As a widely recognized public health problem as well as prevalent and challenging to modern society, chronic insomnia is involved in wide brain areas (such as prefrontal cortex, anterior cingulate cortex, amygdala, hippocampus, and thalamus) and emotion-cognition neuro-circuit. It is closely related to the conditioned hyperarousal and the increased information process and/or the impaired inhibitory ability to withdraw from awaking state. Thus, some specific abnormal mode may exist in the emotion-cognition circuit, which is associated with abnormal cognition load, such as repeated retrieval/intrusion of aversive memories during night. Studies through the combination of multiple techniques including psychology, electrophysiology and neuroimaging methods are needed to further enhance the understanding of chronic insomnia.
Brain ; physiopathology ; Electrophysiology ; Gyrus Cinguli ; Hippocampus ; Humans ; Neuroimaging ; Prefrontal Cortex ; Sleep Initiation and Maintenance Disorders ; pathology ; Thalamus

With a rapid development of neuroscience, the theories related to the pathophysiology of schizophrenia have been changed a lot from a simple hyperdopaminergic one to the various complicated ones. Among these, the theories regarding prefrontal cortex(PFC) pathology as a cause of schizophrenia are gaining more recognition as the results of neuroimaging and neuropsychological tests in schizophrenia consistently report abnormalities in PFC. Therefore, we first reviewed the unique characteristics of PFC in anatomy, neurochemistry and neurophysiology to enhance an understanding of those ones. Secondly, various neurotransmitter, neurodevelopmental and neural network theories of schizophrenia introduced recently were reviewed in terms of PFC pathology.
Dopamine ; Neurochemistry ; Neuroimaging ; Neurophysiology ; Neuropsychological Tests ; Neurosciences ; Neurotransmitter Agents ; Pathology ; Prefrontal Cortex* ; Schizophrenia*

BACKGROUND: Patients with schizophrenia (SCZ) and major depressive disorder (MDD) share significant clinical overlap, although it remains unknown to what extent this overlap reflects shared neural profiles. To identify the shared and specific abnormalities in SCZ and MDD, we performed a whole-brain voxel-based meta-analysis using magnetization transfer imaging, a technique that characterizes the macromolecular structural integrity of brain tissue in terms of the magnetization transfer ratio (MTR). METHODS: A systematic search based on Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines was conducted in PubMed, EMBASE, International Scientific Index (ISI) Web of Science, and MEDLINE for relevant studies up to March 2022. Two researchers independently screened the articles. Rigorous scrutiny and data extraction were performed for the studies that met the inclusion criteria. Voxel-wise meta-analyses were conducted using anisotropic effect size-signed differential mapping with a unified template. Meta-regression was used to explore the potential effects of demographic and clinical characteristics. RESULTS: A total of 15 studies with 17 datasets describing 365 SCZ patients, 224 MDD patients, and 550 healthy controls (HCs) were identified. The conjunction analysis showed that both disorders shared higher MTR than HC in the left cerebellum ( P =0.0006) and left fusiform gyrus ( P =0.0004). Additionally, SCZ patients showed disorder-specific lower MTR in the anterior cingulate/paracingulate gyrus, right superior temporal gyrus, and right superior frontal gyrus, and higher MTR in the left thalamus, precuneus/cuneus, posterior cingulate gyrus, and paracentral lobule; and MDD patients showed higher MTR in the left middle occipital region. Meta-regression showed no statistical significance in either group. CONCLUSIONS The results revealed a structural neural basis shared between SCZ and MDD patients, emphasizing the importance of shared neural substrates across psychopathology. Meanwhile, distinct disease-specific characteristics could have implications for future differential diagnosis and targeted treatment.
Humans ; Depressive Disorder, Major/drug therapy* ; Schizophrenia/pathology* ; Brain/pathology* ; Prefrontal Cortex ; Frontal Lobe ; Magnetic Resonance Imaging/methods*

BACKGROUND AND PURPOSE: Involvement of the corpus callosum (CC) is reported to be a consistent feature of amyotrophic lateral sclerosis (ALS). We examined the CC pathology using diffusion tensor tractography analysis to identify precisely which fiber bundles are involved in ALS. METHODS: Diffusion tensor imaging was performed in 14 sporadic ALS patients and 16 age-matched healthy controls. Whole brain tractography was performed using the multiple-region of interest (ROI) approach, and CC fiber bundles were extracted in two ways based on functional and structural relevance: (i) cortical ROI selection based on Brodmann areas (BAs), and (ii) the sulcal-gyral pattern of cortical gray matter using FreeSurfer software, respectively. RESULTS: The mean fractional anisotropy (FA) values of the CC fibers interconnecting the primary motor (BA4), supplementary motor (BA6), and dorsolateral prefrontal cortex (BA9/46) were significantly lower in ALS patients than in controls, whereas those of the primary sensory cortex (BA1, BA2, BA3), Broca's area (BA44/45), and the orbitofrontal cortex (BA11/47) did not differ significantly between the two groups. The FreeSurfer ROI approach revealed a very similar pattern of abnormalities. In addition, a significant correlation was found between the mean FA value of the CC fibers interconnecting the primary motor area and disease severity, as assessed using the revised Amyotrophic Lateral Sclerosis Functional Rating Scale, and the clinical extent of upper motor neuron signs. CONCLUSIONS: Our findings suggest that there is some degree of selectivity or a gradient in the CC pathology in ALS. The CC fibers interconnecting the primary motor and dorsolateral prefrontal cortices may be preferentially involved in ALS.
Amyotrophic Lateral Sclerosis* ; Anisotropy ; Brain ; Corpus Callosum* ; Diffusion Tensor Imaging ; Diffusion* ; Humans ; Motor Neuron Disease ; Motor Neurons ; Pathology ; Prefrontal Cortex

Micturition is a complex process involving the bladder, spinal cord, and the brain. Highly sophisticated central neural program controls bladder function by utilizing multiple brain regions, including pons and suprapontine structures. Periaqueductal grey, insula, anterior cingulate cortex, and medial prefrontal cortex are components of suprapontine micturition centers. Under pathologic conditions such as epilepsy, urinary dysfunction is a frequent symptom and it seems to be associated with increased suprapontine cortical activity. Interestingly, micturition can also trigger seizures known as reflex epilepsy. During voiding behavior, frontotemporal cortical activation has been reported and it may induce reflex seizures. As current researches are only limited to present clinical cases, more rigorous investigations are needed to elucidate biological mechanisms of micturition to advance our knowledge on the process of micturition in physiology and pathology.
Brain ; Epilepsy* ; Epilepsy, Reflex ; Gyrus Cinguli ; Pathology ; Physiology ; Pons ; Prefrontal Cortex ; Reflex ; Seizures ; Spinal Cord ; Urinary Bladder ; Urination*

OBJECTIVE: To explore the olfactory abilities in patients with allergic rhinitis (AR), analyze the correlation between olfactory bulb (OB) volume with depth of olfactory sulcus (OS) and olfactory function in patients with AR. METHOD: One hundred patients with AR were compared with one hundred controls in terms of olfactory function T&T testing, OB volume and depth of OS assessed with magnetic resonance imaging (MRI). T&T testing and MRI were done after a year in 100 AR patients,the results were compared with the initial results. RESULT: The OB volume in AR patients was (29.53±3.95) mm3 on the left, (29.67±14.21)mm3 on the right, (29.61±4.05) mm3 on average; The OB volume in controls was (48.93±6.73)mm3 on the left side, (48.81±7.43)mm3 on the right side, (48.85±7.11)mm3 on average; The OB volume in AR patients was less then the control group(t= 6.321, 6.141, 6.221, P<0.01). The OS depth had no statistical difference between AR patients and controls (t=1.032, 0.972, 0.991, P>0.05). Olfactory discriminate threshold was negatively correlated with OB volume in AR patients (r=-0.46, P<0.05); and it was no correlated with depth of OS (r=-0.012,P>0.05). Among 100 followed-up AR patients, 43 showed increased in OB volume and olfactory function after a year, but there was no statistical difference (t= 0. 811,0. 843, 0.826, P>0.05; Z=1.911, P>0.05) ,and the other 57 showed no significant changes of OB volume and olfactory function. CONCLUSION In AR patients, the OB volume and olfactory function decreased, but the depth of OS had no significant changes. The OB volume is correlated with olfactory function, while the depth of OS is no correlated with olfactory function. Conservative treatment had some clinical significance on the recovery of olfactory function in patients with AR.
Humans ; Magnetic Resonance Imaging ; Olfaction Disorders ; etiology ; Olfactory Bulb ; pathology ; physiopathology ; Prefrontal Cortex ; Rhinitis, Allergic ; complications ; Smell

OBJECTIVETo investigate the mechanisms of taurine (Tau) preventive effect on neurotoxicity induced by manganese (Mn) in rat's prefrontal cortex.

METHODSSD rats were divided into four groups after one week of observation: normal control:the group animals received daily intraperitoneal (ip.) injections of sterile saline for 3 months; Mn treated group (Mn): rats received ip. injection of MnCl(2).4H(2)O once a day for 3 months; Tau preventive group (Mn + Tau): The Mn level of this group were the same as Mn's, the Tau level 200 mg/kg, three times per week, for 3 months; Tau treated group (Mn-->Tau): After received the daily injection of Mn as Mn group for 3 months, the rats received Tau three times per week for 3 months. The dose of Mn and Tau were the same as above. The experiment lasted 6 months.

RESULTS(1) Mn induced apoptosis of neurons in rat's prefrontal cortex. The ratio of apoptosis of neurons in the Mn treated group [(20.0 +/- 4.3)%] was higher than that of the control group [(1.8 +/- 2.1)%] (P < 0.05) and the ratio of apoptosis in Tau preventive group (Mn + Tau) was lower than that of the Mn treated group (P < 0.05). (2) The production of MDA in Mn treated group was higher than the control group (P < 0.05) and the activity of SOD was lower than that in the control group. In Tau preventive group (Mn + Tau), Tau increased the activity of SOD and decreased the production of the MDA, with the significant difference level compared to the Mn treated group (P < 0.05).

CONCLUSIONMn induces apoptosis in rat's prefrontal cortex neurons. The main mechanisms of Tau preventing cytotoxicity against Mn is the reduction of the oxidative stress in prefrontal cortex neurons.

Animals ; Apoptosis ; drug effects ; Drug Antagonism ; Male ; Manganese ; toxicity ; Neurons ; drug effects ; metabolism ; pathology ; Neurotoxicity Syndromes ; etiology ; metabolism ; pathology ; prevention & control ; Prefrontal Cortex ; drug effects ; metabolism ; pathology ; Rats ; Rats, Sprague-Dawley ; Taurine ; pharmacology

OBJECTIVETo investigate the relation between the progressive effects of chronic intermittent hypoxia (CIH) on cognitive function and the change of cholinergic neuron.

METHODSForty adult male Sprague-Dawley rats were randomly averagely divided into four groups: control group, CIH 1 week group, CIH 3 week group and CIH 5 week group. The cognitive function was assessed by the Morris Water Maze. The necrosis neurons in prefrontal cortex and hippocampus were observed and counted. The cholin acetyltransferase (ChAT) immunostained cells in prefrontal cortex and hippocampus were identified and quantitated.

RESULTSThe spatial learning and memory impairments progressed from 1 to 5 5 weeks in rats. Compared with the control group, the cognitive impairments in CIH5w group were significant (P < 0.05). The degeneration or necrosis neurons in prefrontal cortex and hippocampus were significantly increased in CIH rats, and worsen gradually along with the hypoxia. The ChAT immunostained cells in prefrontal cortex and hippocampus were gradually reduced. The ChAT immunostained cells of prefrontal cortex and hippocampus in CIH3w group and CIH5w group were less than that in control group (P < 0.05).

CONCLUSIONChronic intermittent hypoxia induced slowly progressive spatial learning and memory impairments in rats, which maybe associated with the damage of neurons and the reduction of ChAT in prefrontal cortex and hippocampus.

Animals ; Cholinergic Fibers ; pathology ; physiology ; Cholinergic Neurons ; pathology ; physiology ; Cognition ; physiology ; Hippocampus ; cytology ; physiopathology ; Hypoxia ; physiopathology ; Male ; Maze Learning ; physiology ; Memory Disorders ; etiology ; physiopathology ; Prefrontal Cortex ; cytology ; physiopathology ; Rats ; Rats, Sprague-Dawley

Catechol-O-methyltransferase (COMT) gene encodes catechol-O-methyltransferase, the variant of this gene may affect the expression and metabolic activity of COMT. As the result of the changes of the effective concentration of the catecholamine neurotransmitter in the central nervous system, central nervous system dysfunctions associated with schizophrenia. This review summarizes genetic polymorphism and diversity of COMT gene. It also elaborates the relation between SNP and haplotype of COMT gene and three aspects, which including schizophrenia, attacking and violent tendency, and the frontal cognitive function of the schizophreniac. The correlativity study between genetic variation of the COMT gene and schizophrenia in patients with attacking and violent tendency may be helpful for the assessment of forensic psychiatry.
Aggression/psychology* ; Brain/pathology* ; Catechol O-Methyltransferase/genetics* ; Cognition/physiology* ; Dopamine/metabolism* ; Forensic Genetics ; Gene Expression ; Genetic Predisposition to Disease ; Genetic Variation ; Genotype ; Haplotypes ; Humans ; Polymerase Chain Reaction ; Polymorphism, Genetic ; Prefrontal Cortex/pathology* ; Promoter Regions, Genetic ; Schizophrenia/genetics* ; Violence/psychology*

Cognition and pain share common neural substrates and interact reciprocally: chronic pain compromises cognitive performance, whereas cognitive processes modulate pain perception. In the present study, we established a non-drug-dependent rat model of context-based analgesia, where two different contexts (dark and bright) were matched with a high (52°C) or low (48°C) temperature in the hot-plate test during training. Before and after training, we set the temperature to the high level in both contexts. Rats showed longer paw licking latencies in trials with the context originally matched to a low temperature than those to a high temperature, indicating successful establishment of a context-based analgesic effect in rats. This effect was blocked by intraperitoneal injection of naloxone (an opioid receptor antagonist) before the probe. The context-based analgesic effect also disappeared after optogenetic activation or inhibition of the bilateral infralimbic or prelimbic sub-region of the prefrontal cortex. In brief, we established a context-based, non-drug dependent, placebo-like analgesia model in the rat. This model provides a new and useful tool for investigating the cognitive modulation of pain.
Action Potentials ; drug effects ; physiology ; Analgesics ; pharmacology ; therapeutic use ; Animals ; Disease Models, Animal ; Electric Stimulation ; Female ; In Vitro Techniques ; Naloxone ; pharmacology ; Narcotic Antagonists ; pharmacology ; Optogenetics ; Pain ; drug therapy ; pathology ; physiopathology ; Pain Measurement ; drug effects ; Pain Threshold ; drug effects ; physiology ; Patch-Clamp Techniques ; Physical Stimulation ; Prefrontal Cortex ; drug effects ; metabolism ; pathology ; Pyramidal Cells ; drug effects ; physiology ; Rats ; Rats, Sprague-Dawley ; Time Factors