Accelerometer-based and self-reported physical activity and sedentary time and their relationships with the P300 in a Go/No-Go task in older adults.

Older adults who experience cognitive decline are more likely to have a reduced quality of life. Identifying lifestyle factors that may influence cognitive processing and in turn improve quality of life during older adulthood is an important area of interest. Cognitive function, as measured by the P300 event-related potential (ERP), has been noted to be modified by physical activity; however, no study to date has examined relationships between this neurophysiological measure and physical activity and sedentary time in older adults. Furthermore, there is a gap in understanding as to whether physical activity and sedentary time assessed using self-reported and accelerometer-based methods similarly relate to the P300. This study aimed to assess the P300 during a Go/No-Go task in relation to self-reported and accelerometer-based physical activity and sedentary time in a community sample of 75 older adults. Results indicated that participants engaging in more moderate-to-vigorous physical activity had larger P300 amplitudes across self-reported and accelerometer-based measurements; however, no relationships between sedentary time and P300 amplitude were observed. Notably, accelerometer-based moderate-to-vigorous physical activity explained P300 amplitudes over and above self-reported moderate-to-vigorous physical activity-an effect that remained significant even after accounting for age. Although these results highlight the importance of moderate-to-vigorous physical activity in relation to cognitive function, as measured via the P300 in older adults, a secondary analysis indicated that engaging in lifestyle activity may have similar effects on the P300 as moderate-to-vigorous physical activity. In sum, the present study highlights the role of habitual engagement in physical activity as a possible means for supporting cognitive function during the aging process.

Sex-specific adaptations to VTA circuits following subchronic stress.

Dysregulation of the mesolimbic reward circuitry is implicated in the pathophysiology of stress-related illnesses such as depression and anxiety. These disorders are more frequently diagnosed in females, and sex differences in the response to stress are likely to be one factor that leads to enhanced vulnerability of females. In this study, we use subchronic variable stress (SCVS), a model in which females are uniquely vulnerable to behavioral disturbances, to investigate sexually divergent mechanisms of regulation of the ventral tegmental area by stress. Using slice electrophysiology, we find that female, but not male mice have a reduction in the ex vivo firing rate of VTA dopaminergic neurons following SCVS. Surprisingly, both male and female animals show an increase in inhibitory tone onto VTA dopaminergic neurons and an increase in the firing rate of VTA GABAergic neurons. In males, however, this is accompanied by a robust increase in excitatory synaptic tone onto VTA dopamine neurons. This supports a model by which SCVS recruits VTA GABA neurons to inhibit dopaminergic neurons in both male and female mice, but males are protected from diminished functioning of the dopaminergic system by a compensatory upregulation of excitatory synapses.

Neural deficits in anticipatory and consummatory reward processing are uniquely associated with current depressive symptoms during adolescence.

Deficits within the consummatory phase of reward processing are associated with increased depression symptoms and risk; however, few studies have also examined other aspects of reward processing in relation to depression. In the current study, a community sample of 121 adolescents (Mage  = 13.1, Min = 11.14; Max = 15.12; 54% male) completed self-report questionnaires to assess depressive symptoms and the monetary incentive delay (MID) task while EEG was recorded. Results indicated that a reduced cue-P300 as well as a reduced reward positivity (RewP) and feedback negativity (FN) to gain and loss feedback, respectively, were associated with increased depressive symptoms; on the other hand, SPN and feedback P300 were unrelated to depressive symptoms. An exploratory multiple regression analysis revealed that a reduced money cue-P300, a reduced RewP, and a reduced (i.e., less negative) FN, all explained unique variance in depressive symptoms. The current study demonstrates that reduced cue-P300, RewP, and FN amplitudes may reflect distinct deficits in reward processing among adolescents with increased depressive symptoms. Notably, this study is one of the first to leverage the MID task in adolescents in relation to depressive symptoms, allowing for a more in-depth view of the individual differences in reward processing among adolescents with increased depressive symptomatology.

VTA GABA Neurons at the Interface of Stress and Reward.

The ventral tegmental area (VTA) is best known for its robust dopaminergic projections to forebrain regions and their critical role in regulating reward, motivation, cognition, and aversion. However, the VTA is not only made of dopamine (DA) cells, as approximately 30% of cells in the VTA are GABA neurons. These neurons play a dual role, as VTA GABA neurons provide both local inhibition of VTA DA neurons and long-range inhibition of several distal brain regions. VTA GABA neurons have increasingly been recognized as potent mediators of reward and aversion in their own right, as well as potential targets for the treatment of addiction, depression, and other stress-linked disorders. In this review article, we dissect the circuit architecture, physiology, and behavioral roles of VTA GABA neurons and suggest critical gaps to be addressed.