• Title/Summary/Keyword: Amygdala

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Morphologic Alterations in Amygdala Subregions of Adult Patients with Bipolar Disorder

  • Lee, Hyun-Jae;Han, Kyu-Man;Kim, Aram;Kang, Wooyoung;Kang, Youbin;Kang, June;Won, Eunsoo;Tae, Woo-Suk;Ham, Byung-Joo
    • Korean Journal of Biological Psychiatry
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    • v.26 no.1
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    • pp.22-31
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    • 2019
  • Objectives Previous studies have revealed inconsistent results on amygdala volume in adult bipolar disorder (BD) patients compared to healthy controls (HC). Since the amygdala encompasses multiple subregions, the subtle volume changes in each amygdala nucleus might have not been fully reflected in the measure of the total amygdala volume, causing discrepant results. Thus, we aimed to investigate volume changes in each amygdala subregion and their association with subtypes of BD, lithium use and clinical status of BD. Methods Fifty-five BD patients and 55 HC underwent T1-weighted structural magnetic resonance imaging. We analyzed volumes of the whole amygdala and each amygdala subregion, including the anterior amygdaloid area, cortico-amygdaloid transition area, basal, lateral, accessory basal, central, cortical, medial and paralaminar nuclei using the atlas in the FreeSurfer. The volume difference was analyzed using a one-way analysis of covariance with individual volumes as dependent variables, and age, sex, and total intracranial volume as covariates. Results The volumes of whole right amygdala and subregions including basal nucleus, accessory basal nucleus, anterior amygdaloid area, and cortico-amygdaloid transition area in the right amygdala of BD patients were significantly smaller for the HC group. No significant volume difference between bipolar I disorder and bipolar II disorder was found after the Bonferroni correction. The trend of larger volume in medial nucleus with lithium treatment was not significant after the Bonferroni correction. No significant correlation between illness duration and amygdala volume, and insignificant negative correlation were found between right central nucleus volume and depression severity. Conclusions Significant volume decrements of the whole amygdala, basal nucleus, accessory basal nucleus, anterior amygdaloid area, and cortico-amygdaloid transition area were found in the right hemisphere in adult BD patients, compared to HC group. We postulate that such volume changes are associated with altered functional activity and connectivity of amygdala nuclei in BD.

Effect of Medial Amygdala on Gastric Acid Secretion and Plasma Gastrin Concentration in Conscious Rats (흰쥐에서 내측 편도체가 위산 분비와 혈장 Gastrin 농도에 미치는 영향)

  • Yoon, Shin-Hee;Kim, Chung-Chin;Kim, Myung-Suk;Jo, Yang-Hyeok;Hahn, Sang-June;Kim, Mie-Hye;Choi, Hyun
    • The Korean Journal of Physiology
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    • v.23 no.1
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    • pp.119-127
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    • 1989
  • This study was undertaken to investigate the effect of medial amygdala on the gastric acid secretion and plasma gastrin concentration in the rats with chronic gastric fistula. After the medial nucleus of amygdala was damaged bilaterally by radiofrequency a. c. through stereotaxically inserted electrodes, the gastric juice was collected in the basal and histamine-stimulated states for 1 hour. The gastric juice was also collected while the medial nucleus of amygdala was stimulated with biphasic square wave in the both states. After the collection of the gastric juice, blood samples were drawn from the abdominal aorta for the radioimmunoassay of plasma gastrin. The results were as follows: 1) The damage of the medial amygdala significantly decreased the gastric juice volume and the acid output in the histamine-stimulated state. 2) The electrical stimulation of the medial amygdala significantly increased the gastric juice volume and the acid output in the histamine-stimulated state, and the acid output in the basal state. 3) The damage of the medial amygdala significantly decreased the plasma gastrin concentration but the electrical stimulation of the medial amygdala did not affect the plasma gastrin concentration. It is therefore suggested that the medial amygdala has a facilitatory influence on the histamine-stimulated gastric acid secretion in rats, and the influence may not be attributed to gastrin release.

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Microinjection of Glutamate into the Amygdala Modulates Nociceptive and Cardiovascular Response in Freely Moving Rats

  • Ahn, Dong-Kuk;Kim, Yun-Sook;Park, Jae-Sik
    • The Korean Journal of Physiology and Pharmacology
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    • v.2 no.6
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    • pp.687-693
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    • 1998
  • This study was performed to examine the mean arterial pressure and nociceptive jaw opening reflex after microinjection of glutamate into the amygdala in freely moving rats, and to investigate the mechanisms of antinociceptive action of amygdala. Animals were anesthetized with pentobarbital sodium (40 mg/kg, ip). A stainless steel guide cannula (26 gauge) was implanted in the amygdala and lateral ventricle. Stimulating and recording electrodes were implanted into each of the incisor pulp and anterior digastric muscle. Electrodes were led subcutaneously to the miniature cranial connector sealed on the top of the skull with acrylic resin. After 48 hours of recovery from surgery, mean arterial pressure and digastric electromyogram (dEMG) were monitored in freely moving rats. Electrical shocks (200 ${\mu}sec$ duration, $0.5{\sim}2$ mA intensity) were delivered at 0.5 Hz to the dental pulp every 2 minutes. After injection of 0.35 M glutamate into the amygdala, mean arterial pressure was increased by $8{\pm}2$ mmHg and dEMG was suppressed to $71{\pm}5%$ of the control. Injection of 0.7 M glutamate elevated mean arterial pressure by $25{\pm}5$ mmHg and suppressed dEMG to $20{\pm}7%$ of the control. The suppression of dEMG were maintained for 30 minutes. Naloxone, an opioid receptor antagonist, inhibited the suppression of dEMG elicited by amygdaloid injection of glutamate from $28{\pm}4\;to\;68{\pm}5%$ of the control. Methysergide, a serotonin receptor antagonist, also inhibited the suppression of dEMG from $33{\pm}5\;to\;79{\pm}4%$ of the control. However, phentolamine, an ${\alpha}-adrenergic$ receptor antagonist, did not affect the suppression of dEMG. These results suggest that the amygdala can modulate both cardiovascular and nociceptive responses and that the antinociception of amygdala seems to be attributed to an augmentation of descending inhibitory influences on nociceptive pathways via serotonergic and opioid pathways.

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Modulation of Neural Circuit Actvity by Ethanol in Basolateral Amygdala

  • Chung, Leeyup
    • Development and Reproduction
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    • v.16 no.4
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    • pp.265-270
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    • 2012
  • Ethanol actions in the amygdala formation may underlie in part the reinforcing effects of ethanol consumption. Previously a physiological phenomenon in the basolateral amygdala (BLA) that is dependent on neuronal network activity, compound postsynaptic potentials (cPSPs) were characterized. Effects of acute ethanol application on the frequency of cPSPs were subsequently investigated. Whole cell patch clamp recordings were performed from identified projection neurons in a rat brain slice preparation containing the amygdala formation. Acute ethanol exposure had complex effects on cPSP frequency, with both increases and decreases dependent on concentration, duration of exposure and age of the animal. Ethanol produces complex biphasic effects on synaptically-driven network activity in the BLA. These findings may relate to subjective effects of ethanol on arousal and anxiolysis in humans.

Characteristics of Intrinsic Functional Connectivity of Amygdalar Subregions in Social Anxiety Disorder (사회불안장애에서 편도 하위영역의 내재 기능적 연결성의 특성)

  • Kim, Jinseong;Yoon, Hyung-Jun;Park, Sunyoung;Shin, Yu-Bin;Kim, Jae-Jin
    • Anxiety and mood
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    • v.10 no.1
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    • pp.44-51
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    • 2014
  • Objective : The amygdala has been considered to be a critical region in the pathophysiology of social anxiety disorder, but subregional connectivity pattern has not been examined yet despite lots of previous functional neuroimaging studies. Methods : Resting-state functional magnetic resonance imaging data was obtained in 19 patients with social anxiety disorder and 20 normal controls, and default mode functional connectivity with each of basolateral, centromedial and superficial areas of the amygdala was measured and compared between the two groups. Results : Differential amygdala-based networks between the two groups were distributed to all over the brain. In particular, however, a bias on the amygdala-cingulate pathway was observed in the superficial amygdala only. Connectivity strengths between the superficial amygdala and perigenual anterior cingulate cortex were correlated with scores of social interaction and avoidance. Conclusion : Our findings provide new insights into understanding of the intrinsic cognitive bias model of social anxiety disorder. An abnormality in superficial amygdala-anterior cingulate connectivity may influence on cognitive processing of socially-relevant information in social anxiety disorder.

Modulation of Amygdala Synaptic Transmission by Metabotropic Glutamate Receptors

  • Kim, Jung-Hyun;Park, Eun-Jin;Chang, Duk-Jin;Choi, Suk-Woo
    • The Korean Journal of Physiology and Pharmacology
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    • v.7 no.6
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    • pp.303-306
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    • 2003
  • Metabotropic glutamate receptors (mGluRs), classified into three groups (group I, II, III), play a critical role in modulation of synaptic transmission at central and peripheral synapses. In the present study, extracellular field potential recording techniques were used to investigate effects of mGluR agonists on excitatory synaptic transmission at thalamic input synapses onto the lateral amygdala. The non-selective mGluR agonist t-ACPD ($100{\mu}M$) produced reversible, short-term depression, but the group III mGluR agonist L-AP4 ($50{\mu}M$) did not have any significant effects on amygdala synaptic transmission, suggesting that group I and/or II mGluRs are involved in the modulation by t-ACPD. The group I mGluR agonist DHPG ($100{\mu}M$) produced reversible inhibition as did t-ACPD. Unexpectedly, the group II mGluR agonist LCCG-1 ($10{\mu}M$) induced long-term as well as short-term depression. Thus, our data suggest that activation of group I or II mGluRs produces short-term, reversible depression of excitatory synaptic transmission at thalamic input synapses onto the lateral amygdala. Considering the long-term effect upon activation of group II mGluRs, lack of long-term effects upon activation of group I and II mGluRs may indicate a possible cross-talk among different groups of mGluRs.

Enhancement of Anxiety and Modulation of TH and pERK Expressions in Amygdala by Repeated Injections of Corticosterone

  • Lim, Hee-Na;Jang, So-Yong;Lee, Yeon-Ju;Moon, So-Hyeon;Kim, Ji-Eun;Oh, Sei-Kwan
    • Biomolecules & Therapeutics
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    • v.20 no.4
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    • pp.418-424
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    • 2012
  • Repeated stress induces corticosterone release. However, it is not clear that stress results in further elevation of corticosterone levels, and the roles of released corticosterone to aggravate stress-related symptoms are also not clear. This study investigated whether neuronal modulation was induced in the amygdala after two kinds of stress, that is, such as electric shock and corticosterone injection. It was found that stress by electric shock decreased the expression of tyrosine hydoroxylase (TH) in the amygdala while the expression of pERK was increased. However, there is no difference in the expressions of TH and pERK in the frontal cortex compared with those of the control group. The level of corticosterone was significantly increased in the serum after stress. To determine the effect of corticosterone on the induction of anxiety and the expression of TH, the rats received corticosterone (20 mg or 40 mg/kg i.p.) for 1 day, 1 week, 2 weeks and 3 weeks, respectively. The spent time in open arms of the EPM (elevated plus maze) test was significantly decreased after 1 week, 2 weeks and 3 weeks. The time spent in open arms of the EPM test after repeated injections of corticosterone was significantly decreased in a dose-dependent manner. The expression of TH in the amygdala was reduced after following repeated corticosterone treatment for 2 weeks and 3 weeks. Collectively, this study suggests that corticosterone has a major role in the induction of anxiety and the modulation of TH expression, at least, in the amygdala.

Perioperative stress prolong post-surgical pain via miR-339-5p targeting oprm1 in the amygdala

  • Zhu, Yi;Sun, Mei;Liu, Peng;Shao, Weidong;Xiong, Ming;Xu, Bo
    • The Korean Journal of Pain
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    • v.35 no.4
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    • pp.423-432
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    • 2022
  • Background: The decreased expression of mu-opioid receptors (MOR) in the amygdala may be a key molecular in chronic post-surgical pain (CPSP). It is known that miR-339-5p expression in the amygdala of a stressed rat model was increased. Analyzed by RNAhybrid, miR-339-5p could target opioid receptor mu 1 (oprm1) which codes MOR directly. So, the authors hypothesized that miR-339-5p could regulate the expression of MOR via targeting oprm1 and cause the effects to CPSP. Methods: To simulate perioperative short-term stress, a perioperative stress prolongs incision-induced pain hypersensitivity without changing basal pain perception rat model was built. A pmiR-RB-REPORTTM dual luciferase assay was taken to verify whether miR-339-5p could act on oprm1 as a target. The serum glucocorticoid level of rats was test. Differential expressions of MOR, GFAP, and pERK1/2 in each group of the rats' amygdala were tested, and the expressions of miR-339-5p in each group of rats' amygdalas were also measured. Results: Perioperative stress prolonged the recovery time of incision pain. The expression of MOR was down-regulated in the amygdala of rats in stress + incision (S + IN) group significantly compared with other groups (P < 0.050). miR-339-5p was up-regulated in the amygdala of rats in group S + IN significantly compared with other groups (P < 0.050). miR-339-5p acts on oprm1 3'UTR and take MOR mRNA as a target. Conclusions: Perioperative stress could increase the expression of miR-339-5p, and miR-339-5p could cause the expression of MOR to decrease via targeting oprm1. This regulatory pathway maybe an important molecular mechanism of CPSP.

Effects of Prenatal and Restraint Stress on Astrocytes of Amygdala Complex of Rat: I. Effects on the Astrocytic Cell Body (출생 전 스트레스와 감금 스트레스가 흰쥐 편도복합체 별아교세포에 미치는 영향: I. 별아교세포의 세포체에 미치는 영향)

  • Lee, Ji-Yong;Choi, Byoung-Young;Kim, Dong-Heui;Jung, Won-Sug;Cho, Byung-Pil;Yang, Young-Chul
    • Applied Microscopy
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    • v.38 no.3
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    • pp.213-219
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    • 2008
  • The plasticity of nervous system is generated not only due to changes in neurons but also due to changes in neuroglial cells. Astrocyte is important for maintaining the normal brain function and controlling the neuronal functions. The amygdala receives an array of important sensory information of danger signals. This information is further transduced and integrated to produce the highly adaptive emotion, fear. In this study, morphometric changes in the cell bodies of astrocytes in the amygdala, induced by prenatal stress and restraint stress were examined. For this purpose. rats were classified into 4 groups; control group (CON), only restraint-stressed (starting on P90 for 3 days) group (CONR), prenatally-stressed group (PNS), and prenatally and restraint (on P90 for 3 days) stressed group (PNSR). Astrocytes were verified with anti-GFAP immunohistochemistry, counter stained with methylene blue/azure II and were examined using the Neurolucida. Results showed that astrocytes in the amygdala of PNS rats had significantly larger cell bodies than did CON rats and this was enhanced further by restraint stress. Thus this data showed that hypertrophy of the astrocytic cell bodies of amygdala complex is induced by prenatal and restraint stress.

A Understanding of the Temporal Stem

  • Choi, Chan-Young;Han, Seong-Rok;Yee, Gi-Taek;Lee, Chae-Heuck
    • Journal of Korean Neurosurgical Society
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    • v.47 no.5
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    • pp.365-369
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    • 2010
  • Objective : There has been inconsistency about definition of the temporal stem despite of several descriptions demonstrating its microanatomy using fiber dissection and/or diffusion tensor tractography. This study was designed to clarify three dimensional configurations of the temporal stem. Methods : The fronto-temporal regions of several formalin-fixed human cerebral hemispheres were dissected under an operating microscope using the fiber dissection technique. The consecutive coronal cuts of the dissected specimens were made to define the relationships of white matter tracts comprising the temporal stem and the subcortical gray matters (thalamus, caudate nucleus, amygdala) with inferior limiting (circular) sulcus of insula. Results : The inferior limiting sulcus of insula, limen insulae, medial sylvian groove, and caudate nucleus/amygdala were more appropriate anatomical structures than the roof/dorso-lateral wall of the temporal horn and lateral geniculate body which were used to describe previously for delineating the temporal stem. The particular space located inside the line connecting the inferior limiting sulcus of insula, limen insulae, medial sylvian groove/amygdala, and tail of caudate nucleus could be documented. This space included the extreme capsule, uncinate fasciculus, inferior occipito-frontal fasciculus, anterior commissure, ansa peduncularis, and inferior thalamic peduncle including optic radiations, whereas the stria terminalis, cingulum, fimbria, and inferior longitudinal fiber of the temporal lobe were not passing through this space. Also, this continued posteriorly along the caudate nucleus and limiting sulcus of the insula. Conclusion : The temporal stem is white matter fibers passing through a particular space of the temporal lobe located inside the line connecting the inferior limiting sulcus of insula, limen insulae, medial sylvian groove/amygdala, and tail of caudate nucleus. The three dimensional configurations of the temporal stem are expected to give the very useful anatomical and surgical insights in the temporal lobe.