Neuroscience
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The ventral hippocampus is a component of the neural circuitry involved with context-associated memory for reward and generation of appropriate behavioral responses to context. Glycogen synthase kinase 3 beta (GSK3β) has been linked to the maintenance of synaptic plasticity, contextual memory retrieval, and is involved in the reconsolidation of cocaine-associated contextual memory. In this study, the effects of targeted downregulation of GSK3β in the ventral hippocampus were examined on a series of behavioral tests for assessing drug reward-context association and non-reward related memory. ⋯ Impaired object location memory was observed in mice with GSK3β downregulation in the ventral hippocampus, but novel object recognition remained intact. These results indicate that GSK3β signaling in the ventral hippocampus is differentially involved in the formation of place-drug reward association dependent upon drug class. Additionally, ventral hippocampal GSK3β signaling is important in detection of discrete spatial cues, but not recognition memory for objects.
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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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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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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.