Dorsal BNST DRD2+ neurons mediate sex-specific anxiety-like behavior induced by chronic social isolation.

The dorsal bed nucleus of stria terminalis (dBNST) is a pivotal hub for stress response modulation. Dysfunction of dopamine (DA) network is associated with chronic stress, but the roles of DA network of dBNST in chronic stress-induced emotional disorders remain unclear. We examine the role of dBNST Drd1+ and Drd2+ neurons in post-weaning social isolation (PWSI)-induced behavior deficits. We find that male, but not female, PWSI rats exhibit negative emotional phenotypes and the increase of excitability and E-I balance of dBNST Drd2+ neurons. More importantly, hypofunction of dBNST Drd2 receptor underlies PWSI-stress-induced male-specific neuronal plasticity change of dBNST Drd2+ neurons. Furthermore, chemogenetic activation of dBNST Drd2+ neurons is sufficient to induce anxiogenic effects, while Kir4.1-mediated chronic inhibition of dBNST Drd2+ neurons ameliorate PWSI-induced anxiety-like behaviors. Our findings reveal an important neural mechanism underlying PWSI-induced sex-specific behavioral abnormalities and potentially provide a target for the treatment of social stress-related emotional disorder.

Correction to: Projection from the Anterior Cingulate Cortex to the Lateral Part of Mediodorsal Thalamus Modulates Vicarious Freezing Behavior.

The authors found that in this article.

Spike Phase Shift Relative to Beta Oscillations Mediates Modality Selection.

How does the brain selectively process signals from stimuli of different modalities? Coherent oscillations may function in coordinating communication between neuronal populations simultaneously involved in such cognitive behavior. Beta power (12-30 Hz) is implicated in top-down cognitive processes. Here we test the hypothesis that the brain increases encoding and behavioral influence of a target modality by shifting the relationship of neuronal spike phases relative to beta oscillations between primary sensory cortices and higher cortices. We simultaneously recorded neuronal spike and local field potentials in the posterior parietal cortex (PPC) and the primary auditory cortex (A1) when male rats made choices to either auditory or visual stimuli. Neuronal spikes exhibited modality-related phase locking to beta oscillations during stimulus sampling, and the phase shift between neuronal subpopulations demonstrated faster top-down signaling from PPC to A1 neurons when animals attended to auditory rather than visual stimuli. Importantly, complementary to spike timing, spike phase predicted rats' attended-to target in single trials, which was related to the animals' performance. Our findings support a candidate mechanism that cortices encode targets from different modalities by shifting neuronal spike phase. This work may extend our understanding of the importance of spike phase as a coding and readout mechanism.

Projection from the Anterior Cingulate Cortex to the Lateral Part of Mediodorsal Thalamus Modulates Vicarious Freezing Behavior.

Emotional contagion, a primary form of empathy, is present in rodents. Among emotional contagion behaviors, social transmission of fear is the most studied. Here, we modified a paradigm used in previous studies to more robustly assess the social transmission of fear in rats that experienced foot-shock. We used resting-state functional magnetic resonance imaging to show that foot-shock experience enhances the regional connectivity of the anterior cingulate cortex (ACC). We found that lesioning the ACC specifically attenuated the vicarious freezing behavior of foot-shock-experienced observer rats. Furthermore, ablation of projections from the ACC to the mediodorsal thalamus (MDL) bilaterally delayed the vicarious freezing responses, and activation of these projections decreased the vicarious freezing responses. Overall, our results demonstrate that, in rats, the ACC modulates vicarious freezing behavior via a projection to the MDL and provide clues to understanding the mechanisms underlying empathic behavior in humans.

Neural activity of orbitofrontal cortex contributes to control of waiting.

The willingness to wait for delayed reward and information is of fundamental importance for deliberative behaviors. The orbitofrontal cortex (OFC) is thought to be a core component of the neural circuitry underlying the capacity to control waiting. However, the neural correlates of active waiting and the causal role of the OFC in the control of waiting still remain largely unknown. Here, we trained rats to perform a waiting task (waiting for a pseudorandom time to obtain the water reward), and recorded neuronal ensembles in the OFC throughout the task. We observed that subset OFC neurons exhibited ramping activities throughout the waiting process. Receiver operating characteristic analysis showed that neural activities during the waiting period even predicted the trial outcomes (patient vs. impatient) on a trial-by-trial basis. Furthermore, optogenetic activation of the OFC during the waiting period improved the waiting performance, but did not influence rats' movement to obtain the reward. Taken together, these findings reveal that the neural activity in the OFC contributes to the control of waiting.

[Advances on Drosophila presenilin gene].

In Drosophila, presenilin is an aspartyl protease that plays important roles in the development and calcium homeostasis. It has been expressed all through the fly developmental process. The loss of Drosophila presenilin (DPS) function causes significantly decreased Notch signaling and neuron apoptosis and increased cytoplasm calcium. This subsequently led to impaired long term memory and cognitive deficits. Therefore, study of DPS is one of the most popular models for Alzheimer's disease research, and has provided important insights into the pathological mechanisms of AD. This review is to summarize the AD related function of DPS gene.