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The BNST encompasses an astonishing diversity of cell types that differ across many features including spatial organization, molecular signature, biological sex and hormonal milieu, synaptic input, axonal output, neurophysiological communication mode, and functional role. Given this tremendous complexity, comprehensive elucidation of the BNST neuropeptide circuit mechanisms underlying emotional arousal presents an ambitious set of challenges. In this review, we describe how rigorous investigation of these unresolved questions may reveal key insights to enhancing psychiatric treatments and global psychological wellbeing.

Nicotine is the major addictive component of cigarette smoke and the prime culprit of the failure to quit smoking. Common elements perpetuating the use of addictive drugs are (i) cues associated with the setting in which drug was used and (ii) relapse/reinstatement mediated by an increased glutamatergic tone (iii) associated with drug-induced neuroinflammation and oxidative stress.

The present study assessed the effect of the coadministration of the antioxidant

-acetylcysteine (NAC) plus the anti-inflammatory acetylsalicylic acid (ASA) on oral nicotine reinstatement intake following a post-deprivation re-access in female rats that had chronically and voluntarily consumed a nicotine solution orally. The nicotine-induced oxidative stress and neuroinflammation in the hippocampus and its effects on the glutamate transporters GLT-1 and XCT mRNA levels in prefrontal cortex were also analyzed.

The oral coadministration of NAC (40 mg/kg/day) and ASA (15 mg/kg/day) inhibited by 85% of the oral nicotine reinstaent behaviors.

Nicotine reinstatement, following post-deprivation of chronic oral nicotine intake, downregulates the mRNA levels of GLT-1 and xCT transporters, an effect reversed by the coadministration of N-acetylcysteine and acetylsalicylic acid, leading to a marked inhibition of nicotine intake. The combination of these drugs may constitute a valuable adjunct in the treatment of nicotine-dependent behaviors.The existing computational models used to estimate motion sickness are incapable of describing the fact that the predictability of motion patterns affects motion sickness. Therefore, the present study proposes a computational model to describe the effect of the predictability of dynamics or the pattern of motion stimuli on motion sickness. In the proposed model, a submodel - in which a recursive Gaussian process regression is used to represent human features of online learning and future prediction of motion dynamics - is combined with a conventional model of motion sickness based on an observer theory. A simulation experiment was conducted in which the proposed model predicted motion sickness caused by a 900 s horizontal movement. The movement was composed of a 9 m repetitive back-and-forth movement pattern with a pause. Regarding the motion condition, the direction and timing of the motion were varied as follows (a) Predictable motion (M_P) the direction of the motion and duration of the pause were set to 8 s; (b) Motion with unpredicted direction (M_dU) the pause duration was fixed as in (M_P), but the motion direction was randomly determined; (c) Motion with unpredicted timing (M_tU) the motion direction was fixed as in (M_P), but the pause duration was randomly selected from 4 to 12 s. The results obtained using the proposed model demonstrated that the predicted motion sickness incidence for (M_P) was smaller than those for (M_dU) and (M_tU) and no considerable difference was found between M_dU and M_tU. This tendency agrees with the sickness patterns observed in a previous experimental study in which the human participants were subject to motion conditions similar to those used in our simulations. Moreover, no significant differences were found in the predicted motion sickness incidences at different conditions when the conventional model was used.Slow oscillations are a pattern of synchronized network activity generated by the cerebral cortex. They consist of Up and Down states, which are periods of activity interspersed with periods of silence, respectively. However, even when this is a unique dynamic regime of transitions between Up and Down states, this pattern is not constant there is a range of oscillatory frequencies (0.1-4 Hz), and the duration of Up vs. Down states during the cycles is variable. This opens many questions. Is there a constant relationship between the duration of Up and Down states? How much do they vary across conditions and oscillatory frequencies? Are there different sub regimes within the slow oscillations? To answer these questions, we aimed to explore a concrete aspect of slow oscillations, Up and Down state durations, across three conditions deep anesthesia, light anesthesia, and slow-wave sleep (SWS), in the same chronically implanted rats. selleckchem We found that light anesthesia and SWS have rather similar properties, occupying a small area of the Up and Down state duration space. Deeper levels of anesthesia occupy a larger region of this space, revealing that a large variety of Up and Down state durations can emerge within the slow oscillatory regime. In a network model, we investigated the network parameters that can explain the different points within our bifurcation diagram in which slow oscillations are expressed.Olfactory bulb and higher processing areas are synaptically interconnected, providing rapid regulation of olfactory bulb circuit dynamics and sensory processing. Short-term plasticity changes at any of these synapses could modulate sensory processing and potentially short-term sensory memory. A key olfactory bulb circuit for mediating cortical feedback modulation is granule cells, which are targeted by multiple cortical regions including both glutamatergic excitatory inputs and GABAergic inhibitory inputs. There is robust endocannabinoid modulation of excitatory inputs to granule cells and here we explored whether there was also endocannabinoid modulation of the inhibitory cortical inputs to granule cells. We expressed light-gated cation channel channelrhodopsin-2 (ChR2) in GABAergic neurons in the horizontal limb of the diagonal band of Broca (HDB) and their projections to granule cells in olfactory bulb. Selective optical activation of ChR2 positive axons/terminals generated strong, frequency-dependent short-term depression of GABA A -mediated-IPSC in granule cells.

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