14 results on '"Haram Park"'
Search Results
2. Sexually dimorphic behavior, neuronal activity, and gene expression in Chd8-mutant mice
- Author
-
Su Yeon Choi, Jason P. Lerch, Won Mah, Hwajin Jung, Yonghan Kwon, Sun-Gyun Kim, Yangsik Kim, Seojung Mo, Eunjoon Kim, Hyun Kim, Mihyun Bae, Issac Rhim, Changuk Chung, Jaeseung Kang, Taesun Yoo, Se-Bum Paik, Hyojin Kang, Hanseul Kweon, Eunee Lee, Seung Min Um, Haram Park, Jiseok Lee, Seungmin Ha, Woochul Choi, Yong Chul Bae, Junyeop Daniel Roh, Jacob Ellegood, Hanwool Park, and Yeonsoo Choi
- Subjects
Male ,0301 basic medicine ,Mutant ,Gene Expression ,Neurotransmission ,Biology ,Inhibitory postsynaptic potential ,Hippocampus ,Synaptic Transmission ,Mice ,03 medical and health sciences ,0302 clinical medicine ,Anxiety, Separation ,Gene expression ,Animals ,Premovement neuronal activity ,Social Behavior ,Gene ,Neurons ,Sex Characteristics ,Behavior, Animal ,General Neuroscience ,Object Attachment ,Extracellular Matrix ,Cell biology ,Chromatin ,DNA-Binding Proteins ,Mice, Inbred C57BL ,030104 developmental biology ,Female ,Vocalization, Animal ,Transcriptome ,Neuroscience ,030217 neurology & neurosurgery ,Signal Transduction ,Sex characteristics - Abstract
Autism spectrum disorders (ASDs) are four times more common in males than in females, but the underlying mechanisms are poorly understood. We characterized sexually dimorphic changes in mice carrying a heterozygous mutation in Chd8 (Chd8+/N2373K) that was first identified in human CHD8 (Asn2373LysfsX2), a strong ASD-risk gene that encodes a chromatin remodeler. Notably, although male mutant mice displayed a range of abnormal behaviors during pup, juvenile, and adult stages, including enhanced mother-seeking ultrasonic vocalization, enhanced attachment to reunited mothers, and isolation-induced self-grooming, their female counterparts do not. This behavioral divergence was associated with sexually dimorphic changes in neuronal activity, synaptic transmission, and transcriptomic profiles. Specifically, female mice displayed suppressed baseline neuronal excitation, enhanced inhibitory synaptic transmission and neuronal firing, and increased expression of genes associated with extracellular vesicles and the extracellular matrix. Our results suggest that a human CHD8 mutation leads to sexually dimorphic changes ranging from transcription to behavior in mice.
- Published
- 2018
3. Splice-dependent trans-synaptic PTPδ-IL1RAPL1 interaction regulates synapse formation and non-REM sleep
- Author
-
Frank Koopmans, Hye Min Han, Woong Seob Sim, Suho Lee, Esther Yang, Hyun Kim, August B. Smit, Hanseul Kweon, Eunjoon Kim, Yong Chul Bae, Hwajin Jung, Seoyeong Kim, Yeonsoo Choi, Suwon Kang, Haram Park, Molecular and Cellular Neurobiology, Amsterdam Neuroscience - Cellular & Molecular Mechanisms, and Center for Neurogenomics and Cognitive Research
- Subjects
receptor tyrosine phosphatase ,Neurexin ,Protein tyrosine phosphatase ,Biology ,General Biochemistry, Genetics and Molecular Biology ,Article ,Synapse ,03 medical and health sciences ,Mice ,alternative splicing ,SDG 17 - Partnerships for the Goals ,0302 clinical medicine ,Excitatory synapse ,Postsynaptic potential ,Animals ,Molecular Biology ,030304 developmental biology ,Mice, Knockout ,0303 health sciences ,Mice, Inbred BALB C ,General Immunology and Microbiology ,General Neuroscience ,Alternative splicing ,synaptic adhesion ,Long-term potentiation ,Articles ,sleep behavior and rhythm ,Synapses ,Excitatory postsynaptic potential ,Sleep Stages ,Protein Tyrosine Phosphatases ,synapse development ,Interleukin-1 Receptor Accessory Protein ,Neuroscience ,030217 neurology & neurosurgery - Abstract
Alternative splicing regulates trans‐synaptic adhesions and synapse development, but supporting in vivo evidence is limited. PTPδ, a receptor tyrosine phosphatase adhering to multiple synaptic adhesion molecules, is associated with various neuropsychiatric disorders; however, its in vivo functions remain unclear. Here, we show that PTPδ is mainly present at excitatory presynaptic sites by endogenous PTPδ tagging. Global PTPδ deletion in mice leads to input‐specific decreases in excitatory synapse development and strength. This involves tyrosine dephosphorylation and synaptic loss of IL1RAPL1, a postsynaptic partner of PTPδ requiring the PTPδ‐meA splice insert for binding. Importantly, PTPδ‐mutant mice lacking the PTPδ‐meA insert, and thus lacking the PTPδ interaction with IL1RAPL1 but not other postsynaptic partners, recapitulate biochemical and synaptic phenotypes of global PTPδ‐mutant mice. Behaviorally, both global and meA‐specific PTPδ‐mutant mice display abnormal sleep behavior and non‐REM rhythms. Therefore, alternative splicing in PTPδ regulates excitatory synapse development and sleep by modulating a specific trans‐synaptic adhesion., Global deletion of PTPδ, a presynaptic adhesion molecule, disrupts excitatory synapse formation and NREM sleep. Deletion of the PTPδ‐meA splice insert, critical for trans‐synaptic IL1RAPL1 binding, recapitulates the synaptic and behavioural changes induced by global PTPδ knockout.
- Published
- 2019
4. Single and multiple sevoflurane exposures during pregnancy and offspring behavior in mice
- Author
-
Sang Il Park, Soomin Lee, Xianshu Ju, Woosuk Chung, Seunghwan Yoon, Youngkwon Ko, Jiho Park, Haram Park, Hanwool Park, Yoon Hee Kim, Seok-Hwa Yoon, and Jun Young Heo
- Subjects
Methyl Ethers ,medicine.medical_specialty ,Offspring ,Long-Term Potentiation ,Anxiety ,Sevoflurane ,Mice ,03 medical and health sciences ,0302 clinical medicine ,Memory ,Pregnancy ,030202 anesthesiology ,Internal medicine ,Animals ,Learning ,Medicine ,Social Behavior ,Fetus ,Neuronal Plasticity ,Behavior, Animal ,business.industry ,Excitatory Postsynaptic Potentials ,Long-term potentiation ,Fear ,medicine.disease ,Grooming ,Mice, Inbred C57BL ,Anesthesiology and Pain Medicine ,Endocrinology ,Animals, Newborn ,In utero ,Prenatal Exposure Delayed Effects ,Anesthesia ,Anesthetics, Inhalation ,Pediatrics, Perinatology and Child Health ,Synaptic plasticity ,Gestation ,Female ,business ,030217 neurology & neurosurgery ,medicine.drug - Abstract
SummaryBackground The second trimester is a period of neurogenesis and neuronal migration, which can be affected by exposure to anesthetics. Studies also suggest that multiple exposures may have a greater impact on neurodevelopment. Aim We investigated whether in utero single or multiple exposures to anesthetics caused long-term behavior changes. Methods Pregnant mice were randomly divided into four groups on gestational day 14 (GD 14). Mice in the Control × 1 group were exposed to 100% oxygen for 150 min. Mice in the Sevo × 1 group were also exposed to 100% oxygen for 150 min, except that 2.5% sevoflurane was added during the first 120 min. Mice in the Control × 3 and Sevo × 3 group were identically treated as Control × 1 and Sevo × 1 group for three consecutive days, respectively (GD 14–16). Behavioral tests were performed only with the male offspring at the age of 2–4 months. Synaptic plasticity was also compared by inducing long-term potentiation in acute hippocampal slices. Results Single or multiple sevoflurane exposures in pregnant mice during the second trimester did not cause long-lasting behavioral consequences or changes in long-term synaptic plasticity of their offspring. Conclusion Our study suggests that neither single nor multiple exposures of mice to sevoflurane during the fetal developmental period induces long-term behavioral dysfunctions or affects long-term synaptic plasticity. Additional studies focusing on early stages of neurodevelopment are necessary to confirm the effects of sevoflurane exposure during pregnancy.
- Published
- 2017
5. NGL-1/LRRC4C Deletion Moderately Suppresses Hippocampal Excitatory Synapse Development and Function in an Input-Independent Manner
- Author
-
Yeonsoo Choi, Haram Park, Hwajin Jung, Hanseul Kweon, Seoyeong Kim, Soo Yeon Lee, Hyemin Han, Yisul Cho, Seyeon Kim, Woong Seob Sim, Jeongmin Kim, Yongchul Bae, and Eunjoon Kim
- Subjects
0301 basic medicine ,Hippocampus ,Neurotransmission ,Hippocampal formation ,lcsh:RC321-571 ,Synapse ,03 medical and health sciences ,Cellular and Molecular Neuroscience ,0302 clinical medicine ,Excitatory synapse ,Postsynaptic potential ,synapse ,synaptic transmission ,Molecular Biology ,lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry ,PSD-95 ,Original Research ,synaptic plasticity ,Chemistry ,trans-synaptic adhesion ,Cell biology ,030104 developmental biology ,NGL-1 ,Synaptic plasticity ,Excitatory postsynaptic potential ,030217 neurology & neurosurgery ,LRRC4C ,Neuroscience - Abstract
Netrin-G ligand-1 (NGL-1), also known as LRRC4C, is a postsynaptic densities (PSDs)-95-interacting postsynaptic adhesion molecule that interacts trans-synaptically with presynaptic netrin-G1. NGL-1 and its family member protein NGL-2 are thought to promote excitatory synapse development through largely non-overlapping neuronal pathways. While NGL-2 is critical for excitatory synapse development in specific dendritic segments of neurons in an input-specific manner, whether NGL-1 has similar functions is unclear. Here, we show that Lrrc4c deletion in male mice moderately suppresses excitatory synapse development and function, but surprisingly, does so in an input-independent manner. While NGL-1 is mainly detected in the stratum lacunosum moleculare (SLM) layer of the hippocampus relative to the stratum radiatum (SR) layer, NGL-1 deletion leads to decreases in the number of PSDs in both SLM and SR layers in the ventral hippocampus. In addition, both SLM and SR excitatory synapses display suppressed short-term synaptic plasticity in the ventral hippocampus. These morphological and functional changes are either absent or modest in the dorsal hippocampus. The input-independent synaptic changes induced by Lrrc4c deletion involve abnormal translocation of NGL-2 from the SR to SLM layer. These results suggest that Lrrc4c deletion moderately suppresses hippocampal excitatory synapse development and function in an input-independent manner.
- Published
- 2019
6. GABA Neuronal Deletion of Shank3 Exons 14–16 in Mice Suppresses Striatal Excitatory Synaptic Input and Induces Social and Locomotor Abnormalities
- Author
-
Taesun Yoo, Heejin Cho, Jiseok Lee, Haram Park, Ye-Eun Yoo, Esther Yang, Jin Yong Kim, Hyun Kim, and Eunjoon Kim
- Subjects
0301 basic medicine ,Scaffold protein ,Elevated plus maze ,striatum ,autism ,Striatum ,Biology ,lcsh:RC321-571 ,03 medical and health sciences ,Cellular and Molecular Neuroscience ,0302 clinical medicine ,Postsynaptic potential ,lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry ,Original Research ,repetitive behavior ,social interaction ,Electrophysiology ,030104 developmental biology ,Shank3 ,Excitatory postsynaptic potential ,Phelan-McDermid syndrome ,GABAergic ,Postsynaptic density ,Neuroscience ,030217 neurology & neurosurgery - Abstract
Shank3 is an excitatory postsynaptic scaffolding protein implicated in multiple brain disorders, including autism spectrum disorders (ASD) and Phelan-McDermid syndrome (PMS). Although previous neurobiological studies on Shank3 and Shank3-mutant mice have revealed diverse roles of Shank3 in the regulation of synaptic, neuronal and brain functions, whether Shank3 expression in specific cell types distinctly contributes to mouse phenotypes remains largely unclear. In the present study, we generated two Shank3-mutant mouse lines (exons 14–16) carrying global and GABA neuron-specific deletions and characterized their electrophysiological and behavioral phenotypes. These mouse lines show similar decreases in excitatory synaptic input onto dorsolateral striatal neurons. In addition, the abnormal social and locomotor behaviors observed in global Shank3-mutant mice are strongly mimicked by GABA neuron-specific Shank3-mutant mice, whereas the repetitive and anxiety-like behaviors are only partially mimicked. These results suggest that GABAergic Shank3 (exons 14–16) deletion has strong influences on striatal excitatory synaptic transmission and social and locomotor behaviors in mice.
- Published
- 2018
7. IRSp53/BAIAP2 in dendritic spine development, NMDA receptor regulation, and psychiatric disorders
- Author
-
Haram Park, Jaeseung Kang, and Eunjoon Kim
- Subjects
0301 basic medicine ,medicine.medical_specialty ,Dendritic spine ,Dendritic Spines ,Nerve Tissue Proteins ,Biology ,Receptors, N-Methyl-D-Aspartate ,03 medical and health sciences ,Mice ,Cellular and Molecular Neuroscience ,medicine ,Animals ,Humans ,Protein Interaction Domains and Motifs ,RNA, Messenger ,Psychiatry ,Actin ,IRSp53 ,Pharmacology ,Mental Disorders ,Cell Membrane ,Membrane ,Brain ,Post-Synaptic Density ,medicine.disease ,Actin cytoskeleton ,NMDA receptor ,Cell biology ,Actin Cytoskeleton ,030104 developmental biology ,Phenotype ,Schizophrenia ,Excitatory postsynaptic potential ,Lamellipodium ,Psychiatric disorders ,Filopodia ,Postsynaptic density ,Neuroscience - Abstract
IRSp53 (also known as BAIAP2) is a multi-domain scaffolding and adaptor protein that has been implicated in the regulation of membrane and actin dynamics at subcellular structures, including filopodia and lamellipodia. Accumulating evidence indicates that IRSp53 is an abundant component of the postsynaptic density at excitatory synapses and an important regulator of actin-rich dendritic spines. In addition, IRSp53 has been implicated in diverse psychiatric disorders, including autism spectrum disorders, schizophrenia, and attention deficit/hyperactivity disorder. Mice lacking IRSp53 display enhanced NMDA (N-methyl-d-aspartate) receptor function accompanied by social and cognitive deficits, which are reversed by pharmacological suppression of NMDA receptor function. These results suggest the hypothesis that defective actin/membrane modulation in IRSp53-deficient dendritic spines may lead to social and cognitive deficits through NMDA receptor dysfunction.This article is part of the Special Issue entitled ‘Synaptopathy – from Biology to Therapy’.
- Published
- 2016
- Full Text
- View/download PDF
8. Shank2 Deletion in Parvalbumin Neurons Leads to Moderate Hyperactivity, Enhanced Self-Grooming and Suppressed Seizure Susceptibility in Mice
- Author
-
Seungjoon Lee, Eunee Lee, Ryunhee Kim, Jihye Kim, Suho Lee, Haram Park, Esther Yang, Hyun Kim, and Eunjoon Kim
- Subjects
0301 basic medicine ,Scaffold protein ,medicine.medical_specialty ,Cell type ,seizure ,autism spectrum disorder ,Biology ,Electroencephalography ,lcsh:RC321-571 ,03 medical and health sciences ,Cellular and Molecular Neuroscience ,Basal (phylogenetics) ,0302 clinical medicine ,Postsynaptic potential ,Internal medicine ,parvalbumin ,medicine ,self-grooming ,EEG ,Molecular Biology ,lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry ,Original Research ,medicine.diagnostic_test ,General Neuroscience ,social interaction ,medicine.disease ,SHANK2 ,030104 developmental biology ,Endocrinology ,Shank2 ,biology.protein ,GABAergic ,Autism ,030217 neurology & neurosurgery ,Parvalbumin ,Neuroscience - Abstract
Shank2 is an abundant postsynaptic scaffolding protein implicated in neurodevelopmental and psychiatric disorders, including autism spectrum disorders (ASD). Deletion of Shank2 in mice has been shown to induce social deficits, repetitive behaviors, and hyperactivity, but the identity of the cell types that contribute to these phenotypes has remained unclear. Here, we report a conditional mouse line with a Shank2 deletion restricted to parvalbumin (PV)-positive neurons (Pv-Cre;Shank2fl/fl mice). These mice display moderate hyperactivity in both novel and familiar environments and enhanced self-grooming in novel, but not familiar, environments. In contrast, they showed normal levels of social interaction, anxiety-like behavior, and learning and memory. Basal brain rhythms in Pv-Cre;Shank2fl/fl mice, measured by electroencephalography, were normal, but susceptibility to pentylenetetrazole (PTZ)-induced seizures was decreased. These results suggest that Shank2 deletion in PV-positive neurons leads to hyperactivity, enhanced self-grooming and suppressed brain excitation.
- Published
- 2018
9. Postsynaptic distribution of IRSp53 in spiny excitatory and inhibitory neurons
- Author
-
Haram Park, Richard J. Weinberg, and Alain C. Burette
- Subjects
Dendritic spine ,Neocortex ,General Neuroscience ,Biology ,Medium spiny neuron ,Inhibitory postsynaptic potential ,medicine.anatomical_structure ,nervous system ,Postsynaptic potential ,Excitatory postsynaptic potential ,medicine ,Long-term depression ,Postsynaptic density ,Neuroscience - Abstract
The 53 kDa insulin receptor substrate protein (IRSp53) is highly enriched in the brain. Despite evidence that links mutations of IRSp53 with autism and other neuropsychiatric problems, the functional significance of this protein remains unclear. We here use light and electron microscopic immunohistochemistry to demonstrate that IRSp53 is expressed throughout the adult rat brain. Labeling concentrated selectively in dendritic spines, where it was associated with the postsynaptic density. Surprisingly, its organization within the PSD of spiny excitatory neurons of neocortex and hippocampus differed from that within spiny inhibitory neurons of neostriatum and cerebellar cortex. The present data support previous suggestions that IRSp53 is involved in postsynaptic signaling, while hinting that its signaling role may differ in different types of neurons.
- Published
- 2014
10. Sevoflurane Exposure during the Critical Period Affects Synaptic Transmission and Mitochondrial Respiration but Not Long-term Behavior in Mice
- Author
-
Jun Young Heo, Yangsik Kim, Gi Ryang Kweon, Won Hyung Lee, Youngkwon Ko, Soo-Min Lee, Yong Sup Shin, Sang Il Park, Min Jeong Ryu, Seunghwan Yoon, Woosuk Chung, Yoonhee Kim, Seok Hwa Yoon, Haram Park, and Xianshu Ju
- Subjects
Male ,Methyl Ethers ,Dendritic spine ,Period (gene) ,Mitochondrion ,Neurotransmission ,Biology ,Synaptic Transmission ,Sevoflurane ,03 medical and health sciences ,Mice ,0302 clinical medicine ,Sex Factors ,030202 anesthesiology ,Respiration ,medicine ,Long term behavior ,Animals ,Critical period ,Behavior, Animal ,Mitochondria ,Mice, Inbred C57BL ,Anesthesiology and Pain Medicine ,Anesthetics, Inhalation ,Female ,Neuroscience ,030217 neurology & neurosurgery ,medicine.drug - Abstract
Background Anesthesia during the synaptogenic period induces dendritic spine formation, which may affect neurodevelopment. The authors, therefore, evaluated whether changes in synaptic transmission after dendritic spine formation induced by sevoflurane were associated with long-term behavioral changes. The effects of sevoflurane on mitochondrial function were also assessed to further understand the mechanism behind spinogenesis. Methods Postnatal day 16 to 17 mice were exposed to sevoflurane (2.5% for 2 h), and synaptic transmission was measured in the medial prefrontal cortex 6 h or 5 days later. The expression of postsynaptic proteins and mitochondrial function were measured after anesthesia. Long-term behavioral changes were assessed in adult mice. Results Sevoflurane increased the expression of excitatory postsynaptic proteins in male and female mice (n = 3 to 5 per group). Sevoflurane exposure in male mice transiently increased miniature excitatory postsynaptic current frequency (control: 8.53 ± 2.87; sevoflurane: 11.09 ± 2.58) but decreased miniature inhibitory postsynaptic current frequency (control: 10.18 ± 4.66; sevoflurane: 6.88 ± 2.15). Unexpectedly, sevoflurane increased miniature inhibitory postsynaptic current frequency (control: 1.81 ± 1.11; sevoflurane: 3.56 ± 1.74) in female mice (neurons, n = 10 to 21 per group). Sevoflurane also increased mitochondrial respiration in male mice (n = 5 to 8 per group). However, such changes from anesthesia during the critical period did not induce long-term behavioral consequences. Values are presented as mean ± SD. Conclusions Sevoflurane exposure during the critical period induces mitochondrial hyperactivity and transient imbalance of excitatory/inhibitory synaptic transmission, without long-lasting behavioral consequences. Further studies are needed to confirm sexual differences and to define the role of mitochondrial activity during anesthesia-induced spine formation.
- Published
- 2016
11. Cell type-specific deletion of Shank3 exons 14–16 in mice differentially affects synaptic and behavioral phenotypes
- Author
-
Hee Jin Cho, Eunjoon Kim, Jiseok Lee, Esther Yang, Taesun Yoo, Hyun Uk Kim, Haram Park, Jin Yang Kim, and Ye-Eun Yoo
- Subjects
Genetics ,Behavioral phenotypes ,Exon ,General Neuroscience ,Cell type specific ,Biology - Published
- 2019
12. Social deficits in IRSp53 mutant mice improved by NMDAR and mGluR5 suppression
- Author
-
Sae Geun Park, Yeonsoo Choi, Eunee Lee, Yong Chul Bae, Dong Soo Lee, Min Whan Jung, Issac Rhim, Seung Joon Lee, Eunjoon Kim, Yi Sul Cho, Su Yeon Choi, Ryunhee Kim, Woosuk Chung, Jaeseung Kang, Myoung Hwan Kim, Hanwool Park, Jeonghoon Choi, Daesoo Kim, Haram Park, and Jong Won Lee
- Subjects
Male ,Receptor, Metabotropic Glutamate 5 ,Hippocampus ,Mice, Transgenic ,Nerve Tissue Proteins ,Receptors, N-Methyl-D-Aspartate ,Mice ,mental disorders ,medicine ,Animals ,Prefrontal cortex ,Cells, Cultured ,Neurons ,Metabotropic glutamate receptor 5 ,musculoskeletal, neural, and ocular physiology ,General Neuroscience ,Memantine ,Social Behavior Disorders ,Long-term potentiation ,Recognition, Psychology ,Feeding Behavior ,Grooming ,Mice, Inbred C57BL ,nervous system ,Animals, Newborn ,Gene Expression Regulation ,Case-Control Studies ,Synaptic plasticity ,Mutation ,Exploratory Behavior ,NMDA receptor ,Synaptic signaling ,Vocalization, Animal ,Psychology ,Neuroscience ,Excitatory Amino Acid Antagonists ,medicine.drug - Abstract
Social deficits are observed in diverse psychiatric disorders, including autism spectrum disorders and schizophrenia. We found that mice lacking the excitatory synaptic signaling scaffold IRSp53 (also known as BAIAP2) showed impaired social interaction and communication. Treatment of IRSp53(-/-) mice, which display enhanced NMDA receptor (NMDAR) function in the hippocampus, with memantine, an NMDAR antagonist, or MPEP, a metabotropic glutamate receptor 5 antagonist that indirectly inhibits NMDAR function, normalized social interaction. This social rescue was accompanied by normalization of NMDAR function and plasticity in the hippocampus and neuronal firing in the medial prefrontal cortex. These results, together with the reduced NMDAR function implicated in social impairments, suggest that deviation of NMDAR function in either direction leads to social deficits and that correcting the deviation has beneficial effects.
- Published
- 2014
13. Postsynaptic distribution of IRSp53 in spiny excitatory and inhibitory neurons
- Author
-
Alain C, Burette, Haram, Park, and Richard J, Weinberg
- Subjects
Male ,Neurons ,Dendritic Spines ,Brain ,Fluorescent Antibody Technique ,Post-Synaptic Density ,Nerve Tissue Proteins ,Immunohistochemistry ,Article ,Immunoenzyme Techniques ,Rats, Sprague-Dawley ,Microscopy, Electron ,nervous system ,Synapses ,Image Processing, Computer-Assisted ,Animals ,gamma-Aminobutyric Acid ,Adaptor Proteins, Signal Transducing - Abstract
The 53 kDa insulin receptor substrate protein (IRSp53) is highly enriched in the brain. Despite evidence that links mutations of IRSp53 with autism and other neuropsychiatric problems, the functional significance of this protein remains unclear. We used light and electron microscopic immunohistochemistry to demonstrate that IRSp53 is expressed throughout the adult rat brain. Labeling concentrated selectively in dendritic spines, where it was associated with the postsynaptic density (PSD). Surprisingly, its organization within the PSD of spiny excitatory neurons of neocortex and hippocampus differed from that within spiny inhibitory neurons of neostriatum and cerebellar cortex. The present data support previous suggestions that IRSp53 is involved in postsynaptic signaling, while hinting that its signaling role may differ in different types of neurons.
- Published
- 2013
14. Frontier battery development for hybrid vehicles
- Author
-
Heather Lewis, Maion Paolini, and Haram Park
- Subjects
Battery (electricity) ,Break-even (economics) ,Chemistry(all) ,Operations research ,Chemistry ,Research ,Social cost ,Yield (finance) ,Price premium ,General Chemistry ,Environmental economics ,Software deployment ,Greenhouse gas ,QD1-999 ,Externality - Abstract
Background Interest in hybrid-electric vehicles (HEVs) has recently spiked, partly due to an increasingly negative view toward the U.S. foreign oil dependency and environmental concerns. Though HEVs are becoming more common, they have a significant price premium over gasoline-powered vehicles. One of the primary drivers of this “hybrid premium” is the cost of the vehicles’ batteries. This paper focuses on these batteries used in hybrid vehicles, examines the types of batteries used for transportation applications and addresses some of the technological, environmental and political drivers in battery development and the deployment of HEVs. Methods This paper examines the claim, often voiced by HEV proponents, that by taking into account savings on gasoline and vehicle maintenance, hybrid cars are cheaper than traditional gasoline cars. This is done by a quantitative benefit-cost analysis, in addition to qualitative benefit-cost analysis from political, technological and environmental perspectives. Results The quantitative benefit-cost analysis shows that, taking account of all costs for the life of the vehicle, hybrid cars are in fact more expensive than gasoline-powered vehicles; however, after five years, HEVs will break even with gasoline cars. Conclusions Our results show that it is likely that after 5 years, using hybrid vehicles should be cheaper in effect and yield a positive net benefit to society. There are a number of externalities that could significantly impact the total social cost of the car. These externalities can be divided into four categories: environmental, industrial, R&D and political. Despite short-term implications and hurdles, increased HEV usage forecasts a generally favorable long-term net benefit to society. Most notably, increasing HEV usage could decrease greenhouse gas emissions, while also decreasing U.S. dependence on foreign oil.
- Published
- 2012
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.