OBJECTIVE: To observe the dynamic changes of microvascular injury and repair in the penumbra of traumatic brain injury (TBI) rats with effective cerebral perfusion microvascular imaging using optical coherence tomography angiography (OCTA). METHODS: Transparent closed cranial windows were placed in craniotomy rats after TBI caused by weight drop. All the rats in TBI group and control group underwent head MRI examination on the first postoperative day, and the changes of cerebral cortical microvessel density were measured by OCTA through cranial windows on d0, d2, d4, d6, and d8. On the second day after the operation, the same number of rats in the two groups were selected to complete the immunohistochemical staining of brain tissue with pimonidazole, an indicator of hypoxia. RESULTS: MRI T2W1 and immunohistochemical staining demonstrated that edema and hypoxia in the traumatic brain tissue extended deeply throughout the entire cortex. OCTA showed that the cortical surface veins of the rats in both groups were significantly dilated and tortuous after operation, and recovered to the postoperative day level on d8. The effective perfusion microvessel density of the rats in both groups gradually recovered after a temporary decrease, and the TBI group decreased from 39.38%±4.48% on d0 to 27.84%±6.01% on d2, which was significantly lower than that on d0, d6, and d8 (P < 0.05). The highest value was 61.71%±7.69% on d8, which was significantly higher than that on d0, d2, and d4 (P < 0.05). The control group decreased from 44.59%±7.78% on d0 to 36.69%±5.49% on d2, which was significantly lower than that on d0, d6, and d8 (P < 0.05). The highest value was 51.92%±5.96% on d8, which was significantly higher than that on d2, and d4 (P < 0.05). Comparing the two groups, the effective perfusion microvessel density in the TBI group was significantly lower than that in the control group on d2 (P=0.021), and significantly higher than that in the control group on d8 (P=0.030). CONCLUSION OCTA can be used as a method of imaging and measurement of effective perfusion microvessels in the injured cerebral cortex of TBI rats. After TBI, the effective perfusion microvessel density in the wound penumbra gradually recovered after decreasing, and increased significantly on d8.
Animals ; Brain Injuries, Traumatic/physiopathology* ; Rats ; Tomography, Optical Coherence/methods* ; Male ; Rats, Sprague-Dawley ; Microvessels/pathology* ; Microvascular Density ; Cerebral Cortex/blood supply* ; Cerebrovascular Circulation

The retrosplenial cortex has been implicated in processing sensory information and spatial learning, with abnormal neural activity reported in association with psychedelics and in mouse and non-human primate models of autism spectrum disorders (ASDs). The direct role of the retrosplenial cortex in regulating social behaviors remains unclear. In this work, we reveal that neural activity in the retrosplenial agranular cortex (RSA), a subregion of the retrosplenial cortex, is initially activated, then quickly suppressed upon social contact. This up-down phase of RSA neurons is crucial for normal social behaviors. Parvalbumin-positive GABAergic neurons in the hippocampal CA1 region were found to send inhibitory projections to the RSA. Blocking these CA1-RSA inhibitory inputs significantly impaired social behavior. Notably, enhancing the CA1-RSA inhibitory input rescued the social behavior defects in an ASD mouse model. This work suggests a neural mechanism for the salience processing of social behavior and identifies a potential target for ASD intervention using neural modulation approaches.
Animals ; Social Behavior ; CA1 Region, Hippocampal/physiology* ; Mice ; Male ; Autism Spectrum Disorder/physiopathology* ; Mice, Inbred C57BL ; GABAergic Neurons/drug effects* ; Neural Inhibition/drug effects* ; Parvalbumins/metabolism* ; Neural Pathways/physiology* ; Cerebral Cortex/physiology*

OBJECTIVE: To investigate the changes in gray matter volume in depressive-like mice and explore the possible mechanism. METHODS: Twenty-four 6-week-old C57 mice were randomized equally into control group and model group, and the mice in the model group were subjected to chronic unpredictable mild stimulation (CUMS) for 35 days. Magnetic resonance imaging was performed to examine structural changes of the grey matter volume in depressive-like mice. The expression of brain-derived neurotrophic factor (BDNF) in the grey matter of the mice was detected using Western blotting and immunofluorescence staining. RESULTS: Compared with the control mice, the mice with CUMS showed significantly decreased central walking distance in the open field test (P < 0.05) and increased immobile time in forced swimming test (P < 0.05). Magnetic resonance imaging showed that the volume of the frontal cortex was significantly decreased in CUMS mice (P < 0.001, when the mass level was greater than or equal to 10 756, the FDRc was corrected with P=0.05). Western blotting showed that the expression of mature BDNF in the frontal cortex was significantly decreased in CUMS mice (P < 0.05), and its expression began to decrease after the exposure to CUMS as shown by immunofluorescence staining. The volume of different clusters obtained by voxel-based morphometry (VBM) analysis was correlated with the expression level of mature BDNF detected by Western blotting (P < 0.05). CONCLUSION The decrease of frontal cortex volume after CUMS is related with the reduction of mature BDNF expression in the frontal cortex.
Animals ; Mice ; Blotting, Western ; Brain-Derived Neurotrophic Factor ; Cerebral Cortex ; Depression/physiopathology* ; Frontal Lobe/pathology*

A 68-year-old man presented with a three-week history of rapidly progressive dementia, gait ataxia and myoclonus. Subsequent electroencephalography showed periodic sharp wave complexes, and cerebrospinal fluid assay revealed the presence of a 14-3-3 protein. A probable diagnosis of sporadic Creutzfeldt-Jakob disease was made, which was further supported by magnetic resonance (MR) imaging of the brain showing asymmetric signal abnormality in the cerebral cortices and basal ganglia. The aetiology, clinical features, diagnostic criteria, various MR imaging patterns and radiologic differential diagnosis of sporadic Creutzfeldt-Jakob disease are discussed in this article.
Aged ; Brain ; pathology ; Cerebral Cortex ; Cerebrospinal Fluid ; metabolism ; Creutzfeldt-Jakob Syndrome ; diagnostic imaging ; Dementia ; physiopathology ; Diagnosis, Differential ; Diffusion Magnetic Resonance Imaging ; Electroencephalography ; Humans ; Hypoxia-Ischemia, Brain ; diagnostic imaging ; Male ; Prion Diseases ; physiopathology

The neurocircuitries that constitute the cortico-striato-thalamo-cortical (CSTC) circuit provide a framework for bridging gaps between neuroscience and executive function in attention deficit hyperactivity disorder (ADHD), but it has been difficult to identify the mechanisms for regulating emotional problems from the understanding of ADHD comorbidity with disruptive behavior disorders (DBD). Research based on "cool" and "hot" executive functional theory and the dual pathway models, which are thought of as applied response inhibition and delay aversion, respectively, within the neuropsychological view of ADHD, has shed light on emotional responding before and after decontextualized stimuli, while CSTC circuit-related domains have been suggested to explain the different emotional symptoms of ADHD with or without comorbid DBD. This review discusses the role of abnormal connections in each CSTC circuit, especially in the emotion circuit, which may be responsible for targeted executive dysfunction at the neuroscience level. Thus, the two major domains - abstract thinking (cool) and emotional trait (hot) - trigger the mechanism of onset of ADHD.
Animals ; Attention Deficit Disorder with Hyperactivity ; complications ; pathology ; psychology ; Attention Deficit and Disruptive Behavior Disorders ; complications ; pathology ; psychology ; Brain ; physiopathology ; Cerebral Cortex ; physiopathology ; Corpus Striatum ; physiopathology ; Emotions ; Humans ; Inhibition (Psychology) ; Neuropsychological Tests ; Thalamus ; physiopathology

Human functional MRI studies in acute and various chronic pain conditions have revolutionized how we view pain, and have led to a new theory that complex multi-dimensional pain experience (sensory-discriminative, affective/motivational, and cognitive) is represented by concurrent activity in widely-distributed brain regions (termed a network or pain matrix). Despite these breakthrough discoveries, the specific functions proposed for these regions remain elusive, because detailed electrophysiological characterizations of these regions in the primate brain are lacking. To fill in this knowledge gap, we have studied the cortical areas around the central and lateral sulci of the non-human primate brain with combined submillimeter resolution functional imaging (optical imaging and fMRI) and intracranial electrophysiological recording. In this mini-review, I summarize and present data showing that the cortical circuitry engaged in nociceptive processing is much more complex than previously recognized. Electrophysiological evidence supports the engagement of a distinct nociceptive-processing network within SI (i.e., areas 3a, 3b, 1 and 2), SII, and other areas along the lateral sulcus. Deafferentation caused by spinal cord injury profoundly alters the relationships between fMRI and electrophysiological signals. This finding has significant implications for using fMRI to study chronic pain conditions involving deafferentation in humans.
Animals ; Cerebral Cortex ; diagnostic imaging ; physiopathology ; Humans ; Pain ; diagnostic imaging ; pathology ; physiopathology ; Primates ; Touch ; physiology

Hypoxic-ischemic brain damage (HIBD) is referred to a common type of cerebral damage, which is caused by injury, leading to shallow bleeding in the cortex with intact cerebral pia mater. In recent years, studies show that a various kinds of immune cells and immune cellular factors are involved in the occurrence of HIBD. CC chemokine receptor 2 (CCR2) is a representative of CC chemokine receptor, and is widely distributed in cerebral neuron, astrocyte, and microglial cells, and is the main chemo-tactic factor receptor in brain tissue. CC chemokine ligand 2 (CCL2) is a kind of basophilic protein and the ligand of CCR2, and plays an important role in inflammation. In order to provide evidence for correlational studies in HIBD, this review will introduce the biological characteristics of CCR2 and CCL2, and illustrate the relationship between the immunoreactivity and HIBD.
Animals ; Brain Injuries/pathology* ; Cerebral Cortex/physiopathology* ; Chemokine CCL2/metabolism* ; Chemokines, CC/metabolism* ; Hypoxia-Ischemia, Brain/metabolism* ; Macrophage Inflammatory Proteins/metabolism* ; RNA, Messenger/metabolism* ; Rats ; Rats, Sprague-Dawley ; Receptors, CCR2/metabolism*

OBJECTIVETo explore the morphometric abnormalities of brain gray matter (GM) in patients with chronic low back pain (CLBP).

METHODSThirty patients with CLBP and 30 healthy individuals were enrolled and examined with a 3.0 T magnetic resonance (MR) scanner. High-resolution T1 structural MR data were acquired and data analysis was performed using voxel-based morphometry (VBM) in FMRIB Software Library. The morphological differences were compared between the two groups.

RESULTSs Compared with the healthy control subjects, patients with CLBP showed decreased GM volumes in several brain cortical areas including the bilateral superior frontal gyrus, right frontal pole, left insular cortex, left middle and left inferior temporal gyrus (P<0.05, after TFCE correction). Increased GM volumes were found in the patients in the subcortical structures including the left thalamus, bilateral putamen, bilateral nucleus accumben and right caudate nucleus (P<0.05, after TFCE correction).

CONCLUSIONPatients with CLBP have different patterns of GM abnormalities in different brain regions, characterized by reduced GM volume in cerebral cortical regions and increased GM volume in the subcortical nuclei. Such changes might be associated with the maladaptation of the brain in chronic pain state.

Cerebral Cortex ; Frontal Lobe ; Gray Matter ; diagnostic imaging ; pathology ; Humans ; Low Back Pain ; physiopathology ; Magnetic Resonance Imaging ; Temporal Lobe ; Thalamus

OBJECTIVE: To research the serum levels of BDNF, H2S and S-100β as metabolic product of hippocampus and cerebral cortex in moderate to severe obstructive sleep apnea hypopnea syndrome(OSAHS) patients before and after surgery, and to analyze their correlations with cognitive impairment. METHOD: Forty-four randomly selected diagnosed OSAHS patients were divided into two groups according to Montreal Cognitive Assessment (MoCA), 19 cases in cognitively normal group and 25 cases in cognitive dysfunction group. Cases in cognitive dysfunction group underwent UPPP oriented surgery, and received 6 months follow-up, 21 cases were remained as treament group, 4 cases lost. 19 cases of healthy subjects were randomly selected as the normal control group. All groups were detected for the serum BDNF, H2S and S-100β levels to analyze the correlations between the biochemical indexes and sleep disorders indexes, hypoxia levels and cognitive function scores. RESULT: (1) In the comparison between the treatment group and the normal control group regarding PSG monitoring results, the AHI, I + II, LA/HT and SLT90% indexes of OSAHS patients increased, and the III + IV phase, REM phase, MSaO2 and LSaO2 decreased. In the comparison between the cognitive dysfunction group and the cognitively normal group, the III + IV, REM and LSaO2 indexes of the cognitive dysfunction group decreased. (2) In the comparison between cognitive dysfunction group and cognitively normal group, and between the treatment group and the normal control group, BDNF and H2S levels increased and S-100β levels decreased, and the MoCA total scores, attention, memory/delayed recall scores decreased. (3) The correlation between biochemical indexes with PSG indexes was as follows. The serum BNDF and H2S levels were negatively correlated with AHI index. The serum BNDF and H2S levels were positively correlated with III + IV stage, REM stage and MSaO2 indexes. The S-100β level was positively correlated with AHI index, and S-100β levels were negatively correlated with III + IV stage, REM stage, MSaO2 and LSaO2 indexes. (4) The correlation between biochemical indexes and MoCA scores was as follows. The serum BNDF and H2S levels were positively correlated with MoCA total scores, attention, and memory/delayed recall scores. The serum S-100β levels were negatively correlated with MoCA total scores, attention and memory/ delayed recall scores. (5) The linear regression equation between MoCA total scores in cognitive dysfunction group of OSAHS patients and the serum BNDF, H2S and S-100β levels was as follows: Y(MoCA) = 40.131 + 0.22 X(BDNF) + 0.012 X(H2S)-0.647X(S-100β) (R2 = 0.461). CONCLUSION OSAHS patients with sleep disorder and nocturnal hypoxemia might suffer from cognitive dysfunction in which attention and memory predominates. Serum BNDF, H2S and S-100β levels, which could indirectly reflect the metabolic abnormalities degree of hippocampus and cerebral cortex, are sensitive indicators of early cognitive dysfunction in OSAHS patients.
Brain-Derived Neurotrophic Factor ; metabolism ; Cerebral Cortex ; physiopathology ; Cognition Disorders ; complications ; Hippocampus ; physiopathology ; Humans ; Hypoxia ; Memory ; Metabolic Diseases ; physiopathology ; S100 Calcium Binding Protein beta Subunit ; metabolism ; Sleep Apnea, Obstructive ; complications

OBJECTIVE: To observe the time-course expression of zonula occludens-1 (ZO-1) in cerebral cortex after traumatic brain injury (TBI). METHODS: The TBI model of mouse was established. The mice were divided in 1 h, 3 h, 6 h, 12 h, 24 h, 3 d, 7 d after TBI, sham and control groups. The permeability of the blood brain barrier was evaluated by measuring the extravasation of Evans blue (EB) dye. The expression of ZO-1 in cerebral cortex in the injured area was detected by Western blotting and immunohistochemistry. RESULTS: The extravasation of EB dye of injured cortex gradually increased from 1 h, peaked at 1-3 d and approximately decreased to normal at 7 d after TBI. Western blotting revealed that the expression of ZO-1 gradually decreased after 1 h, was at the lowest at 1-3 d, and then significantly increased after 7 d but was still lower than that of normal and sham groups. The result of immunohistochemistry showed that ZO-1 had strong expression in vessel of normal cortex, gradually decreased after TBI, and almost disappeared at 3 d after TBI and gradually recovered to normal level later. CONCLUSION The expression of ZO-1 in the injured cortex after TBI initially decreases and then increases. The negative correlation between ZO-1 expression and EB extravasation after TBI could be used as a new indicator for wound age estimation.
Animals ; Blood-Brain Barrier ; Blotting, Western ; Brain Injuries/physiopathology* ; Cerebral Cortex/metabolism* ; Immunohistochemistry ; Mice ; Permeability ; Tight Junctions/metabolism* ; Zonula Occludens-1 Protein/metabolism*