Introduction The medial orbitofrontal cortex (mOFC) and rostral part of the anterior cingulate cortex (rACC) are brain regions that are important in the neural network involving emotional processing and decision making, as well as playing an important role in social behavior and interaction. Considering the schizophrenia dysconnectivity hypothesis, observed abnormalities in emotional response and social behavior in schizophrenia might be associated with connectivity abnormalities between mOFC and rACC. Methods Twenty-seven patients with chronic schizophrenia and 26 healthy controls were examined using Diffusion Tensor Imaging (DTI). White matter properties in bilateral mOFC-rACC connections were examined using stochastic tractography, which has been shown to be among the most effective DTI methods for examining tracts between adjacent gray matter regions. Results Reductions in fractional anisotropy (FA) were observed in left anterior mOFC-rACC connections (p<0.0001), and bilateral posterior mOFC-rACC connections (left: p<0.0001; right: p<0.0001) in patients compared to controls. In addition, reduced FA in left posterior mOFC-rACC connections were associated with more severe anhedonia-asociality (R=−0.396, P=0.041) and avolition-apathy (R=−0.426, p=0.027) using the Scale for the Assessment of Negative Symptoms. Discussion White matter abnormalities within connections between mOFC and rACC are associated with more severe anhedonia-asociality and avolition-apathy, which suggest that these brain regions may be important in understanding abnormal emotional responses and social behavior in patients with schizophrenia.

General anesthesia is characterized by loss of consciousness, amnesia, analgesia, and immobility. Important molecular targets of general anesthetics have been identified, but the neural circuits underlying the discrete end points of general anesthesia remain incompletely understood. General anesthesia and natural sleep share the common feature of reversible unconsciousness, and recent developments in neuroscience have enabled elegant studies that investigate the brain nuclei and neural circuits underlying this important end point. A common approach to measure cortical activity across the brain is electroencephalogram (EEG), which can reflect local neuronal activity as well as connectivity among brain regions. The EEG oscillations observed during general anesthesia depend greatly on the anesthetic agent as well as dosing, and only some resemble those observed during sleep. For example, the EEG oscillations during dexmedetomidine sedation are similar to those of stage 2 nonrapid eye movement (NREM) sleep, but high doses of propofol and ether anesthetics produce burst suppression, a pattern that is never observed during natural sleep. Sleep is primarily driven by withdrawal of subcortical excitation to the cortex, but anesthetics can directly act at both subcortical and cortical targets. While some anesthetics appear to activate specific sleep-active regions to induce unconsciousness, not all sleep-active regions play a significant role in anesthesia. Anesthetics also inhibit cortical neurons, and it is likely that each class of anesthetic drugs produces a distinct combination of subcortical and cortical effects that lead to unconsciousness. Conversely, arousal circuits that promote wakefulness are involved in anesthetic emergence and activating them can induce emergence and accelerate recovery of consciousness. Modern neuroscience techniques that enable the manipulation of specific neural circuits have led to new insights into the neural circuitry underlying general anesthesia and sleep. In the coming years, we will continue to better understand the mechanisms that generate these distinct states of reversible unconsciousness.