Reorganization of Basolateral Amygdala-Subiculum Circuitry in Mouse Epilepsy Model

Ma, Dongliang; Qu, Jian Qiang; Goh, Eyleen L. K.; Tang, Feng Ru

doi:10.3389/fnana.2015.00167

Cited by 9 publications

(4 citation statements)

References 59 publications

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“…Our study also found that the Eyes Task score decreased with an increase in several previous manic episodes, accounting for decreased socio-perception. These findings, together with data from other studies, are indicative that neuronal loss in the brain is associated with many previous episodes rather than early-onset [17][18][19].…”

Section: Discussionsupporting

confidence: 74%

Theory of mind deficits in bipolar disorder in remission

Kılınçel¹,

Eker²,

Kılınçel³

2020

Journal of Surgery and Medicine

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Aims: Theory of Mind (ToM), a concept used to describe an individual's social cognitive abilities that play roles in social interaction, may have a significant role in explaining the clinical variables and social problems of affective disorders. This study aims to determine whether ToM functions are impaired in Bipolar Disorder (BD) compared to healthy controls as well as investigate the association between clinical variables of ToM deficit and social competence. Methods: A total of 50 patients diagnosed with BD who were in remission and 50 healthy control subjects were included in this crosssectional study. Demographic data and medical history of participants were assessed, and Beck Depression Inventory (BDI), Beck Anxiety Inventory (BAI), Eyes test, Hinting Task, Social Adaptation and Self-Evaluation Scale (SASS), Wechsler Adult Intelligence Scale-Revised (WAIS-R) tests were administered. Results: There were no significant differences with regards to age, gender and BDI scores between patient and control groups. Hinting test (P=0.001), Eyes test (P=0.001), SASS (P=0.007) and WAIS-R (P=0.001) scores were higher in the control group. There was a significant correlation between Hinting Test and WAIS-R (r=0.430, P=0.001), and between Eyes Test and age (r.-0.590, P=0.001), duration of bipolar disorder (r=-0.554, P=0.001), number of manic attacks (r=0.590, P=0.001) and WAIS-R (r=0.343, P=0.050). Logistic regression analysis showed that compared to the patient group, control group was related to Eyes test by 1.2-fold for each point increase in Eyes test (P=0.001) and 1.3-fold for each point increase in Hinting test (P=0.003). Conclusion: ToM deficit was an essential factor that separated BD patients in remission from healthy individuals. ToM deficit may play a role in the essential pathology or affect the presence, or even onset, of BD.

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Section: Discussionsupporting

confidence: 74%

Theory of mind deficits in bipolar disorder in remission

Kılınçel¹,

Eker²,

Kılınçel³

2020

Journal of Surgery and Medicine

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“…After SE, axon sprouting of granule cells would increase recurrent excitation in the dentate gyrus (Tauck and Nadler, 1985), whereas axonal sprouting of CA1 pyramidal cell would increase CA1 to subiculum excitation (Cavazos et al, 2004). Anatomical projections from the basolateral amygdala to ventral subiculum were also increased after pilocarpine SE (Ma et al, 2015). In the hippocampus, kainate-induced SE resulted in loss of inhibitory interneurons in the distal dendritic layer (Cossart et al, 2001), increase in dendritic excitation and spike excitability (Bernard et al, 2004, Wu and Leung, 2003).…”

Section: Discussionmentioning

confidence: 99%

Resting state functional network disruptions in a kainic acid model of temporal lobe epilepsy

Gill

Mirsattari

Leung

2017

NeuroImage: Clinical

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We studied the graph topological properties of brain networks derived from resting-state functional magnetic resonance imaging in a kainic acid induced model of temporal lobe epilepsy (TLE) in rats. Functional connectivity was determined by temporal correlation of the resting-state Blood Oxygen Level Dependent (BOLD) signals between two brain regions during 1.5% and 2% isoflurane, and analyzed as networks in epileptic and control rats. Graph theoretical analysis revealed a significant increase in functional connectivity between brain areas in epileptic than control rats, and the connected brain areas could be categorized as a limbic network and a default mode network (DMN). The limbic network includes the hippocampus, amygdala, piriform cortex, nucleus accumbens, and mediodorsal thalamus, whereas DMN involves the medial prefrontal cortex, anterior and posterior cingulate cortex, auditory and temporal association cortex, and posterior parietal cortex. The TLE model manifested a higher clustering coefficient, increased global and local efficiency, and increased small-worldness as compared to controls, despite having a similar characteristic path length. These results suggest extensive disruptions in the functional brain networks, which may be the basis of altered cognitive, emotional and psychiatric symptoms in TLE.

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“…was injected to antagonize the peripheral cholinergic response caused by pilocarpine. Behavioral changes were observed, and seizures were evaluated by the Racine score [ 34 ]. Mice with seizures grade IV or V were used in subsequent experiments.…”

Section: Methodsmentioning

confidence: 99%

miR-485 inhibits histone deacetylase HDAC5, HIF1α and PFKFB3 expression to alleviate epilepsy in cellular and rodent models

Pan

Song

et al. 2021

Aging

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We investigated the role of microRNA (miR)-485 and its downstream signaling molecules on mediating epilepsy in cellular and rat models. We established a cellular epilepsy model by exposing hippocampal neurons to magnesium and a rat model by treating ICR mice with lithium chloride (127 mg/kg) and pilocarpine (30 mg/kg). We confirmed that miR-485 could bind and inhibit histone deacetylase 5 (HDAC5) and then measured expression of miR-485 and in mice and cells. Cells were transfected with overexpression or knockdown of miR-485, HDAC5, hypoxia-inducible factor-1alpha (HIF1α), or 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 enzyme (PFKFB3) to verify their roles in apoptosis, oxidative stress, and inflammation in epileptic hippocampal neurons. Binding relationship between miR-485, HDAC5, HIF1α, and PFKFB3 was verified. Oxidative stress and inflammation marker levels in epilepsy model mice were assessed. miR-485 was downregulated and HDAC5 was upregulated in cell and animal model of epilepsy. Seizure, neuronal apoptosis, oxidative stress (increased SOD and GSH-Px expression and decreased MDA and 8-OHdG expression) and inflammation (reduced IL-1β, TNF-α, and IL-6 expression) were reduced by miR-485 in epileptic cells. HIF1α and PFKFB3 expression was reduced by HDAC5 knockdown in cells, which was recapitulated in vivo . Thus, miR-485 alleviates neuronal damage and epilepsy by inhibiting HDAC5, HIF1α, and PFKFB3.

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Reorganization of Basolateral Amygdala-Subiculum Circuitry in Mouse Epilepsy Model

Cited by 9 publications

References 59 publications

Theory of mind deficits in bipolar disorder in remission

Theory of mind deficits in bipolar disorder in remission

Resting state functional network disruptions in a kainic acid model of temporal lobe epilepsy

miR-485 inhibits histone deacetylase HDAC5, HIF1α and PFKFB3 expression to alleviate epilepsy in cellular and rodent models

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