702 results match your criteria Molecular Brain [Journal]


Assessment of mGluR5 KO mice under conditions of low stress using a rodent touchscreen apparatus reveals impaired behavioural flexibility driven by perseverative responses.

Mol Brain 2019 04 11;12(1):37. Epub 2019 Apr 11.

Department of Pharmacology, BK21 PLUS Project for Medical Science, Brain Research Institute, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seoul, 03722, Republic of Korea.

Genetic and pharmacological manipulations targeting metabotropic glutamate receptor 5 (mGluR5) affect performance in behavioural paradigms that depend on cognitive flexibility. Many of these studies involved exposing mice to highly stressful conditions including electric foot shocks or water immersion and forced swimming. Because mGluR5 is also implicated in resilience and stress responses, however, apparent impairments in inhibitory learning may have been an artifact of manipulation-induced changes in affective state. Read More

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http://dx.doi.org/10.1186/s13041-019-0441-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6458840PMC

Development of GABARAP family protein-sensitive LIR-based probes for neuronal autophagy.

Mol Brain 2019 04 8;12(1):33. Epub 2019 Apr 8.

Department of Biological Sciences and Biotechnology, College of Life Sciences and Nanotechnology, Hannam University, 461-6 Jeonmin-dong, Yuseong-gu, Daejeon, 34054, Republic of Korea.

Autophagy allows for lysosomal cellular degradation of cytosolic components. In particular, neuronal autophagy is essential for cellular homeostasis and neuronal survival and is tightly regulated by several autophagy-related (ATG) proteins in post-mitotic neurons. Among these ATG proteins, the LC3/GABARAP proteins are known to regulate autophagosome biogenesis/maturation and cargo recognition. Read More

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http://dx.doi.org/10.1186/s13041-019-0458-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6454701PMC

Identification of a molecular gating determinant within the carboxy terminal region of Ca3.3 T-type channels.

Mol Brain 2019 04 8;12(1):34. Epub 2019 Apr 8.

Institute of Organic Chemistry and Biochemistry, Czech Academy of Sciences, Flemingovo nam. 2, 16610, Prague, Czech Republic.

The physiological functions controlled by T-type channels are intrinsically dependent on their gating properties, and alteration of T-type channel activity is linked to several human disorders. Therefore, it is essential to develop a clear understanding of the structural determinants responsible for the unique gating features of T-type channels. Here, we have investigated the specific role of the carboxy terminal region by creating a series a deletion constructs expressed in tsA-201 cells and analyzing them by patch clamp electrophysiology. Read More

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http://dx.doi.org/10.1186/s13041-019-0457-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6454634PMC

Modulation of mTOR and CREB pathways following mGluR5 blockade contribute to improved Huntington's pathology in zQ175 mice.

Mol Brain 2019 04 8;12(1):35. Epub 2019 Apr 8.

University of Ottawa Brain and Mind Institute, University of Ottawa, 451 Smyth Road, Ottawa, Ontario, K1H 8M5, Canada.

Huntington's disease (HD) is a neurodegenerative disorder caused by a genetic abnormality in the huntingtin gene that leads to a polyglutamine repeat expansion of the huntingtin protein. The cleaved polyglutamine expansion of mutant huntingtin (mHTT) protein can form aggregates strongly correlated with HD progression. We have previously shown that the inhibition of mGluR5 using CTEP, a selective negative allosteric mGluR5 modulator, can delay disease progression and reduce in mHTT aggregates in the zQ175 mouse model of HD. Read More

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http://dx.doi.org/10.1186/s13041-019-0456-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6454676PMC

Anxiolytic effects of Formononetin in an inflammatory pain mouse model.

Mol Brain 2019 04 8;12(1):36. Epub 2019 Apr 8.

Department of Pharmacology, School of Pharmacy, and Precision Pharmacy & Drug Development Center, Department of Pharmacy, Tangdu Hospital, Fourth Military Medical University, Xi'an, 710032, China.

Chronic pain is commonly accompanied with anxiety disorder, which complicates treatment. In this study, we investigated the analgesic and anxiolytic effects of Formononetin (FMNT), an active component of traditional Chinese medicine red clover (Trifolium pratense L.) that is capable of protecting neurons from N-methyl-D-aspartate (NMDA)-evoked excitotoxic injury, on mice suffering from complete Freund's adjuvant (CFA)-induced chronic inflammatory pain. Read More

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http://dx.doi.org/10.1186/s13041-019-0453-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6454770PMC
April 2019
4.345 Impact Factor

Overexpression of activated CaMKII in the CA1 hippocampus impairs context discrimination, but not contextual conditioning.

Mol Brain 2019 04 5;12(1):32. Epub 2019 Apr 5.

School of Biological Sciences, Seoul National University, Gwanak-gu, Seoul, 08826, South Korea.

Calcium/Calmodulin-dependent protein kinase II (CaMKII) plays a key role in the molecular mechanism of memory formation. CaMKII is known to be activated specifically in the activated spines during memory formation. However, it is unclear whether the specific activation of CaMKII is necessary for encoding information. Read More

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https://molecularbrain.biomedcentral.com/articles/10.1186/s1
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http://dx.doi.org/10.1186/s13041-019-0454-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6449978PMC
April 2019
2 Reads

Effects of norepinephrine and β2 receptor antagonist ICI 118,551 on whisker hair follicle mechanoreceptors dissatisfy Merkel discs being adrenergic synapses.

Mol Brain 2019 04 3;12(1):31. Epub 2019 Apr 3.

Department of Anesthesiology and Perioperative Medicine, School of Medicine, University of Alabama at Birmingham, Birmingham, AL, 35294, USA.

Merkel discs, located in skin touch domes and whisker hair follicles, are tactile end organs essential for environmental exploration, social interaction, and tactile discrimination. Recent studies from our group and two others have shown that mechanical stimulation excites Merkel cells via Piezo2 channel activation to subsequently activate sensory neural pathways. We have further shown that mechanical stimulation leads to the release of 5-HT from Merkel cells to synaptically transmit tactile signals to whisker afferent nerves. Read More

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http://dx.doi.org/10.1186/s13041-019-0450-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6448341PMC

Differential sensitivity of three forms of hippocampal synaptic potentiation to depotentiation.

Mol Brain 2019 04 3;12(1):30. Epub 2019 Apr 3.

Department of Biological Sciences and Brain and Cognitive Sciences, College of Natural Sciences, Seoul National University, Seoul, 151-746, Korea.

Theta-burst stimulation (TBS) induces short-term potentiation (STP) plus two types of transcriptionally-independent forms of long-term potentiation (LTP), termed LTP1 and LTP2. We have compared the susceptibility of these three types of synaptic plasticity to depotentiation, induced by low frequency stimulation (LFS; 2 Hz for 10 min) at the Schaffer collateral-commissural pathway in area CA1 of adult rat hippocampal slices. In interleaved experiments, STP and LTP were induced by three episodes of either compressed or spaced TBS (cTBS or sTBS). Read More

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http://dx.doi.org/10.1186/s13041-019-0451-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6446328PMC
April 2019
2 Reads

Prenatal selective serotonin reuptake inhibitor (SSRI) exposure induces working memory and social recognition deficits by disrupting inhibitory synaptic networks in male mice.

Mol Brain 2019 04 1;12(1):29. Epub 2019 Apr 1.

Molecular Neurophysiology Laboratory, Signature Program in Neuroscience and Behavioral Disorders, Duke-National University of Singapore (NUS) Medical School, 8 College Road, Singapore, 169857, Singapore.

Selective serotonin reuptake inhibitors (SSRIs) are commonly prescribed antidepressant drugs in pregnant women. Infants born following prenatal exposure to SSRIs have a higher risk for behavioral abnormalities, however, the underlying mechanisms remains unknown. Therefore, we examined the effects of prenatal fluoxetine, the most commonly prescribed SSRI, in mice. Read More

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http://dx.doi.org/10.1186/s13041-019-0452-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6444596PMC
April 2019
2 Reads

Conditioned stimulus presentations alter anxiety level in fear-conditioned mice.

Mol Brain 2019 03 29;12(1):28. Epub 2019 Mar 29.

State key laboratory of chemical oncogenomics, School of Chemical Biology and Biotechnology, Peking University Shenzhen Graduate School, Shenzhen, China.

It is generally believed that fear is rapidly triggered by a distinct cue while anxiety onset is less precise and not associated with a distinct cue. Although it has been claimed that both processes can be measured with certain independence of each other, it is unclear how exactly they differ. In this study, we measured anxiety in mice that received discriminative fear conditioning using behavioral, heart rate and calcium (Ca) responses in the ventral hippocampal CA1 (vCA1) neurons. Read More

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http://dx.doi.org/10.1186/s13041-019-0445-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6441152PMC
March 2019
1 Read

Region- and time-dependent gene regulation in the amygdala and anterior cingulate cortex of a PTSD-like mouse model.

Mol Brain 2019 03 28;12(1):25. Epub 2019 Mar 28.

Department of Anatomy, Physiology and Genetics, Uniformed Services University of Health Sciences, 4301 Jones Bridge Rd, Bethesda, MD, 20814, USA.

Posttraumatic stress disorder is developed by exposure to a threatening and/or a horrifying event and characterized by the presence of anxiety, hyperarousal, avoidance, and sleep abnormality for a prolonged period of time. To elucidate the potential molecular mechanisms, we constructed a mouse model by electric foot shock followed by situational reminders and performed transcriptome analysis in brain tissues. The stressed mice acquired anxiety-like behavior after 2 weeks and exaggerated startle response after 4 weeks. Read More

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http://dx.doi.org/10.1186/s13041-019-0449-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6438009PMC
March 2019
1 Read

Blood-based molecular biomarkers for Alzheimer's disease.

Mol Brain 2019 03 28;12(1):26. Epub 2019 Mar 28.

CSIRO Health and Biosecurity, Parkville, Victoria, 3052, Australia.

A major barrier to the effective conduct of clinical trials of new drug candidates against Alzheimer's disease (AD) and to identifying patients for receiving future disease-modifying treatments is the limited capacity of the current health system to find and diagnose patients with early AD pathology. This may be related in part to the limited capacity of the current health systems to select those people likely to have AD pathology in order to confirm the diagnosis with available cerebrospinal fluid and imaging biomarkers at memory clinics. In the current narrative review, we summarize the literature on candidate blood tests for AD that could be implemented in primary care settings and used for the effective identification of individuals at increased risk of AD pathology, who could be referred for potential inclusion in clinical trials or future approved treatments following additional testing. Read More

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http://dx.doi.org/10.1186/s13041-019-0448-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6437931PMC
March 2019
2 Reads

The secreted APP ectodomain sAPPα, but not sAPPβ, protects neurons against Aβ oligomer-induced dendritic spine loss and increased tau phosphorylation.

Mol Brain 2019 03 29;12(1):27. Epub 2019 Mar 29.

Institute for Regenerative Medicine, University of Zurich, Schlieren, Switzerland.

Aim: The amyloid precursor protein (APP) is endoproteolytically processed to generate either the neurotoxic beta-amyloid peptide (Aβ) or the secreted ectodomain APP alpha (sAPPα). While neurotrophic properties of sAPPα were suggested in several studies, it is still unclear if and how sAPPα counteracts pathogenic effects of Aβ. Direct comparisons with sAPPβ, produced in the Aβ-generating pathway, are missing in order to determine the role of sAPPα's carbonyl-terminal end in its possible neuroprotective activity. Read More

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http://dx.doi.org/10.1186/s13041-019-0447-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6440141PMC

ZnT3 expression levels are down-regulated in the brain of Mcoln1 knockout mice.

Mol Brain 2019 03 26;12(1):24. Epub 2019 Mar 26.

Department of Biological Science, California State University Fullerton, 800 N. State College Blvd., Fullerton, CA, 92831, USA.

Aim: Zinc is a critical divalent cation in mammalian brain, but its concentration must be strictly-controlled. Within certain subsets of glutamatergic neurons, ZnT3 (encoded by the Slc30a3 gene) facilitates the transport and storage of zinc in synaptic vesicles. It has been previously reported that Slc30a3 mRNA levels are perturbed in numerous neurodegenerative disorders. Read More

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http://dx.doi.org/10.1186/s13041-019-0446-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6434829PMC
March 2019
1 Read

Roles for osteocalcin in brain signalling: implications in cognition- and motor-related disorders.

Mol Brain 2019 03 25;12(1):23. Epub 2019 Mar 25.

Department of Endocrine and Metabolic Diseases, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Rui-jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Institute of Endocrine and Metabolic Diseases, Shanghai, China.

It is now generally accepted that the extra-skeleton functionalities of bone are multifaceted. Its endocrine functions came first to light when it was realized that osteoblasts, the bone forming cells, maintain energy homeostasis by improving glucose metabolism, insulin sensitivity and energy expenditure through osteocalcin, a multipurpose osteokine secreted by osteoblasts. Recently, the emerging knowledge on the functional aspects of this osteokine expanded to properties including adult and maternal regulation of cognitive functions. Read More

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http://dx.doi.org/10.1186/s13041-019-0444-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6434857PMC
March 2019
1 Read

Structural plasticity of the hippocampus in response to estrogens in female rodents.

Mol Brain 2019 03 18;12(1):22. Epub 2019 Mar 18.

Department of Psychology, Graduate Program in Neuroscience, Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, BC, V6T 1Z3, Canada.

It is well established that estrogens affect neuroplasticity in a number of brain regions. In particular, estrogens modulate and mediate spine and synapse formation as well as neurogenesis in the hippocampal formation. In this review, we discuss current research exploring the effects of estrogens on dendritic spine plasticity and neurogenesis with a focus on the modulating factors of sex, age, and pregnancy. Read More

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http://dx.doi.org/10.1186/s13041-019-0442-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6423800PMC

Prior observation of fear learning enhances subsequent self-experienced fear learning with an overlapping neuronal ensemble in the dorsal hippocampus.

Mol Brain 2019 03 14;12(1):21. Epub 2019 Mar 14.

Laboratory of Chemical Pharmacology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, 113-0033, Japan.

Information from direct experience and observation of others is integrated in the brain to enable appropriate responses to environmental stimuli. Fear memory can be acquired by observing a conspecific's distress. However, it remains unclear how prior fear observation affects self-experienced fear learning. Read More

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http://dx.doi.org/10.1186/s13041-019-0443-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6419346PMC

LAMP5 in presynaptic inhibitory terminals in the hindbrain and spinal cord: a role in startle response and auditory processing.

Mol Brain 2019 03 12;12(1):20. Epub 2019 Mar 12.

Department of Applied Biological Sciences, Tokyo University of Science, Chiba, 278-8510, Japan.

Lysosome-associated membrane protein 5 (LAMP5) is a mammalian ortholog of the Caenorhabditis elegans protein, UNC-46, which functions as a sorting factor to localize the vesicular GABA transporter UNC-47 to synaptic vesicles. In the mouse forebrain, LAMP5 is expressed in a subpopulation of GABAergic neurons in the olfactory bulb and the striato-nigral system, where it is required for fine-tuning of GABAergic synaptic transmission. Here we focus on the prominent expression of LAMP5 in the brainstem and spinal cord and suggest a role for LAMP5 in these brain regions. Read More

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http://dx.doi.org/10.1186/s13041-019-0437-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6416879PMC

Sacs R272C missense homozygous mice develop an ataxia phenotype.

Mol Brain 2019 03 12;12(1):19. Epub 2019 Mar 12.

Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, Room 622, 3801, University Street, Montreal, Québec, H3A 2B4, Canada.

Autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSACS [MIM 270550]) is an early-onset neurodegenerative disorder caused by mutations in the SACS gene. Over 200 SACS mutations have been identified. Most mutations lead to a complete loss of a sacsin, a large 520 kD protein, although some missense mutations are associated with low levels of sacsin expression. Read More

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http://dx.doi.org/10.1186/s13041-019-0438-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6416858PMC
March 2019
1 Read

Lysosomal dysfunction in proteinopathic neurodegenerative disorders: possible therapeutic roles of cAMP and zinc.

Mol Brain 2019 03 12;12(1):18. Epub 2019 Mar 12.

Asan Institute for Life Sciences, Asan Medical Center, Seoul, South Korea.

A number of neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis, share intra- and/or extracellular deposition of protein aggregates as a common core pathology. While the species of accumulating proteins are distinct in each disease, an increasing body of evidence indicates that defects in the protein clearance system play a crucial role in the gradual accumulation of protein aggregates. Among protein degradation systems, the endosome-autophagosome-lysosome pathway (EALP) is the main degradation machinery, especially for large protein aggregates. Read More

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http://dx.doi.org/10.1186/s13041-019-0439-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6417073PMC
March 2019
1 Read

Proteomics of the corpus callosum to identify novel factors involved in hypomyelinated Niemann-Pick Type C disease mice.

Mol Brain 2019 03 11;12(1):17. Epub 2019 Mar 11.

Albrecht-Kossel-Institute for Neuroregeneration, University Medical Center Rostock, Gehlsheimer Strasse 20, 18147, Rostock, Germany.

Hypomyelination in the central nerves system (CNS) is one of the most obviously pathological features in Niemann-Pick Type C disease (NPC), which is a rare neurodegenerative disorder caused by mutations in the NPC intracellular cholesterol transporter 1 or 2 (Npc1 or Npc2). Npc1 plays key roles in both neurons and oligodendrocytes during myelination, however, the linkage between the disturbed cholesterol transport and inhibited myelination is unrevealed. In this study, mass spectrometry (MS)-based differential quantitative proteomics was applied to compare protein composition in the corpus callosum between wild type (WT) and NPC mice. Read More

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http://dx.doi.org/10.1186/s13041-019-0440-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6417209PMC

Gene expression meta-analysis of Parkinson's disease and its relationship with Alzheimer's disease.

Mol Brain 2019 02 28;12(1):16. Epub 2019 Feb 28.

Faculty of Medicine and Dentistry, Plymouth University, Plymouth, PL6 8BU, UK.

Parkinson's disease (PD) and Alzheimer's disease (AD) are the most common neurodegenerative diseases and have been suggested to share common pathological and physiological links. Understanding the cross-talk between them could reveal potentials for the development of new strategies for early diagnosis and therapeutic intervention thus improving the quality of life of those affected. Here we have conducted a novel meta-analysis to identify differentially expressed genes (DEGs) in PD microarray datasets comprising 69 PD and 57 control brain samples which is the biggest cohort for such studies to date. Read More

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http://dx.doi.org/10.1186/s13041-019-0436-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6396547PMC
February 2019
5 Reads

Neuronal scaffolding protein spinophilin is integral for cocaine-induced behavioral sensitization and ERK1/2 activation.

Mol Brain 2019 02 25;12(1):15. Epub 2019 Feb 25.

Department of Cellular and Molecular Medicine and University of Ottawa Brain and Mind Institute, University of Ottawa, 451 Smyth Road, Ottawa, ON, K1H 8M5, Canada.

Spinophilin is a scaffolding protein enriched in dendritic spines with integral roles in the regulation of spine density and morphology, and the modulation of synaptic plasticity. The ability of spinophilin to alter synaptic strength appears to involve its scaffolding of key synaptic proteins, including the important structural element F-actin, AMPA/NMDA modulator protein phosphatase 1, and neuromodulatory G-protein coupled receptors, including dopamine receptor D2 and metabotropic glutamate receptor 5. Additionally, spinophilin is highly expressed in the striatum, a brain region that is fundamentally involved in reward-processing and locomotor activity which receives both glutamatergic and dopaminergic inputs. Read More

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http://dx.doi.org/10.1186/s13041-019-0434-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6388481PMC
February 2019
1 Read

DA-JC1 improves learning and memory by antagonizing Aβ31-35-induced circadian rhythm disorder.

Mol Brain 2019 02 11;12(1):14. Epub 2019 Feb 11.

Department of Pathology, Shanxi Medical University, Taiyuan, People's Republic of China.

Studies have shown that a normal circadian rhythm is crucial to learning and memory. Circadian rhythm disturbances that occur at early stages of Alzheimer's disease (AD) aggravate the progression of the disease and further reduce learning and memory in AD patients. The novel, dual GLP-1R/GIPR agonist DA-JC1 has been found to exert a stronger hypoglycemic effect than a GLP-1R agonist alone and has been shown to exert neuroprotective effects. Read More

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http://dx.doi.org/10.1186/s13041-019-0432-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6371467PMC
February 2019
1 Read
4.345 Impact Factor

Determination of circuit-specific morphological adaptations in ventral tegmental area dopamine neurons by chronic morphine.

Mol Brain 2019 02 8;12(1):10. Epub 2019 Feb 8.

Neuroscience Program and Department of Physiology, Michigan State University, 567 Wilson Road, BPS 3182, East Lansing, MI, 48824, USA.

Chronic opiate exposure induces neuroadaptations in the mesocorticolimbic system including ventral tegmental area (VTA) dopamine (DA) neurons, whose soma size is decreased following opiate exposure. Yet it is now well documented that VTA DA neurons are heterogeneous, with notable differences between VTA DA neurons based on their projection target. Therefore, we sought to determine whether chronic morphine induced similar changes in the morphology of VTA DA neurons that project to the nucleus accumbens (NAc) and prefrontal cortex (PFC). Read More

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http://dx.doi.org/10.1186/s13041-019-0435-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6368752PMC
February 2019
1 Read

Cav3.2 calcium channel interactions with the epithelial sodium channel ENaC.

Mol Brain 2019 02 8;12(1):12. Epub 2019 Feb 8.

Molecular Neuroscience, Department of Physiology and Pharmacology, Hotchkiss Brain Institute and Alberta Children's Hospital Research Institute, Cumming School of Medicine, University of Calgary, 3330 Hospital Dr. NW, Calgary, T2N 4N1, Canada.

This study describes the functional interaction between Cav3.2 calcium channels and the Epithelial Sodium Channel (ENaC). β-ENaC subunits showed overlapping expression with endogenous Cav3. Read More

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https://molecularbrain.biomedcentral.com/articles/10.1186/s1
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http://dx.doi.org/10.1186/s13041-019-0433-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6368719PMC
February 2019
17 Reads

Baicalin regulates the dopamine system to control the core symptoms of ADHD.

Mol Brain 2019 02 8;12(1):11. Epub 2019 Feb 8.

Nanjing University of Chinese Medicine, Xianlin road no.138, Qixia District, Nanjing City, Jiangsu Province, 210023, China.

We aimed to test the therapeutic effects of baicalin on attention deficit hyperactivity disorder (ADHD) in an animal model and to explain the potential mechanism. We investigated the therapeutic effects and mechanisms of baicalin in a spontaneously hypertensive rat (SHR) model of ADHD depending on the dopamine (DA) deficit theory. In this study, fifty SHRs were randomly divided into five groups: methylphenidate (MPH), baicalin (50 mg/kg, 100 mg/kg, or 150 mg/kg), and saline-treated. Read More

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http://dx.doi.org/10.1186/s13041-019-0428-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6368814PMC
February 2019
2 Reads

Motor skills mediated through cerebellothalamic tracts projecting to the central lateral nucleus.

Mol Brain 2019 02 8;12(1):13. Epub 2019 Feb 8.

Department of Molecular Genetics, Institute of Biomedical Sciences, Fukushima Medical University, Fukushima, 960-1295, Japan.

The cerebellum regulates complex animal behaviors, such as motor control and spatial recognition, through communication with many other brain regions. The major targets of the cerebellar projections are the thalamic regions including the ventroanterior nucleus (VA) and ventrolateral nucleus (VL). Another thalamic target is the central lateral nucleus (CL), which receives the innervations mainly from the dentate nucleus (DN) in the cerebellum. Read More

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http://dx.doi.org/10.1186/s13041-019-0431-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6368787PMC
February 2019
1 Read

Correction to: The effect of Neuroligin-2 absence on sleep architecture and electroencephalographic activity in mice.

Mol Brain 2019 01 30;12(1). Epub 2019 Jan 30.

Research Center and Center for Advanced Research in Sleep Medicine, Hôpital du Sacré-Cœur de Montréal (CIUSSS-NIM), 5400 Gouin West blvd, Montréal, QC H4J 1C5, Canada.

Correction to: Molecular Brain (2018) 11:52 https://doi.org/10.1186/s13041-018-0394-3Following publication of the original article [1], the authors reported that the article was mistakenly submitted with the omission of two authors: Feng Cao and Zhengping Jia. Read More

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http://dx.doi.org/10.1186/s13041-019-0425-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6352436PMC
January 2019

Genetic risk variants for brain disorders are enriched in cortical H3K27ac domains.

Mol Brain 2019 01 28;12(1). Epub 2019 Jan 28.

University of Exeter Medical School, RILD Building, Royal Devon & Exeter Hospital, University of Exeter, Barrack Rd, Exeter, EX2 5DW, UK.

Most variants associated with complex phenotypes in genome-wide association studies (GWAS) do not directly index coding changes affecting protein structure. Instead they are hypothesized to influence gene regulation, with common variants associated with disease being enriched in regulatory domains including enhancers and regions of open chromatin. There is interest, therefore, in using epigenomic annotation data to identify the specific regulatory mechanisms involved and prioritize risk variants. Read More

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https://molecularbrain.biomedcentral.com/articles/10.1186/s1
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http://dx.doi.org/10.1186/s13041-019-0429-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6348673PMC
January 2019
7 Reads

Quantitative profiling brain proteomes revealed mitochondrial dysfunction in Alzheimer's disease.

Mol Brain 2019 01 28;12(1). Epub 2019 Jan 28.

School of Biological Sciences, Division of Structural Biology and Biochemistry, Nanyang Technological University, 60 Nanyang Drive, Singapore, 637551, Singapore.

Mitochondrial dysfunction is a key feature in both aging and neurodegenerative diseases including Alzheimer's disease (AD), but the molecular signature that distinguishes pathological changes in the AD from healthy aging in the brain mitochondria remain poorly understood. In order to unveil AD specific mitochondrial dysfunctions, this study adopted a discovery-driven approach with isobaric tag for relative and absolute quantitation (iTRAQ) and label-free quantitative proteomics, and profiled the mitochondrial proteomes in human brain tissues of healthy and AD individuals. LC-MS/MS-based iTRAQ quantitative proteomics approach revealed differentially altered mitochondriomes that distinguished the AD's pathophysiology-induced from aging-associated changes. Read More

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http://dx.doi.org/10.1186/s13041-019-0430-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6350377PMC
January 2019
2 Reads

Hyperexcitability of the local cortical circuit in mouse models of tuberous sclerosis complex.

Mol Brain 2019 01 25;12(1). Epub 2019 Jan 25.

Department of Anatomy & Cell Biology, University of Illinois at Chicago, Chicago, IL, USA.

Tuberous sclerosis complex (TSC) is a neurogenetic disorder associated with epilepsy, intellectual disabilities, and autistic behaviors. These neurological symptoms result from synaptic dysregulations, which shift a balance between excitation and inhibition. To decipher the synaptic substrate of hyperexcitability, we examined pan-neuronal Tsc1 knockout mouse and found a reduction in surface expression of a GABA receptor (GABAR) subunit but not AMPA receptor (AMPAR) subunit. Read More

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http://dx.doi.org/10.1186/s13041-019-0427-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6347813PMC
January 2019
1 Read

Reduced expression of somatostatin in GABAergic interneurons derived from induced pluripotent stem cells of patients with parkin mutations.

Mol Brain 2019 01 18;12(1). Epub 2019 Jan 18.

Department of Pharmacology, Hoshi University School of Pharmacy and Pharmaceutical Sciences, Ebara, Shinagawa-ku, Tokyo, 142-8501, Japan.

Parkinson's disease (PD) is associated with both motor and non-motor symptoms, including constipation, sensory neuropathy, depression, dementia and sleep disorder. Somatostatin (SST) is considered to be a modulator of GABAergic inhibitory transmission, and its levels are reduced in cerebrospinal fluid of PD patients. In the present study, we evaluated the changes in the expression of SST in GABAergic neurons derived from induced pluripotent stem cells (iPSCs) of PD patients. Read More

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https://molecularbrain.biomedcentral.com/articles/10.1186/s1
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http://dx.doi.org/10.1186/s13041-019-0426-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6339354PMC
January 2019
8 Reads

Pathological changes of distal motor neurons after complete spinal cord injury.

Mol Brain 2019 01 9;12(1). Epub 2019 Jan 9.

Department of Orthopaedic Surgery, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.

Traumatic spinal cord injury (SCI) causes serious disruption of neuronal circuits that leads to motor functional deficits. Regeneration of disrupted circuits back to their original target is necessary for the restoration of function after SCI, but the pathophysiological condition of the caudal spinal cord has not been sufficiently studied. Here we investigated the histological and biological changes in the distal part of the injured spinal cord, using a mice model of complete thoracic SCI in the chronic stage (3 months after injury). Read More

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http://dx.doi.org/10.1186/s13041-018-0422-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6327522PMC
January 2019
1 Read

Artificial association of memory events by optogenetic stimulation of hippocampal CA3 cell ensembles.

Mol Brain 2019 01 8;12(1). Epub 2019 Jan 8.

Department of Biochemistry, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama, 930-0194, Japan.

Previous gain-of-function studies using an optogenetic technique showed that manipulation of the hippocampal dentate gyrus or CA1 cell ensembles is important for memory reactivation and to generate synthetic or false memory. However, gain-of-function study manipulating CA3 cell ensembles has not been reported. The CA3 area of the hippocampus comprises a recurrent excitatory circuit, which is thought to be important for the generation of associations among the stored information within one brain region. Read More

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https://molecularbrain.biomedcentral.com/articles/10.1186/s1
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http://dx.doi.org/10.1186/s13041-018-0424-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6323779PMC
January 2019
3 Reads

Effects of rapamycin on social interaction deficits and gene expression in mice exposed to valproic acid in utero.

Mol Brain 2019 01 8;12(1). Epub 2019 Jan 8.

Addictive Substance Project, Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Setagaya-ku, Tokyo, Japan.

The mammalian target of rapamycin (mTOR) signaling pathway plays a crucial role in cell metabolism, growth, and proliferation. The overactivation of mTOR has been implicated in the pathogenesis of syndromic autism spectrum disorder (ASD), such as tuberous sclerosis complex (TSC). Treatment with the mTOR inhibitor rapamycin improved social interaction deficits in mouse models of TSC. Read More

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http://dx.doi.org/10.1186/s13041-018-0423-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6325753PMC
January 2019
2 Reads

The peacefulness gene promotes aggression in Drosophila.

Mol Brain 2019 01 3;12(1). Epub 2019 Jan 3.

Department of Neurology and Neurosurgery, McGill Centre for Research in Neuroscience, 1650 Cedar Avenue, Montreal, Quebec, H3G 1A4, Canada.

Natural aggressiveness is commonly observed in all animal species, and is displayed frequently when animals compete for food, territory and mating. Aggression is an innate behaviour, and is influenced by both environmental and genetic factors. However, the genetics of aggression remains largely unclear. Read More

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http://dx.doi.org/10.1186/s13041-018-0417-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6318936PMC
January 2019
2 Reads

What does LTP tell us about the roles of CaMKII and PKMζ in memory?

Mol Brain 2018 12 28;11(1):77. Epub 2018 Dec 28.

Department of Physiology and Pharmacology, The Robert F. Furchgott Center for Neural and Behavioral Science, State University of New York Downstate Medical Center, Brooklyn, NY, 11203, USA.

In "Criteria for identifying the molecular basis of the engram (CaMKII, PKMζ)," Lisman proposes that elucidating the mechanism of LTP maintenance is key to understanding memory storage. He suggests three criteria for a maintenance mechanism to evaluate data on CaMKII and PKMζ as memory storage molecules: necessity, occlusion, and erasure. Here we show that when the criteria are tested, the results reveal important differences between the molecules. Read More

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http://dx.doi.org/10.1186/s13041-018-0420-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6309091PMC
December 2018
1 Read

In memoriam: John Lisman - commentaries on CaMKII as a memory molecule.

Mol Brain 2018 12 28;11(1):76. Epub 2018 Dec 28.

Department of Biological Sciences, Seoul National University, Gwanak-gu, Seoul, Republic of Korea.

Shortly before he died in October 2017, John Lisman submitted an invited review to Molecular Brain on 'Criteria for identifying the molecular basis of the engram (CaMKII, PKMζ)'. John had no opportunity to read the referees' comments, and as a mark of the regard in which he was held by the neuroscience community the Editors decided to publish his review as submitted. This obituary takes the form of a series of commentaries on Lisman's review. Read More

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https://molecularbrain.biomedcentral.com/articles/10.1186/s1
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http://dx.doi.org/10.1186/s13041-018-0419-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6309094PMC
December 2018
16 Reads

EriB targeted inhibition of microglia activity attenuates MPP induced DA neuron injury through the NF-κB signaling pathway.

Mol Brain 2018 12 18;11(1):75. Epub 2018 Dec 18.

Department of Neurology and Institute of Neurology, Ruijin Hospital affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.

Accumulating evidence indicates that microglia activation is associated with an increased risk for developing Parkinson's disease (PD). With the progressive and selective degeneration of dopaminergic (DA) neurons, proinflammatory cytokines are elevated in the substantia nigra (SN) of PD patients. Thus, anti-inflammation has become one of the therapeutic strategies of PD. Read More

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http://dx.doi.org/10.1186/s13041-018-0418-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6299497PMC
December 2018
4.345 Impact Factor

Hyperpolarized [1-13C] pyruvate MR spectroscopy detect altered glycolysis in the brain of a cognitively impaired mouse model fed high-fat diet.

Mol Brain 2018 12 18;11(1):74. Epub 2018 Dec 18.

Department of Anatomy, BK21 Project for Medical Science and Research Institute of Radiological Science, Yonsei University College of Medicine, 50-1 Yonsei-ro, Seodaemun-gu, Seoul, 03722, Republic of Korea.

Higher dietary intakes of saturated fatty acid increase the risk of developing Alzheimer's disease and dementia, and even in people without diabetes higher glucose levels may be a risk factor for dementia. The mechanisms causing neuronal dysfunction and dementia by consuming high-fat diet degrading the integrity of the blood-brain barrier (BBB) has been suggested but are not yet fully understood, and metabolic state of the brain by this type of insult is still veiled. The objective of this study was to investigate the effect of high-fat diet on the brain metabolism by a multimodal imaging method using the hyperpolarizedcarbon 13 (C)-pyruvate magnetic resonance (MR) spectroscopy and dynamic contrast-enhanced MR imaging in conjunction with the biochemical assay and the behavior test in a mouse model fed high-fat diet (HFD). Read More

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http://dx.doi.org/10.1186/s13041-018-0415-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6299662PMC
December 2018

Systemic functional enrichment and ceRNA network identification following peripheral nerve injury.

Mol Brain 2018 12 17;11(1):73. Epub 2018 Dec 17.

Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-innovation Center of Neuroregeneration, Nantong University, 19 Qixiu Road, Nantong, Jiangsu Province, People's Republic of China, 226001.

Peripheral nerve injury is a worldwide clinical issue that impacts patients' quality of life and causes huge society and economic burden. Injured peripheral nerves are able to regenerate by themselves. However, for severe peripheral nerve injury, the regenerative abilities are very limited and the regenerative effects are very poor. Read More

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http://dx.doi.org/10.1186/s13041-018-0421-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6297964PMC
December 2018

Dual roles of anterior cingulate cortex neurons in pain and pleasure in adult mice.

Mol Brain 2018 12 4;11(1):72. Epub 2018 Dec 4.

Center for Neuron and Disease, Frontier Institute of Science and Technology, Xi'an Jiaotong University, Xi'an, 710049, China.

Human and animal studies indicate that some brain regions are activated during painful and pleasant situations, such as the anterior cingulate cortex (ACC). In the present study, we wanted to determine if some of the same neurons in the ACC may be activated by both pain and pleasure. We labeled neurons activated by two stimuli by using two immediate early genes (IEGs), Arc and Homer1a, and detected the intranuclear transcription of the IEG mRNA in situ. Read More

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https://molecularbrain.biomedcentral.com/articles/10.1186/s1
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http://dx.doi.org/10.1186/s13041-018-0416-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6280384PMC
December 2018
2 Reads

Transcriptome analysis of Shank3-overexpressing mice reveals unique molecular changes in the hypothalamus.

Mol Brain 2018 11 27;11(1):71. Epub 2018 Nov 27.

Department of Neuroscience, College of Medicine, Korea University, 73, Inchon-ro, Seongbuk-gu, Seoul, 02841, South Korea.

Various mutations in the SH3 and multiple ankyrin repeat domains 3 (SHANK3) gene are associated with neurodevelopmental and neuropsychiatric disorders. Thus far, synaptic abnormalities in multiple brain regions, including the hippocampus, prefrontal cortex, striatum, and ventral tegmental area, have been investigated in several lines of Shank3 mutant mice. However, although some reports have shown loss and gain of body weight in Shank3 knock-out and overexpressing transgenic (TG) mice, respectively, the potential functions of Shank3 in the hypothalamus, a brain region critically involved in energy intake and expenditure, are unknown. Read More

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http://dx.doi.org/10.1186/s13041-018-0413-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6257967PMC
November 2018

Accelerated FRET-PAINT microscopy.

Mol Brain 2018 11 22;11(1):70. Epub 2018 Nov 22.

Department of Physics and Astronomy, Seoul National University, Seoul, 08826, Republic of Korea.

Recent development of FRET-PAINT microscopy significantly improved the imaging speed of DNA-PAINT, the previously reported super-resolution fluorescence microscopy with no photobleaching problem. Here we try to achieve the ultimate speed limit of FRET-PAINT by optimizing the camera speed, dissociation rate of DNA probes, and bleed-through of the donor signal to the acceptor channel, and further increase the imaging speed of FRET-PAINT by 8-fold. Super-resolution imaging of COS-7 microtubules shows that high-quality 40-nm resolution images can be obtained in just tens of seconds. Read More

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http://dx.doi.org/10.1186/s13041-018-0414-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6249777PMC
November 2018
9 Reads

Digestion of the glycosaminoglycan extracellular matrix by chondroitinase ABC supports retinal ganglion cell dendritic preservation in a rodent model of experimental glaucoma.

Mol Brain 2018 11 21;11(1):69. Epub 2018 Nov 21.

School of Optometry and Vision Sciences, Cardiff University, Cardiff, Wales, CF24 4HQ, UK.

Retinal ganglion cell dendritic atrophy is an early feature of glaucoma, and the recovery of retinal ganglion cell dendrites is a viable option for vision improvement in glaucoma. Retinal ganglion cell neurites are surrounded by a specialised glycosaminoglycan extracellular matrix which inhibits dendritic plasticity. Since digestion of the extracellular matrix by chondroitinase ABC has been reported to have neuro-regenerative and neuro-plastic effects within the central nervous system, we explored its potential for dendritic recovery in a rat model of ocular hypertension. Read More

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http://dx.doi.org/10.1186/s13041-018-0412-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6249825PMC
November 2018
19 Reads

proBDNF is modified by advanced glycation end products in Alzheimer's disease and causes neuronal apoptosis by inducing p75 neurotrophin receptor processing.

Mol Brain 2018 11 14;11(1):68. Epub 2018 Nov 14.

Serra Húnter fellow, Associate Professor, Generalitat de Catalunya, Barcelona, Spain.

Alzheimer disease (AD) is a complex pathology related to multiple causes including oxidative stress. Brain-derived neurotrophic factor (BDNF) is a neutrotrophic factor essential for the survival and differentiation of neurons and is considered a key target in the pathophysiology of various neurodegenerative diseases, as for example AD. Contrarily to BDNF, the precursor form of BDNF (proBDNF) induces apoptosis through the specific interaction with p75 and its co-receptor, Sortilin. Read More

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http://dx.doi.org/10.1186/s13041-018-0411-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6237019PMC
November 2018
1 Read

Enhancement of dendritic persistent Na currents by mGluR5 leads to an advancement of spike timing with an increase in temporal precision.

Mol Brain 2018 11 9;11(1):67. Epub 2018 Nov 9.

Department of Physiology, Seoul National University College of Medicine, 103 Daehak-ro, Jongno-gu, Seoul, 03080, Republic of Korea.

Timing and temporal precision of action potential generation are thought to be important for encoding of information in the brain. The ability of single neurons to transform their input into output action potential is primarily determined by intrinsic excitability. Particularly, plastic changes in intrinsic excitability represent the cellular substrate for spatial memory formation in CA1 pyramidal neurons (CA1-PNs). Read More

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http://dx.doi.org/10.1186/s13041-018-0410-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6230299PMC
November 2018

Development of a peptide targeting dopamine transporter to improve ADHD-like deficits.

Mol Brain 2018 11 9;11(1):66. Epub 2018 Nov 9.

Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Toronto, ON, M5T 1R8, Canada.

Attention-deficit hyperactivity disorder (ADHD) is a neurocognitive disorder characterized by hyperactivity, inattention, working memory deficits and impulsivity. Its worldwide prevalence is estimated to be 3-5% in children and adolescents. The mainstay treatment for ADHD is stimulant medications (e. Read More

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https://molecularbrain.biomedcentral.com/articles/10.1186/s1
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http://dx.doi.org/10.1186/s13041-018-0409-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6234781PMC
November 2018
18 Reads
4.345 Impact Factor

Exposure to mild blast forces induces neuropathological effects, neurophysiological deficits and biochemical changes.

Mol Brain 2018 11 9;11(1):64. Epub 2018 Nov 9.

Departments of Surgery, Neurobiology, and Neurology, The University of Alabama at Birmingham Medical Center, 1720 2nd Ave S, THT 1052, Birmingham, AL, 35294, USA.

Direct or indirect exposure to an explosion can induce traumatic brain injury (TBI) of various severity levels. Primary TBI from blast exposure is commonly characterized by internal injuries, such as vascular damage, neuronal injury, and contusion, without external injuries. Current animal models of blast-induced TBI (bTBI) have helped to understand the deleterious effects of moderate to severe blast forces. Read More

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https://molecularbrain.biomedcentral.com/articles/10.1186/s1
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http://dx.doi.org/10.1186/s13041-018-0408-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6225689PMC
November 2018
7 Reads