. In the context of obesity, these data suggest that reduced D2R is more likely to diminish effort and behavioral energy expenditure rather than increase appetitive motivation and consumption, possibly contributing to reduced physical activity commonly observed in obesity.
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Fluoro-Jade C (FJC) staining is widely used for the specific detection of all degenerating mature neurons, including apoptotic, necrotic, and autophagic cells. However, whether FJC staining can detect degenerating immature neurons and neural stem/precursor cells remains unclear. In addition, some conflicting studies have shown that FJC and its ancestral dyes, Fluoro-Jade (FJ) and FJB, can label resting/activated astrocytes and microglia. ⋯ Surprisingly degenerating mesenchymal cells were also FJC(+). The present study indicates that FJC is a reliable marker for degenerating neuronal cells during all differentiation stages. However, FJC could also label degenerating non-neuronal cells under some conditions.
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The neural mechanisms associated with the limited capacity of working memory (WM) has long been studied, but it is still unclear which neural regions are associated with the precision of visual WM. Here, an orientation recall task for estimating the trial-wise precision of visual WM was performed and then repeated two weeks later in an fMRI scanner. Results showed that activity in frontal and parietal regions during WM maintenance scaled with WM load, but not with the precision of WM (i.e., recall error in radians). ⋯ Interestingly, a region within the prefrontal cortex, the inferior frontal junction (IFJ), exhibited greater functional connectivity with LOC when the WM load increased. Together, our findings provide unique evidence that the LOC supports visual WM precision, while communication between the IFJ and LOC varies based on WM load demands. These results suggest an intriguing possibility that distinct neural mechanisms may be associated with general content (load) or detailed information (precision) of WM.
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Associations between Turning Characteristics and Corticospinal Inhibition in Young and Older Adults.
The effects of aging are multifaceted including deleterious changes to the structure and function of the nervous system which often results in reduced mobility and quality of life. Turning while walking (dynamic) and in-place (stable) are ubiquitous aspects of mobility and have substantial consequences if performed poorly. Further, turning is thought to require higher cortical control compared to bouts of straight-ahead walking. ⋯ Finally, all associations between corticospinal inhibition and turning performance were specific to the right hemisphere, reflecting that those OA who maintained high levels of inhibition performed turning similar to their younger counterparts. These results compliment the right hemisphere model of aging and lateralization specification of cortically regulated temporal measures of dynamic movement. While additional investigations are required, these pilot findings provide an additional understanding as to the neural control of dynamic movements.
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Static magnetic field (SMF) is gaining interest as a potential technique for modulating CNS neuronal activity. Previous studies have shown a pro-neurogenic effect of short periods of extremely low frequency pulsatile magnetic fields (PMF) in vivo and pro-survival effect of low intensity SMF in cultured neurons in vitro, but little is known about the in vivo effects of low to moderate intensity SMF on brain functions. We investigated the effect of continuously-applied SMF on subventricular zone (SVZ) neurogenesis and immature doublecortin (DCX)-expressing cells in the neocortex of young adult rats and in primary cultures of cortical neurons in vitro. ⋯ We found that low intensity SMF exposure enhances cell proliferation in SVZ and new DCX-expressing cells in neocortical regions of young adult rats. In primary cortical neuronal cultures, SMF exposure increased the expression of newly generated cells co-labelled with EdU and DCX or the mature neuronal marker NeuN, while activating a set of pro neuronal bHLH genes. SMF exposure has potential for treatment of neurodegenerative disease and conditions such as CNS trauma and affective disorders in which increased neurogenesis is desirable.