Transactivation of TrkB by Sigma-1 receptor mediates cocaine-induced changes in dendritic spine density and morphology in hippocampal and cortical neurons

Ka, Minhan; Kook, Yeon Hee; Liao, Ke; Buch, Shilpa; Kim, Woo Yang

doi:10.1038/cddis.2016.319

Cited by 36 publications

(23 citation statements)

References 72 publications

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“…Immunostaining of brain sections or dissociated cells was performed as described previously 42 , 43 . Primary antibodies used were mouse anti-ARID1B (Abcam, ab57461, 1:500; Abnova, H00057492-M02, 1:500), rabbit anti-GABA (Sigma, A2052, 1:500), mouse anti-parvalbumin (Millipore, MAB1572, 1:500), rabbit anti-cleaved caspase-3 (Cell Signaling Technology, #9664, 1:300), mouse anti-BrdU (BD Biosciences, #555627, 1:800), rabbit anti-Phospho-Histone H3 (Cell Signaling Technology, #9701, 1:800), rabbit anti-VIAAT (Phosphosolution, 2100-VGAT, 1:500), guinea pig anti- VGluT11 (Millipore, AB5905, 1:500), rat anti-GAD2 (Developmental Studies Hybridoma Bank, GAD6, 1:500), rat anti-somatostatin (Millipore, MAB354, 1:500), rabbit anti-calbindin-D 28k (Millipore, AB1778, 1:500), mouse anti-calretinin (Millipore, MAB1568, 1:500), rabbit anti-Cux1 (Santa Cruz, sc-13024, 1:500), mouse anti-NeuN (Millipore, MAB377, 1:1000), rabbit anti-TBR1 (Millipore, AB10554, 1:500), rabbit anti-Olig2 (Millipore, AB9610, 1:500), rabbit anti-GFAP (DAKO, Z0334, 1:500), rabbit anti-PSD95 (Abcam, ab18258, 1:500) and chicken anti-GFP (Invitrogen, A10262, 1:1,500) antibodies.…”

Section: Methodsmentioning

confidence: 99%

Arid1b haploinsufficiency disrupts cortical interneuron development and mouse behavior

et al. 2017

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Haploinsufficiency of the AT-rich interactive domain 1B (ARID1B) gene causes autism spectrum disorder (ASD) and intellectual disability, however, the neurobiological basis for this is unknown. Here, we generated Arid1b knockout mice and examined heterozygotes to model human patients. Arid1b heterozygous mice showed a decreased number of cortical GABAergic interneurons and reduced proliferation of interneuron progenitors in the ganglionic eminence. Arid1b haploinsufficiency also led to an imbalance between excitatory and inhibitory synapses in the cerebral cortex. Furthermore, we found that Arid1b haploinsufficiency suppressed histone H3 lysine 9 acetylation (H3K9Ac) overall, and in particular reduced H3K9Ac of the Pvalb promoter, resulting in decreased transcription. Arid1b heterozygous mice exhibited abnormal cognitive and social behavior, which was rescued by treatment with a positive allosteric GABAA receptor modulator. Our results demonstrate a critical role for the Arid1b gene in interneuron development and behavior, and provide insight into the pathogenesis of ASD and intellectual disability.

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Section: Methodsmentioning

confidence: 99%

Arid1b haploinsufficiency disrupts cortical interneuron development and mouse behavior

et al. 2017

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“…Immunostaining. Immunostaining of brain sections was performed as described previously 61,62 . The following primary antibodies were used: anti-Parvalbumin (Millipore, Rabbit, AB1572; 1:200), anti-Arid1b (Abcam, Mouse, ab57461; 1:200), anti-VIAAT (PhosphoSolutions, Rabbit, 2100-VGAT, 1:500), anti-VGLUT1 (Millipore, Guinea pig, AB5905, 1:1000), GAD2 (Developmental Studies Hybridoma Bank, Rat, GAD6, 1:200), and anti-Somatostatin (MilliporeSigma, Rat, MAB354; 1:200).…”

Section: Methodsmentioning

confidence: 99%

Arid1b haploinsufficiency in parvalbumin- or somatostatin-expressing interneurons leads to distinct ASD-like and ID-like behavior

Smith

Jung

Jeon

et al. 2020

Sci Rep

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Inhibitory interneurons are essential for proper brain development and function. Dysfunction of interneurons is implicated in several neurodevelopmental disorders, including autism spectrum disorder (ASD) and intellectual disability (ID). We have previously shown that Arid1b haploinsufficiency interferes with interneuron development and leads to social, cognitive, and emotional impairments consistent with ASD and ID. It is unclear, however, whether interneurons play a major role for the behavioral deficits in Arid1b haploinsufficiency. Furthermore, it is critical to determine which interneuron subtypes contribute to distinct behavioral phenotypes. In the present study, we generated Arid1b haploinsufficient mice in which a copy of the Arid1b gene is deleted in either parvalbumin (PV) or somatostatin (SST) interneurons, and examined their ASD-and ID-like behaviors. We found that Arid1b haploinsufficiency in PV or SST interneurons resulted in distinct features that do not overlap with one another. Arid1b haploinsufficiency in PV neurons contributed to social and emotional impairments, while the gene deletion in the SST population caused stereotypies as well as learning and memory dysfunction. These findings demonstrate a critical role of interneurons in Arid1b haploinsufficient pathology and suggest that PV and SST interneurons may have distinct roles in modulating neurological phenotypes in Arid1b haploinsufficiency-induced ASD and ID. Autism spectrum disorder (ASD) and intellectual disability (ID) are highly prevalent neurodevelopmental disorders, characterized by social communication impairments and cognitive dysfunction, respectively 1,2. Emotional disturbance such as aggressive behavior, depression, and anxiety is another significant aspect of ASD and ID 3-8. While behaviors of ASD and ID are relatively well characterized, the neuropathogenesis of these conditions is poorly understood. Accordingly, no pharmacologic or genetic interventions are available for ASD or ID. Haploinsufficiency of the AT-rich interactive domain 1B (ARID1B) gene has been shown to cause ASD and ID in humans 9-11. ARID1B is a component of the Brg/Brm associated factor (BAF) chromatin remodeling complex in the brain 12,13. It binds to DNA through its AT-rich DNA-binding domain and alters chromatin structure, facilitating transcription factor access and regulating gene expression. Many neurodevelopmental disorders exhibit improper inhibitory interneuron development, resulting in excitatory/inhibitory (E/I) imbalance 14-16. We have previously generated an Arid1b mouse model and showed that Arid1b haploinsufficient (Arid1b +/−) mice recapitulate ASD and ID behavior 17. Importantly, Arid1b haploinsufficient mice exhibit a reduction and abnormal distribution of interneurons as well as abnormal inhibitory synaptic activity in the cerebral cortex 17. No clear anatomical or physiological phenotype has been found in excitatory neurons, suggesting a more prominent effect on interneuron abnormalities in potentially creating a range of social, intelle...

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“…A recent study provided evidence for a role of zinc-mediated TrkB transactivation in regulating both dendritic morphology and spine density in mature primary hippocampal neurons (Zagrebelsky et al 2018 ). Moreover, cocaine treatment has been shown to increase dendritic spine density in hippocampal neurons by promoting TrkB transactivation via the Sigma-1 receptor (Ka et al 2016 ). Transactivation of TrkB results in biologically relevant consequences both in the healthy brain, where it regulates neuronal migration, architecture.…”

Section: The Role Of Bdnf In Regulating Dendritic Spine Developmentmentioning

confidence: 99%

BDNF signaling during the lifetime of dendritic spines

2020

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Dendritic spines are tiny membrane specialization forming the postsynaptic part of most excitatory synapses. They have been suggested to play a crucial role in regulating synaptic transmission during development and in adult learning processes. Changes in their number, size, and shape are correlated with processes of structural synaptic plasticity and learning and memory and also with neurodegenerative diseases, when spines are lost. Thus, their alterations can correlate with neuronal homeostasis, but also with dysfunction in several neurological disorders characterized by cognitive impairment. Therefore, it is important to understand how different stages in the life of a dendritic spine, including formation, maturation, and plasticity, are strictly regulated. In this context, brain-derived neurotrophic factor (BDNF), belonging to the NGF-neurotrophin family, is among the most intensively investigated molecule. This review would like to report the current knowledge regarding the role of BDNF in regulating dendritic spine number, structure, and plasticity concentrating especially on its signaling via its two often functionally antagonistic receptors, TrkB and p75NTR. In addition, we point out a series of open points in which, while the role of BDNF signaling is extremely likely conclusive, evidence is still missing.

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Transactivation of TrkB by Sigma-1 receptor mediates cocaine-induced changes in dendritic spine density and morphology in hippocampal and cortical neurons

Cited by 36 publications

References 72 publications

Arid1b haploinsufficiency disrupts cortical interneuron development and mouse behavior

Arid1b haploinsufficiency disrupts cortical interneuron development and mouse behavior

Arid1b haploinsufficiency in parvalbumin- or somatostatin-expressing interneurons leads to distinct ASD-like and ID-like behavior

BDNF signaling during the lifetime of dendritic spines

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