• Anxiety and mood
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• v.10 no.2
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• pp.143-150
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• 2014

Objective : The subgenual cingulate cortex, a part of default-mode network, has been known to playa key role in the pathophysiology of depression. The previous studies have reported abnormal functional connectivity between the subgenual cingulate cortex and other brain regions in the patients with depression. The goal of this shldy was to explore the resting-state functional connectivity of the subgenual cingulate cortex between the patients with depression and healthy subjects. Methods : Twenty patients with major depression and age- and sex-matched 20 healthy subjects underwent 5-minute resting state fMRI scans. The functional connectivity map in each subject was acquired using seed-based correlation analysis with the seed located in the subgenual cingulate cortex (Talairach coordinates; x=-10, y=5, z=-10). The functional connectivity maps were calculated using AFNI and compared between the patient and healthy subject group via two-sample T-test using 3dttest++ in AFNI package. Results : Functional connectivity was decreased between the subgenual cingulate cortex and both sides of fusiform gyrus in depressed subjects. Connectivity was also decreased between the subgenual cingulate cortex and the left cerebellum in the patient group. There was no correlation between the severity of depression and the degree of functional connectivity between the subgenual cingulate cortex and the regions showing decreased functional connectivity. Conclusion : Decreased resting-state functional connectivity between the subgenual cingulate cortex and both sides of fusiform gyrus, and decreased connectivity between the subgenual cingulate cortex and the left cerebellum found in the patients with major depression in comparison to the healthy subjects might be related to abnormal emotional and cognitive processing of depressed patients.

• Journal of Acupuncture Research
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• v.21 no.2
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• pp.205-222
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• 2004

Objective: To investigate the effects of acupointed Choksamni(ST36), Kokchi(LI11) and Arbitrary acupoint on NADPH-diaphorase, neuronal nitric oxide synthase(nNOS), neuropeptide Y(NPY) and vasoactive intestinal peptide(VIP) in the cerebral cortex of spontaneously hypertensive rats. Methods: The experimental groups were divided into four groups: Normal, Choksamni(ST36), Kokchi(LI11), arbitrary group. Needles were inserted into acupoints at the depth of 0.5 cm with basic insertion method. Such stimulation was applied continuously for 10 minutes, every other day, for 10 sessions of treatments. Thereafter we evaluated changes in NADPH-d-positive neurons histochemically and changes in nNOS, NPY and VIP-positive neurons immunohistochemically. Results : The optical densities of NADPH-d-positive neurons of all the Choksamni & Kokchi groups were significantly different in all areas of cerebral cortex as compared to arbitrary group. In motor1, sensory2, cingulate2, insular, peripheral, visual cortex there was a significant difference between Choksamni & Kokchi group. The optical densities of nNOS-positive neurons of Choksamni group were significantly different in all areas except for auditory, visual and pisiform cortex and Kokchi group in all areas except for auditory and pisiform cortex as compared to arbitrary group. And there was a significant difference in cingulate1, cingulate2, ectohinal, visual cortex between Choksamni & Kokchi group. The optical densities of NPY neurons of Choksamni group were significantly different in cingulate2, insular, pisiform cortex and Kokchi group in motor1, motor2, sensory1, cingulate2, ectorhinal cortex as compared to arbitrary group. And there was no significant difference between Choksamni & Kokchi group. The optical densities of VIP neurons of Choksamni group were significantly different in all areas except for motor1, auditory cortex and Kokchi group in sensory1, insular, ectorhinal, perirhinal, visual, pisiform cortex as compared to arbitrary group. And there was a significant difference in cingulate1, cingulate2, retrosplenial, auditory corterx between Choksamni & Kokchi group. Conclusion : Our results demonstrated that acupuncture on Choksamni(ST36) & Kokchi(LI11) changes the control activities of the NO system in the cerebral cortex of SHR and according to areas there were significant difference between two groups. In all cerebral cortex areas there were distributed NPY & VIP and there were no significant difference among Choksamni(ST36), Kokchi(LI11) and arbitrary group.

• The Korean Journal of Physiology
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• v.11 no.1
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• pp.45-50
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• 1977

This study was undertaken to investigate the effect of cingulate cortical ablation upon gastric ulceration, and the pathway through which cingulate cortex exerts the effect. 56 female rats were divided equally into cingulate (cingulate cortical ablation), cingulate-vagal (cingulate cortical ablation and vagotomy), normal control and vagal (vagotomy) groups. Cingulate cortex was ablated through a slit-shaped opening (1 mm in width, 13 mm in length) which was made symmetrically on both sides of, and parallel to, the sagittal suture by removing a bone flap from parietal and frontal bones on each side. Vagus nerves on both sides were transected around the distal end of the esophagus. In the normal control animals, surgical intervention ended with scalp incision. All rats were kept without restraint or food deprivation for 3 weeks after surgery. The stomach of each rat was inflated with 7 ml of physiological saline and then removed under deep anesthesia. The mucosal surface was examined under dissecting microscope for the location, shape and number of ulcers, and then enlarged photograph $(4{\times})$was taken. The incidence of ulcer in each group was counted and the number of ulceration as well as the total area of glandular mucosa were measured on the photograph. Results obtained were as follows: 1. The mean number of ulcer per stomach and the total area of ulcer exprssed as permillage of the total area of glandular mucosa were significantly higher in the cingulate group than the cingulate-vagal, the normal control and the vagal groups. There was no difference among the latter three groups. 2. The incidence of ulcer in the cingulate group was significantly higher than that in the .normal control group and was also higher, though not significantly, than those in the cingulate-vagal and the vagal groups. There was no difference among the normal control, the cingulate-vagal and the vagal groups. It is inferred from the above results that the cingulate cortex exerts an inhibitory influence upon gastric ulceration and that this influence is mediated by controlling the vagal activity.

• Korean Journal of Biological Psychiatry
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• v.13 no.2
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• pp.117-120
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• 2006

Localized amnesia is characterized by a failure to recall events that occurred during a circumscribed period of time. Localized amnesia is the most common type of dissociative amnesia. It is assumed that this is a disorder of memory retrieval. Recent neuroimaing studies reported that posterior cingulate cortex may play a important role in memory(autobiographical) retrieval. The authors reported a case of localized amnesia with mass on left posterior cingulate cortex.

• Journal of Pharmacopuncture
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• v.4 no.1
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• pp.125-139
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• 2001

In order to study the effects of bee venom herbal acupuncture on the neurotransmitters of the rat brain cortex, herbal acupuncture with the bee venom group and normal saline group was performed bilaterally on the point corresponding to LI 4 of the rat. The average optical density of the neurotransmitters from the cerebral cortex was analyzed 30 minutes after the herbal acupuncture with immunohistochemical methods. The results were as follows: 1. The density of NADPH-diaphorase in the bee venom group was increased significantly at the motor cortex, visual cortex, auditory cortex, cingulate cortex, retrosplenial cortex, and perirhinal cortex, compared to the normal saline group. 2. The average optical density of vasoactive intestinal peptide in the bee venom group had significant changes at the insular cortex, retrosplenial cortex, and perirhinal cortex, compared to the normal saline group. 3. The average optical density of neuropeptide-Y in the bee venom group increased significantly at the visual cortex and cingulate cortex, compared to the normal saline group.

• Investigative Magnetic Resonance Imaging
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• v.15 no.1
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• pp.67-71
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• 2011

Purpose : To compare T2 relaxation times (T2) in the cingulate cortex, amygdaloid body, hippocampal body, and insular cortex between 1.5T and 3.0T MR imagers. Materials and Methods : Twelve healthy volunteers underwent FLAIR and CPMG imaging perpendicular to the hippocampal body at both 3.0T and 1.5T. T2 was measured in the cingulate cortex, amygdaloid body, hippocampal body, and insular cortex. The T2 relaxation time ratios of the cingulate cortex, insular cortex, and amygdaloid body to the hippocampal body were compared between 1.5T and 3.0T. Results : The mean T2 of the cingulate cortex, amygdaloid body, hippocampal body, and insular cortex at 1.5T were $109.5{\pm}3.1$, $117.0{\pm}7.1$, $114.7{\pm}2.4$, and $111.3{\pm}2.4$, respectively; $99.7{\pm}3.8$, $100.7{\pm}4.3$, $97.9{\pm}3.4$, and $96.2{\pm}2.0$, respectively, at 3.0T. Percentage changes of T2 in the cingulate cortex, insular cortex, amygdaloid body, and hippocampal body at 3.0T with respect to those at 1.5T were -8.9%, -13.5%, -14.6%, and -13.5%, respectively. The mean T2 ratios of the cingulate gyrus, insular cortex, and amygdaloid body to the hippocampal body at 1.5T and 3.0T were 0.96 and 1.02 (p = 0.003); 1.02 and 1.03 (p>0.05); 0.97 and 0.98 (p>0.05), respectively. Conclusion : T2 decrease in the cingulate cortex was less than the amygdaloid body, insular cortex, and hippocampal body at 3.0T. The mean T2 ratio of the cingulate gyrus to the hippocampal body was significantly different between 1.5T and 3.0T.

• The Korean Journal of Physiology
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• v.18 no.2
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• pp.117-124
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• 1984

It has been recently reported that cingulate cortex mar facilitate gastric acid secretion, but its facilitatory mechanism on the gastric acid secretion is still unclear. This study was undertaken to investigate the facilitatory mechanism of the cingulate cortex upon gastric acid secretion in rats. Twenty·three male albino rats were divided into the cingulate(N= 13) and the operated control(N= 10) groups. The cingulate group in which cingulate cortex was removed by suction through a slit-shaped opening on each side of, and parallel to, the sagittal suture. In the operated control group, the surgical procedure was ended with the skull opening and the incision of dura mater. The gastric juice was collected via a chronic gastric cannula after 24 hours of fast, with water ad libitum. The juice was collected continuously for 6 hours, starting 3 hours prior to the injection of gastric secretagogue, pentagastrin$(12\;{\mu}g/kg)$ or histamine dihydrochloride $(320\;{\mu}g/kg)$. Three one·hour samples were obtained before ana after the administration of each secretagogue. The two agents were injected separately and subcutaneously at intervals of 1 week, the blood samples were drawn from the abdominal aorta for the radioimmunoassay of postprandial plasma gastrin concentration in response to the forced feeding of 10% cod liver oil. 1) After pentagastrin administration, the volume of gastric juice tended to decrease, but its acidity tended to increase in the cingulate group compared with those of the operated control group. However, there was no any difference in the acid output between the two groups. 2) Histamine-stimulated acid output and volume of the gastric juice of the cingulate group decreased significantly compared with those of the operated control group, while there was not significantly different in the acidity between the two groups. 3) Before pentagastrin or histamine administration, any change was not observed in the gastric acid secretion following the cingulate cortical ablation. 4) Postprandial plasma gastrin concentration in response to the forced feeding of 10% cod liver oil was insignificantly lower in the cingulate group than in the operated control group. It is inferred from the above results that the cingulate cortex exerts a facilitatory influence upon the histamine-stimulated gastric acid secretion in rats, and its influence may not be mediated by the stimulation of gastrin secretion.

• The Korean Journal of Physiology
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• v.11 no.2
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• pp.67-71
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• 1977

This study was undertaken to investigate the effect of cingulate cortical ablation upon gastric secretion and its components in rats. 23 male rats were divided into the cingulate(N=9) and the operated control(N= 14) groups. Cingulate cortex was ablated through a slit-shaped opening(1 mm in width, 5 mm in length) which was made symmetrically on both sides of, and parallel to, the sagittal suture by removing a bone flap from frontal bone on each side. In the operated control group, the surgical procedure was ended by the removal of the bone flap. Under light ether anesthesia, experimental animals were placed in a restraining jacket of fine mesh wire and gastric juice was collected for 5 hours via a canula which had been inserted through the anterior abdominal wall into the antral portion of the lumen of the stomach. Volume of the gastric juice was measured, and total acid output and free acid output were titrated with 0.04 N NaOH solution by using phenolphthalein and Topfer's reagent at indicator, and chloride ion output was estimated by means of chloridometer. Results obtained were that volume, total acid output, free acid output and chloride ion output of the gastric juice were higher significantly in the cingulate group than in the operated control group. It is inferred from the above results that the cingulate cortex exerts a fascilitatory influence upon gastric secretion and acid output in rats.

• Molecules and Cells
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• v.28 no.6
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• pp.501-507
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• 2009

Fragile X syndrome (FXS) is caused by a lack of the fragile X mental retardation protein (FMRP) due to silencing of the Fmr1 gene. As an RNA binding protein, FMRP is thought to contribute to synaptic plasticity by regulating plasticity-related protein synthesis and other signaling pathways. Previous studies have mostly focused on the roles of FMRP within the hippocampus - a key structure for spatial memory. However, recent studies indicate that FMRP may have a more general contribution to brain functions, including synaptic plasticity and modulation within the prefrontal cortex. In this brief review, we will focus on recent studies reported in the prefrontal cortex, including the anterior cingulate cortex (ACC). We hypothesize that alterations in ACC-related plasticity and synaptic modulation may contribute to various forms of cognitive deficits associated with FXS.

• Korean Journal of Biological Psychiatry
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• v.24 no.4
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• pp.225-234
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• 2017

Objectives Local gyrification reflects the early neural development of cortical connectivity, and is regarded as a potential neural endophenotype in psychiatric disorders. Several studies have suggested altered local gyrification in patients with bipolar I disorder (BD-I). The purpose of the present study was to investigate the alterations in the cortical gyrification of whole brain cortices in patients with BD-I. Methods Twenty-two patients with BD-I and age and sex-matched 22 healthy controls (HC) were included in this study. All participants underwent T1-weighted structural magnetic resonance imaging (MRI). The local gyrification index (LGI) of 66 cortical regions were analyzed using the FreeSurfer (Athinoula A. Martinos Center for Biomedical Imaging). One-way analysis of covariance (ANCOVA) was used to analyze the difference of LGI values between two groups adjusting for age and sex as covariates. Results The patients with BD-I showed significant hypogyria in the left pars opercularis (uncorrected-p = 0.049), the left rostral anterior cingulate gyrus (uncorrected-p = 0.012), the left caudal anterior cingulate gyrus (uncorrected-p = 0.033). However, these findings were not significant after applying the multiple comparison correction. Severity or duration of illness were not significantly correlated with LGI in the patients with BD-I. Conclusions Our results of lower LGI in the anterior cingulate cortex and the ventrolateral prefrontal cortex in the BD-I group implicate that altered cortical gyrification in neural circuits involved in emotion-processing may contribute to pathophysiology of BD-I.