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1.
Neuroscience Bulletin ; (6): 16-28, 2022.
Article in English | WPRIM | ID: wpr-922663

ABSTRACT

Chronic stress leads to many psychiatric disorders, including social and anxiety disorders that are associated with over-activation of neurons in the basolateral amygdala (BLA). However, not all individuals develop psychiatric diseases, many showing considerable resilience against stress exposure. Whether BLA neuronal activity is involved in regulating an individual's vulnerability to stress remains elusive. In this study, using a mouse model of chronic social defeat stress (CSDS), we divided the mice into susceptible and resilient subgroups based on their social interaction behavior. Using in vivo fiber photometry and in vitro patch-clamp recording, we showed that CSDS persistently (after 20 days of recovery from stress) increased BLA neuronal activity in all the mice regardless of their susceptible or resilient nature, although impaired social interaction behavior was only observed in susceptible mice. Increased anxiety-like behavior, on the other hand, was evident in both groups. Notably, the CSDS-induced increase of BLA neuronal activity correlated well with the heightened anxiety-like but not the social avoidance behavior in mice. These findings provide new insight to our understanding of the role of neuronal activity in the amygdala in mediating stress-related psychiatric disorders.


Subject(s)
Amygdala , Animals , Anxiety/etiology , Anxiety Disorders , Avoidance Learning , Mice , Mice, Inbred C57BL , Social Behavior , Stress, Psychological/complications
2.
Neuroscience Bulletin ; (6): 1493-1509, 2021.
Article in English | WPRIM | ID: wpr-922651

ABSTRACT

The periaqueductal gray (PAG) is a complex mesencephalic structure involved in the integration and execution of active and passive self-protective behaviors against imminent threats, such as immobility or flight from a predator. PAG activity is also associated with the integration of responses against physical discomfort (e.g., anxiety, fear, pain, and disgust) which occurs prior an imminent attack, but also during withdrawal from drugs such as morphine and cocaine. The PAG sends and receives projections to and from other well-documented nuclei linked to the phenomenon of drug addiction including: (i) the ventral tegmental area; (ii) extended amygdala; (iii) medial prefrontal cortex; (iv) pontine nucleus; (v) bed nucleus of the stria terminalis; and (vi) hypothalamus. Preclinical models have suggested that the PAG contributes to the modulation of anxiety, fear, and nociception (all of which may produce physical discomfort) linked with chronic exposure to drugs of abuse. Withdrawal produced by the major pharmacological classes of drugs of abuse is mediated through actions that include participation of the PAG. In support of this, there is evidence of functional, pharmacological, molecular. And/or genetic alterations in the PAG during the impulsive/compulsive intake or withdrawal from a drug. Due to its small size, it is difficult to assess the anatomical participation of the PAG when using classical neuroimaging techniques, so its physiopathology in drug addiction has been underestimated and poorly documented. In this theoretical review, we discuss the involvement of the PAG in drug addiction mainly via its role as an integrator of responses to the physical discomfort associated with drug withdrawal.


Subject(s)
Amygdala , Humans , Morphine , Nociception , Periaqueductal Gray , Substance-Related Disorders
3.
Braz. j. med. biol. res ; 53(8): e9950, 2020. graf
Article in English | ColecionaSUS, LILACS, ColecionaSUS | ID: biblio-1132542

ABSTRACT

Pathophysiological mechanisms involved in orofacial pain and their relationship with emotional disorders have emerged as an important research area for multidisciplinary studies. In particular, temporomandibular disorders (TMD) have been evaluated clinically from both physiological and psychological perspectives. We hypothesized that an altered neuronal activity occurs in the amygdala and the dorsal raphe nucleus (DR), encephalic regions involved in the modulation of painful and emotional information. Adult male Wistar rats were used in an experimental complete Freund's adjuvant (CFA)-induced temporomandibular joint (TMJ) inflammation model. CFA was applied for 1 or 10 days, and the animals were euthanized for brain samples dissection for FosB/ΔFosB and parvalbumin (PV) immunostaining. Our results were consistent in showing that the amygdala and DR were activated in the persistent inflammatory phase (10 days) and that the expression of PV+ interneurons in the amygdala was decreased. In contrast, in the DR, the expression of PV+ interneurons was increased in persistent states of CFA-induced TMJ inflammation. Moreover, at 10 days of inflammation, there was an increased co-localization of PV+ and FosB/ΔFosB+ neurons in the basolateral and central nucleus of the amygdala. Different nuclei of the amygdala, as well as portions of the DR, were activated in the persistent phase (10 days) of TMJ inflammation. In conclusion, altered activity of the amygdala and DR was detected during persistent inflammatory nociception in the temporomandibular joint. These regions may be essential for both sensory and affective dimensions of orofacial pain.


Subject(s)
Animals , Male , Rats , Parvalbumins/metabolism , Temporomandibular Joint/physiology , Dorsal Raphe Nucleus/metabolism , Amygdala/metabolism , Rats, Wistar , Rats, Sprague-Dawley , Inflammation , Neurons
4.
Rev. chil. neuropsicol. (En línea) ; 14(2): 35-39, dic. 2019. ilus
Article in Spanish | LILACS | ID: biblio-1102455

ABSTRACT

La isquemia cerebral es el tipo de accidente cerebrovascular más común, generando altas tasas de mortalidad y morbilidad a nivel mundial. El entendimiento de la fisiopatología de la lesión cerebral ha requerido de la implementación de modelos experimentales que permitan evaluar los fenómenos celulares, sobre todo aquellos a largo plazo. Por tal razón, el objetivo del presente trabajo fue evaluar las áreas exofocales a un mes y cuatro meses post-isquemia cerebral en un modelo experimental. Ratas Wistar fueron sometidas a una isquemia focal transitoria (t-MCAo) y un grupo fueron sacrificados al mes y otro grupo a los cuatro meses post-isquemia para su posterior análisis histológico. Los cortes fueron teñidos con Nissl y se realizó inmunohistoquímica de la proteína Tau. Nuestros resultados muestran tres áreas de lesión exofocal tanto al mes como a los cuatro meses post-isquemia: el giro dentado, la amígdala y el tálamo. Estas regiones se han asociado al control emocional, lo cual sugiere que a largo término post-isquemia se tengan en cuenta hallazgos clínicos que evalúen cambios emocionales en los pacientes que han sufrido un evento isquémico cerebral.


Cerebral ischemia is the most common type of stroke, which generates high mortality and morbidity rates worldwide. The understanding of the pathophysiology of brain injury has required the implementation of experimental models that allow the evaluation of cellular phenomena, especially those in the long-term. For this reason, the objective of the present work was to evaluate the exofocal areas at one month and four months after cerebral ischemia. Wistar rats were subjected to transient focal ischemia (t-MCAo) and one group was sacrificed one month and another group at four months' post-ischemia for subsequent histological analysis. The cuts were stained with Nissl and immunohistochemistry of the Tau protein was performed. Our results show three areas of exofocal lesion both one month and four months' post-ischemia: the thalamus, the dentate gyrus, and the amygdala. These regions have been associated with emotional control, which suggests that in the long-term post-ischemia clinical findings that evaluate emotional changes in patients who have suffered a cerebral ischemic event should be considered.


Subject(s)
Animals , Rats , Thalamus/pathology , Brain Ischemia/pathology , Dentate Gyrus/pathology , Amygdala/pathology , Immunohistochemistry , Disease Models, Animal
5.
Article in Korean | WPRIM | ID: wpr-759573

ABSTRACT

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.


Subject(s)
Adult , Amygdala , Basolateral Nuclear Complex , Bipolar Disorder , Cerebellar Nuclei , Corticomedial Nuclear Complex , Depression , Humans , Image Processing, Computer-Assisted , Lithium , Magnetic Resonance Imaging
6.
Psychiatry Investigation ; : 662-670, 2019.
Article in English | WPRIM | ID: wpr-760982

ABSTRACT

The neuroimaging has been applied in the study of pathophysiology in major depressive disorder (MDD). In this review article, several kinds of methodologies of neuroimaging would be discussed to summarize the promising biomarkers in MDD. For the magnetic resonance imaging (MRI) and magnetoencephalography field, the literature review showed the potentially promising roles of frontal lobes, such as anterior cingulate cortex (ACC), dorsolateral prefrontal cortex (DLPFC) and orbitofrontal cortex (OFC). In addition, the limbic regions, such as hippocampus and amygdala, might be the potentially promising biomarkers for MDD. The structures and functions of ACC, DLPFC, OFC, amygdala and hippocampus might be confirmed as the biomarkers for the prediction of antidepressant treatment responses and for the pathophysiology of MDD. The functions of cognitive control and emotion regulation of these regions might be crucial for the establishment of biomarkers. The near-infrared spectroscopy studies demonstrated that blood flow in the frontal lobe, such as the DLPFC and OFC, might be the biomarkers for the field of near-infrared spectroscopy. The electroencephalography also supported the promising role of frontal regions, such as the ACC, DLPFC and OFC in the biomarker exploration, especially for the sleep electroencephalogram to detect biomarkers in MDD. The positron emission tomography (PET) and single-photon emission computed tomography (SPECT) in MDD demonstrated the promising biomarkers for the frontal and limbic regions, such as ACC, DLPFC and amygdala. However, additional findings in brainstem and midbrain were also found in PET and SPECT. The promising neuroimaging biomarkers of MDD seemed focused in the fronto-limbic regions.


Subject(s)
Amygdala , Biomarkers , Brain Stem , Depression , Depressive Disorder, Major , Electroencephalography , Frontal Lobe , Gyrus Cinguli , Hippocampus , Magnetic Resonance Imaging , Magnetoencephalography , Mesencephalon , Neuroimaging , Positron-Emission Tomography , Prefrontal Cortex , Spectroscopy, Near-Infrared , Tomography, Emission-Computed , Tomography, Emission-Computed, Single-Photon
7.
Article in Korean | WPRIM | ID: wpr-787410

ABSTRACT

Mindfulness is a process in which all thoughts, feelings, sensations, and all phenomena that happen to me are uncritically recognized as they are, so that they are eventually accepted and released without identifying or automatically responding to them. The clinical effects of mindfulness-based therapy have already been demonstrated in several studies. However, consistent results have not been reported for the mechanism of mindfulness-based treatment. Thus, this review aimed to describe a systematic review of the literature and research on the mechanisms of mindfulness-based interventions. Experienced meditators showed a physiological change in a ‘wakeful hypometabolic state’ during mindfulness meditation. In mindfulness meditation, it is known that certain areas other than brain activation during relaxation are additionally activated, particularly activation of fronto-limbic and fronto-parietal neural networks. The psychological mechanisms include meta-cognitive awareness, emotion regulation, reduction of automatic and self-referential thinking, concentration control, self-compassion, improvement of value clarification and self-regulation, exposure, extinction, and reconsolidation. Of the brain regions with changes in activity associated with mindfulness meditation, prefrontal cortex, the default mode network including cortical midline structures were associated with emotion regulation, concentration control, and reduction of automatic and self-referential thinking. In addition, brain regions associated with mindfulness meditation have been reported in the hippocampus, amygdala, and medical frontal cortices associated with memory reconsolidation and fear extinction. Thus, mindfulness-based interventions have a psychological and neurobiological effect with a special mechanism different from other psychological interventions, so that mindfulness based intervention can be an effective therapeutic intervention with a different mechanism from other psychological techniques.


Subject(s)
Amygdala , Brain , Frontal Lobe , Hippocampus , Meditation , Memory , Mindfulness , Prefrontal Cortex , Psychological Techniques , Relaxation , Self-Control , Sensation , Thinking
8.
Article in Chinese | WPRIM | ID: wpr-776567

ABSTRACT

OBJECTIVE@#To investigate the effects of central nucleus of amygdala (CeA) lesion on the initiation and expression of sodium appetite in sodium-deficient rats.@*METHODS@#Three groups of SD rats (n=6 in each group) were treated with bilateral CeA lesion, sham lesion or no lesion. After the recovery, the rats were fed with low-sodium diets for 14 days to establish a sodium-deficient rat model. The double-bottle selection in single cage test was used to observe the intake of 0.3 mol/L NaCl and DW in 5 timepoint with 24 hours in sodium-deficient rats. Immunofluorescence staining of aldosterone-sensitive neurons in the nucleus tractus solitarii (NTS)was used to investigate the effect of CeA lesion or not on the activity of aldosterone-sensitive neurons in rats with or without sodium deficiency.@*RESULTS@#After fed with low-sodium diet for14 days, the volume and preference rate of 0.3 mol/L NaCl intake of the rats within 24 h were significantly increased compared with those before low-sodium diet (P<0.01). The intake volume and the preference rate of 0.3 mol/L NaCl in CeA lesion rats were significantly decreased than those in CeA sham lesion rats and normal rats in the sodium-deficient condition (P<0.01). The CeA lesion had no effects on the activity of aldosterone-sensitive neurons in NTS in rats with low-sodium diet.@*CONCLUSION@#Low-sodium diet induces an increase in the expression of sodium appetite in rats. CeA lesions inhibit the behavioral expression of sodium appetite in sodium-deficient rats but have no effects on the initiation of sodium appetite in rats with sodium-deficient rats.


Subject(s)
Amygdala , Pathology , Animals , Appetite , Diet, Sodium-Restricted , Neurons , Rats , Rats, Sprague-Dawley , Sodium , Sodium, Dietary , Pharmacology
9.
Article in English | WPRIM | ID: wpr-761820

ABSTRACT

Nociceptin/orphanin FQ (N/OFQ) and its receptor, nociceptin opioid peptide (NOP) receptor, are localized in brain areas implicated in depression including the amygdala, bed nucleus of the stria terminalis, habenula, and monoaminergic nuclei in the brain stem. N/OFQ inhibits neuronal excitability of monoaminergic neurons and monoamine release from their terminals by activation of G protein-coupled inwardly rectifying K⁺ channels and inhibition of voltage sensitive calcium channels, respectively. Therefore, NOP receptor antagonists have been proposed as a potential antidepressant. Indeed, mounting evidence shows that NOP receptor antagonists have antidepressant-like effects in various preclinical animal models of depression, and recent clinical studies again confirmed the idea that blockade of NOP receptor signaling could provide a novel strategy for the treatment of depression. In this review, we describe the pharmacological effects of N/OFQ in relation to depression and explore the possible mechanism of NOP receptor antagonists as potential antidepressants.


Subject(s)
Amygdala , Antidepressive Agents , Brain , Brain Stem , Calcium Channels , Depression , Habenula , Models, Animal , Neurons , Neuropeptides , Opioid Peptides , Receptors, Drug , Septal Nuclei
10.
Article in English | WPRIM | ID: wpr-741921

ABSTRACT

OBJECTIVE: Classifying mental disorders on the basis of objective makers might clarify their aetiology, help in making the diagnosis, identify “at risk” individuals, determine the severity of mental illness, and predict the course of the disorder. This study aims to review biological and clinical markers of panic disorder (PD). METHODS: A computerized search was carried out in PubMed and Science Direct using the key words: “marker/biomarker/clinical marker/neurobiology/staging” combined using Boolean AND operator with “panic.” In addition, the reference lists from existing reviews and from the articles retrieved were inspected. Only English language papers published in peer-reviewed journals were included. RESULTS: Structural changes in the amygdala, hippocampus, cerebral blood level in the left occipital cortex, serotonin 5-TH and noradrenergic systems activation, aberrant respiratory regulation, hearth rate variability, blood cells and peripheral blood stem cells, hypothalamic–pituitary–adrenal axis dysregulation were identified as potential candidate biomarkers of PD. Staging was identified as clinical marker of PD. According to the staging model, PD is described as follows: prodromal phase (stage 1); acute phase (stage 2); panic attacks (stage 3); chronic phase (stage 4). CONCLUSION: The clinical utility, sensitivity, specificity, and the predictive value of biomarkers for PD is still questionable. The staging model of PD might be a valid susceptibility, diagnostic, prognostic, and predictive marker of PD. A possible longitudinal model of biological and clinical markers of PD is proposed.


Subject(s)
Amygdala , Biomarkers , Blood Cells , Diagnosis , Hippocampus , Mental Disorders , Occipital Lobe , Panic Disorder , Panic , Prodromal Symptoms , Sensitivity and Specificity , Serotonin , Stem Cells
11.
Gac. méd. Méx ; 155(supl.1): 62-69, dic. 2019. tab, graf
Article in Spanish | LILACS | ID: biblio-1286567

ABSTRACT

Resumen Antecedentes: El tratamiento neuroquirúrgico, aunque polémico, se considera un recurso útil en el tratamiento de enfermedades psiquiátricas crónicas como la agresividad refractaria. Objetivo: Evaluar los resultados clínicos y los efectos colaterales de la hipotalamotomía posteromedial (HPM) asociada a amigdalotomía en pacientes con agresividad refractaria. Método: Se realizó un ensayo clínico en pacientes con agresividad crónica y refractaria a tratamiento farmacológico. Se les realizó amigdalotomía central asociada a HPM mediante termocoagulación por radiofrecuencia. El grado de agresividad se cuantificó mediante la escala global de agresividad de Yudofsky. Los cambios postoperatorios en la conducta agresiva continuaron siendo evaluados cada 6 meses durante al menos 36 meses. Resultados: Se observó un cambio estadísticamente significativo de la conducta agresiva, a lo largo de 36 meses de seguimiento. Se describen los efectos colaterales de la asociación de ambos procedimientos, siendo el de mayor frecuencia la somnolencia y algunos casos de reducción en la conducta sexual. Conclusión: Las lesiones unilaterales simétricas y simultáneas del núcleo central de la amígdala y del hipotálamo posteromedial contralaterales a la dominancia motora dan el mismo efecto clínico en la reducción de la agresividad patológica que las lesiones bilaterales.


Abstract Background: Neurosurgical treatment, although controversial, is considered a useful resource in the treatment of chronic psychiatric diseases such as refractory aggressiveness. Objective: To evaluate the clinical results and side effects of posteromedial hypothalamotomy associated with amygdalotomy in patients with refractory aggressiveness. Method: A clinical trial was conducted in patients with chronic aggressiveness and refractory to pharmacological treatment. A central amygdalotomy associated with posteromedial hypothalamotomy was performed using thermo-coagulation by radiofrequency. The degree of aggressiveness was quantified by the Yudofsky's global scale of aggression. Postoperative changes in aggressive behavior continued to be evaluated every 6 months for at least 36 months. Results: A statistically significant change in aggressive behavior was observed during 36 months of follow-up. The collateral effects of the association of both procedures are described, the most frequent being drowsiness and some cases of reduction in sexual behavior. Conclusion: Symmetric and simultaneous unilateral lesions of the central nucleus of the amygdala and the posteromedial hypothalamus contralateral to motor dominance give the same clinical effect in the reduction of the pathological aggression that the bilateral lesions.


Subject(s)
Humans , Male , Female , Adult , Middle Aged , Young Adult , Psychosurgery/methods , Aggression , Amygdala/surgery , Hypothalamus/surgery , Mental Disorders/surgery
12.
Dement. neuropsychol ; 12(2): 105-113, Apr.-June 2018. tab, graf
Article in English | LILACS | ID: biblio-952960

ABSTRACT

Abstract The limbic-reticular coupling theory suggests that the hippocampus and amygdala regulate such descending limbic structures as the mammillary bodies, septum, hypothalamus and epithalamus to regulate the ascending noradrenergic, serotonergic, dopaminergic and cholinergic systems, performing declarative memory consolidation and recall. Recent studies have revealed that, less sensitive to familiarity, the hippocampus functions via the fornix, mammillary bodies and hypothalamus for memory recall. Lesions to the thalamic nuclei were complicated with damage to adjacent fornix, stria medullaris and habenula, simultaneously destroying two kinds of structures respectively for familiarity and recall. Furthermore, the orbitofrontal cortex was shown to be clinically irrelevant for memory recall. Electrophysiologically, the hippocampus regulates the raphe nuclei in complex ways, and the hippocampal theta wave activates the dopaminergic cells in ventral tegmental area and cholinergic neurons in basal forebrain, while cholinergic-modulated theta-gamma coupling mediates cortical recall. These concurrent advances support the limbic-reticular coupling theory for elucidation of memory recall.


Resumo A teoria do acoplamento límbico-reticular sugere que o hipocampo e a amígdala regulam estruturas límbicas descendentes como os corpos mamilares, septum, hipotálamo e epitálamo para regular os sistemas ascendentes noradrenérgico, serotoninérgico, dopaminérgico e colinérgico, realizando a consolidação da memória declarativa e a recordação. Estudos recentes revelaram que, menos sensível à familiaridade, o hipocampo funcionava via fórnice, corpos mamilares e hipotálamo para a recordação da memória. Lesões aos núcleos talâmicos são complicadas com danos ao fórnice, estria medullaris e habenula adjacentes, destruindo simultaneamente dois tipos de estruturas, respectivamente, para familiaridade e recordação. Além disso, o córtex orbitofrontal mostrou-se clinicamente irrelevante para a recordação da memória. Eletrofisiologicamente, o hipocampo regula os núcleos da rafe de maneiras complexas, e a onda teta hipocampal ativa as células dopaminérgicas na área tegmentar ventral e os neurônios colinérgicos no prosencéfalo basal, enquanto que o acoplamento teta-gama colinergicamente modulado medeia a evocação cortical. Esses avanços concorrentes sugerem que a teoria do acoplamento límbico-reticular apropriada para a elucidação da recordação da memória.


Subject(s)
Memory/physiology , Mental Recall , Hippocampus , Amygdala
13.
Experimental Neurobiology ; : 508-525, 2018.
Article in English | WPRIM | ID: wpr-719052

ABSTRACT

Astrocyte is the most abundant cell type in the central nervous system and its importance has been increasingly recognized in the brain pathophysiology. To study in vivo function of astrocyte, astrocyte-specific gene-targeting is regarded as a powerful approach. Especially, hGFAP-CreERT2, which expresses tamoxifen-inducible Cre recombinase under the human GFAP promoter, has been developed and characterized from several research groups. However, one of these mouse lines, [Tg(GFAP-Cre/ERT2)13Kdmc] from Ken McCarthy group has not been quantitatively analyzed, despite its frequent use. Here, we performed comprehensive characterization of this mouse line with quantitative analysis. By crossing this mouse line with Ai14 (RCL-tdTomato), a very sensitive Cre reporter mouse line, we visualized the Cre-expressing cells in various brain regions. For quantitative analysis, we immunostained S100β as an astrocytic marker and NeuN, tyrosine hydroxylase or calbindin as a neuronal marker in different brain regions. We calculated ‘astrocyte specificity’ as the proportion of co-labelled S100β and tdTomato positive cells in the total number of tdTomato positive cells and the ‘astrocyte coverage’ as the proportion of co-labelled S100β and tdTomato positive cells in the total number of S100β positive cells. Interestingly, we found varying degree of astrocyte specificity and coverage in each brain region. In cortex, hypothalamus, substantia nigra pars compacta and cerebellar Purkinje layer, we observed high astrocyte specificity (over 89%) and relatively high astrocyte coverage (over 70%). In striatum, hippocampal CA1 layer, dentate gyrus and cerebellar granule layer, we observed high astrocyte specificity (over 80%), but relative low astrocyte coverage (50–60%). However, thalamus and amygdala showed low astrocyte specificity (about 65%) and significant neuron specificity (over 30%). This hGFAP-CreERT2 mouse line can be useful for genetic modulations of target gene either in gain-of-function or loss-of-function studies in the brain regions with high astrocyte specificity and coverage. However, the use of this mouse line should be restricted to gain-of-function studies in the brain regions with high astrocyte specificity but low coverage. In conclusion, hGFAP-CreERT2 mouse line could be a powerful tool for gene-targeting of astrocytes in cortex, striatum, hippocampus, hypothalamus, substantia nigra pars compacta and cerebellum, but not in thalamus and amygdala.


Subject(s)
Amygdala , Animals , Astrocytes , Brain , Calbindins , Central Nervous System , Cerebellum , Dentate Gyrus , Hippocampus , Humans , Hypothalamus , Mice , Neurons , Pars Compacta , Recombinases , Sensitivity and Specificity , Thalamus , Tyrosine 3-Monooxygenase
14.
Article in English | WPRIM | ID: wpr-715987

ABSTRACT

OBJECTIVES: The purpose of this study was to investigate whether the neural activity of autism spectrum disorder (ASD) patients is different from that of normal individuals when performing aesthetic judgments. METHODS: We recruited typical ASD patients without savant skills (ASD group, n=17) and healthy controls (HC group, n=19) for an functional magnetic resonance imaging study. All subjects were scanned while performing aesthetic judgment tasks on two kinds of artwork (magnificent landscape images and fractal images). Differences in brain activation between the two groups were assessed by contrasting neural activity during the tasks. RESULTS: The aesthetic judgment score for all images was significantly lower in the ASD group than in the HC group. During the aesthetic judgment tasks, the ASD group showed less activation than the HC group in the anterior region of the superior frontal gyrus, and more activation in the temporoparietal area and insula, regardless of the type of images being judged. In addition, during the aesthetic judgment task for the fractal images, the ASD group exhibited greater neural activity in the amygdala and the posterior region of the middle/inferior temporal gyrus (Brodmann area 37) than the HC group. CONCLUSION: The results of this study suggest that the brain activation patterns associated with aesthetic experiences in ASD patients may differ from those of normal individuals.


Subject(s)
Amygdala , Autism Spectrum Disorder , Autistic Disorder , Beauty , Brain , Fractals , Humans , Judgment , Magnetic Resonance Imaging , Prefrontal Cortex , Temporal Lobe
15.
Psychiatry Investigation ; : 1000-1006, 2018.
Article in English | WPRIM | ID: wpr-717817

ABSTRACT

OBJECTIVE: Post weanling isolation-reared (IR) rats are featured with depressive phenotype, yet its mechanism is not clearly defined particularly in terms of the involvement of central 5-HT1A receptors. The present study aims to examine the effects of 5HT1A activation on forced swim test (FST) in IR rats following 5-HT depletion. METHODS: Social control (SOC) and IR rats received an intracerebraoventricular (ICV) injection of 5-HT depletion agent, 5,7-DHT. 14 days after the surgery, rats were assessed their performance in FST with or without the challenge with a 5-HT1A agonist, 8-OH-DPAT. Rats were then sacrificed for analyzing their 5-HT tissue levels and the expressions of their 5-HA1A receptors in prefrontal cortex (PFC), hippocampus (HPX), and amygdala (AMY). RESULTS: 5,7-DHT decreased the tissue concentration of 5-HT in both IR and SOC rats. IR rats were more immobile and less sensitive to the lesion-induced immobility, however this effect was reversed by acute challenge of 8-OH-DPAT. 5,7-DHT lesion increased the expression of PFC 5-HT1A receptors. CONCLUSION: The integrity of central 5-HT system is developmentally crucial for the 5-HT1A-relevant depression profile in rats of social isolation.


Subject(s)
8-Hydroxy-2-(di-n-propylamino)tetralin , Amygdala , Animals , Depression , Hippocampus , Phenotype , Prefrontal Cortex , Rats , Receptor, Serotonin, 5-HT1A , Serotonin 5-HT1 Receptor Agonists , Serotonin , Social Control, Formal , Social Isolation
16.
Article in English | WPRIM | ID: wpr-718218

ABSTRACT

OBJECTIVE: Neuropsychiatric manifestations like depression and cognitive dysfunction commonly occur in inflammatory bowel disease (IBD). In the context of the brain-gut axis model, colitis can lead to alteration of brain function in a bottom-up manner. Here, the changes in the response of the hypothalamic-pituitary-adrenal axis and inflammation-related markers in the brain in colitis were studied. METHODS: Dextran sodium sulfate (DSS) was used to generate a mouse model of colitis. Mice were treated with DSS for 3 or 7 days and sacrificed. We analyzed the gene expression of brain-derived neurotrophic factor (BDNF), cyclo-oxygenase 2 (COX-2), and glial fibrillary acidic protein (GFAP), and the expression of GFAP, in the hippocampus, hypothalamus, and amygdala. Additionally, the levels of C-reactive protein (CRP) and serum cortisol/corticosterone were measured. RESULTS: Alteration of inflammatory-related markers varied depending on the brain region and exposure time. In the hippocampus, COX-2 mRNA, GFAP mRNA, and GFAP expression were upregulated during exposure to DSS. However, in the hypothalamus, COX-2 mRNA was upregulated only 3 days after treatment. In the amygdala, BDNF and COX-2 mRNAs were downregulated. CRP and corticosterone expression increased with DSS treatment at day 7. CONCLUSION: IBD could lead to neuroinflammation in a bottom-up manner, and this effect varied according to brain region. Stress-related hormones and serum inflammatory markers, such as CRP, were upregulated from the third day of DSS treatment. Therefore, early and active intervention is required to prevent psychological and behavioral changes caused by IBD, and region-specific studies can help understand the precise mechanisms by which IBD affects the brain.


Subject(s)
Amygdala , Animals , Brain , Brain-Derived Neurotrophic Factor , C-Reactive Protein , Colitis , Corticosterone , Cyclooxygenase 2 , Depression , Dextrans , Gene Expression , Glial Fibrillary Acidic Protein , Hippocampus , Hypothalamus , Inflammation , Inflammatory Bowel Diseases , Mice , Prostaglandin-Endoperoxide Synthases , RNA, Messenger , Sodium
17.
Article in English | WPRIM | ID: wpr-718216

ABSTRACT

OBJECTIVE: Prior functional magnetic resonance imaging (fMRI) work has revealed that children/adolescents with disruptive behavior disorders (DBDs) show dysfunctional reward/non-reward processing of non-social reinforcements in the context of instrumental learning tasks. Neural responsiveness to social reinforcements during instrumental learning, despite the importance of this for socialization, has not yet been previously investigated. METHODS: Twenty-nine healthy children/adolescents and 19 children/adolescents with DBDs performed the fMRI social/non-social reinforcement learning task. Participants responded to random fractal image stimuli and received social and non-social rewards/non-rewards according to their accuracy. RESULTS: Children/adolescents with DBDs showed significantly reduced responses within the caudate and posterior cingulate cortex (PCC) to non-social (financial) rewards and social non-rewards (the distress of others). Connectivity analyses revealed that children/adolescents with DBDs have decreased positive functional connectivity between the ventral striatum (VST) and the ventromedial prefrontal cortex (vmPFC) seeds and the lateral frontal cortex in response to reward relative to non-reward, irrespective of its sociality. In addition, they showed decreased positive connectivity between the vmPFC seed and the amygdala in response to non-reward relative to reward. CONCLUSION: These data indicate compromised reinforcement processing of both non-social rewards and social non-rewards in children/adolescents with DBDs within core regions for instrumental learning and reinforcement-based decision-making (caudate and PCC). In addition, children/adolescents with DBDs show dysfunctional interactions between the VST, vmPFC, and lateral frontal cortex in response to rewarded instrumental actions potentially reflecting disruptions in attention to rewarded stimuli.


Subject(s)
Amygdala , Attention Deficit and Disruptive Behavior Disorders , Conditioning, Operant , Fractals , Frontal Lobe , Gyrus Cinguli , Learning , Magnetic Resonance Imaging , Prefrontal Cortex , Problem Behavior , Reinforcement, Social , Reward , Socialization , Ventral Striatum
18.
Arq. neuropsiquiatr ; 75(11): 801-808, Nov. 2017. tab, graf
Article in English | LILACS | ID: biblio-888266

ABSTRACT

ABSTRACT Mesial temporal sclerosis creates a focal epileptic syndrome that usually requires surgical resection of mesial temporal structures. Objective: To describe a novel operative technique for treatment of temporal lobe epilepsy and its clinical results. Methods: Prospective case-series at a single institution, performed by a single surgeon, from 2006 to 2012. A total of 120 patients were submitted to minimally-invasive keyhole transtemporal amygdalohippocampectomy. Results: Of the patients, 55% were male, and 85% had a right-sided disease. The first 70 surgeries had a mean surgical time of 2.51 hours, and the last 50 surgeries had a mean surgical time of 1.62 hours. There was 3.3% morbidity, and 5% mild temporal muscle atrophy. There was no visual field impairment. On the Engel Outcome Scale at the two-year follow-up, 71% of the patients were Class I, 21% were Class II, and 6% were Class III. Conclusion: This novel technique is feasible and reproducible, with optimal clinical results.


RESUMO A esclerose mesial temporal é uma síndrome epiléptica focal que requer ablação de estruturas mesiais temporais. Objetivo: Descrever e padronizar a técnica operatória e resultados clínicos. Métodos: Série prospectiva de casos de uma única instituição, realizadas por um único cirurgião, de 2006 a 2012. 120 doentes foram submetidos a amigdalo-hipocampectomia transtemporal por acesso mínimo (keyhole). Resultados: 55% eram do sexo masculino, 85% apresentavam doença do lado direito. As primeiras 70 cirurgias tiveram um tempo cirúrgico médio de 2,51 horas, e as últimas 50 cirurgias tiveram um tempo cirúrgico médio de 1,62 horas. Houve morbidade de 3,3%. 5% dos doentes apresentaram atrofia leve de músculo temporal. O controle das convulsões foi avaliado com a Escala de Engel no segundo ano de pós operatorio, 71% eram Classe I, 21% Classe II, 6% Classe III. Conclusão: Esta nova técnica é viável, reprodutível e com resultados clínicos adequados.


Subject(s)
Humans , Male , Female , Child , Adolescent , Adult , Middle Aged , Aged , Young Adult , Sclerosis/surgery , Temporal Lobe/surgery , Epilepsy, Temporal Lobe/surgery , Hippocampus/surgery , Amygdala/surgery , Treatment Outcome , Minimally Invasive Surgical Procedures/economics , Minimally Invasive Surgical Procedures/methods , Neurosurgical Procedures/economics , Neurosurgical Procedures/methods
20.
Campinas; s.n; 2017. 65 p. ilus.
Thesis in Portuguese | LILACS | ID: biblio-914476

ABSTRACT

Resumo: A AMP-activated protein kinase (AMPK) regula o balanço energético por ações no hipotálamo. Sua ativação está ligada ao aumento da ingestão alimentar e sua inibição leva a redução da ingestão alimentar. Recentes evidências demonstram que outras regiões do sistema nervoso podem contribuir para o controle da ingestão alimentar. O núcleo central da amígdala (CeA) é parte integrante do sistema dopaminérgico de recompensa e juntamente com o hipotálamo participa do controle da homeostase energética. Na amígdala vias moleculares como a via da insulina participam do controle da ingestão alimentar, contudo ainda não foi avaliado se a AMPK poderia contribuir com esse controle. Em vista disso, o presente estudo avaliou a possível fosforilação da AMPK no CeA e sua participação no controle da ingestão alimentar em resposta a diversas situações. A AMPK estava expressa no CeA. O jejum aumentou a fosforilação em treonina da AMPK?1/2Thr172 e a realimentação reduziu essa fosforilação. A injeção de glicose no CeA diminuiu a fosforilação em AMPK?1/2Thr172, ao passo que, a injeção de 2DG aumentou essa fosforilação, assim como a ingestão alimentar. A injeção de grelina no CeA aumentou a ingestão alimentar e a fosforilação em AMPK?1/2Thr172. Esse resultado foi acompanhado pelo aumento da expressão gênica do NPY e redução de ocitocina. Em contrapartida, a insulina reduziu a fosforilação em AMPK?1/2Thr172 no CeA. A ativação farmacológica da AMPK no CeA, com AICAR, aumentou a ingestão como esperado. A infusão crônica de MTII reduziu a massa corporal, a ingestão e a fosforilação em AMPK?1/2Thr172 no CeA. O tratamento por 14 dias com siRNA-AMPK?2 no CeA, inibiu a expressão gênica da AMPK e reduziu a massa corporal. Essa redução foi acompanhada de aumento na expressão gênica de UCP1 no tecido adiposo marrom sem alteração na ingestão alimentar. Em adição, houve redução na expressão gênica de NPY e aumento de ocitocina no CeA. Esses resultados sugerem que a ativação da AMPK no CeA, participa do controle da homeostase energética por modular a ingestão alimentar em reposta a ação de nutrientes e hormônios como grelina e insulina(AU)


Abstract: AMP-activated protein kinase (AMPK) is a cellular energy sensor that regulates energy balance at cellular and whole body nivel. Several studies demonstrate that hypothalamic AMPK participates in the control of food intake in response to nutrients and hormones such as insulin and ghrelin. Increased AMPK activity in hypothalamus is associated with enhance in food intake and its inhibition leads to reduced food intake. Recent evidence demonstrates that other regions from central nervous system may contribute to control energy metabolism and food intake. The central nucleus of the amygdala (CeA) is part of the dopaminergic reward system and jointly with the hypothalamus participates in control of food intake. In amygdala molecular pathways such as insulin pathway participate in the control of food intake, however other cellular pathways, such as AMPK may contribute to this control. In this sense, the present study investigated AMPK activation in CeA and its participation in food intake control. Fasting increased phosphorylation in Thr172 of AMPK?1/2 and refeeding reduced this phosphorylation. Injection of glucose in CeA decreased the phosphorylation in Thr172 of AMPK?1/2, whereas 2DG injection increased this phosphorylation as well as food intake. Ghrelin injection in CeA increased food intake and Thr172 phosphorylation of AMPK?1/2. In adiction, NPY gene expression was increased and oxytocin gene expression was lower. In contrast, insulin reduced Thr172 phosphorylation of AMPK?1/2 in CeA. As expected, AMPK pharmacological activation in CeA with AICAR increased food intake. Chronic injection of MTII in CeA reduced body mass, food intake and phosphorylation in Thr172 of AMPK?1/2. Further, knocking down Alpha 1/2 AMPK in the CeA for 14 days was sufficient to decrease body mass without altering food intake. AMPK?2 and NPY gene expression in CeA was reduced and oxytocin gene expression in CeA and UCP-1 in BAT was increased. These results suggest that once active in CeA, AMPK participates in control of energy homeostasis by modulating food intake in response to nutrients and hormones such as ghrelin and insulin(AU)


Subject(s)
Animals , Rats , AMP-Activated Protein Kinases , Amygdala , Central Amygdaloid Nucleus , Eating , Energy Metabolism , Nervous System , Rats, Wistar
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