Gavin S Dawe

National University Health System, Singapore

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Publications (71)283.66 Total impact

  • Lilia L. Kuleshova · Feng Wen · Yingnan Wu · Sok Siam Gouk · Gavin Stewart Dawe · Eng Hin Lee

    No preview · Article · Dec 2015 · Cryobiology
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    ABSTRACT: Rationale The G-protein-coupled relaxin family receptors RXFP1 and RXFP3 are widely expressed in the cortex and are involved in stress responses and memory and emotional processing. However, the identification of these receptors in human cortex and their status in Alzheimer’s disease (AD), which is characterized by both cognitive impairments and neuropsychiatric behaviours, have not been reported. Objectives In this study, we characterized RXFP receptors for immunoblotting and measured RXFP1 and RXFP3 immunoreactivities in the postmortem neocortex of AD patients longitudinally assessed for depressive symptoms. Methods RXFP1 and RXFP3 antibodies were characterized by immunoblotting with lysates from transfected HEK cells and preadsorption with RXFP3 peptides. Also, postmortem neocortical tissues from behaviourally assessed AD and age-matched controls were processed for immunoblotting with RXFP1 and RXFP3 antibodies. Results Compared to controls, putative RXFP1 immunoreactivity was reduced in parietal cortex of non-depressed AD patients but unchanged in depressed patients. Furthermore, putative RXFP3 immunoreactivity was increased only in depressed AD patients. RXFP1 levels in the parietal cortex also correlated with severity of depression symptoms. In contrast, RXFP1 and RXFP3 levels did not correlate with dementia severity or β-amyloid burden. Conclusion Alterations of RXFP1 and RXFP3 may be neurochemical markers of depression in AD, and relaxin family receptors warrant further preclinical investigations as possible therapeutic targets for neuropsychiatric symptoms in dementia.
    No preview · Article · Nov 2015 · Psychopharmacology
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    ABSTRACT: The nucleus incertus (NI) is a small brainstem cluster of neurons presumed to play a role in stress responses. We show that swim stress (normal water: 30min and cold water: 20min) and elevation stress robustly induced c-Fos expression in the NI and significantly suppressed long term potentiation (LTP) in the hippocampo-medial prefrontal cortical (HP-mPFC) pathway. To examine whether activation of CRF1 receptors in the NI plays a role in the suppression of HP-mPFC LTP, antalarmin, a specific CRF1 receptor antagonist, was infused directly into the NI either before presentation of (1) elevation stress or (2) high frequency stimulation. As predicted, the intra-NI infusion of antalarmin reversed the elevation stress-induced suppression of LTP in the HP-mPFC pathway. This short report suggests that the CRF1 receptor system in the NI contributes to stress-related impairment in the plasticity of HP-mPFC pathway. The findings suggest that the NI-HP-mPFC is a stress responsive circuit in the rodent brain.
    Preview · Article · Nov 2015 · Brain research bulletin
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    ABSTRACT: Adaptation of the nervous system to different chemical and physiologic conditions is important for the homeostasis of brain processes and for learning and remembering appropriate responses to challenges. Although processes such as tolerance and dependence to various drugs of abuse have been known for a long time, it was recently discovered that even a single pharmacologically relevant dose of various drugs of abuse induces neuroplasticity in selected neuronal populations, such as the dopamine neurons of the ventral tegmental area, which persist long after the drug has been excreted. Prolonged (self-) administration of drugs induces gene expression, neurochemical, neurophysiological, and structural changes in many brain cell populations. These region-specific changes correlate with addiction, drug intake, and conditioned drugs effects, such as cue- or stress-induced reinstatement of drug seeking. In rodents, adolescent drug exposure often causes significantly more behavioral changes later in adulthood than a corresponding exposure in adults. Clinically the most impairing and devastating effects on the brain are produced by alcohol during fetal development. In adult recreational drug users or in medicated patients, it has been difficult to find persistent functional or behavioral changes, suggesting that heavy exposure to drugs of abuse is needed for neurotoxicity and for persistent emotional and cognitive alterations. This review describes recent advances in this important area of research, which harbors the aim of translating this knowledge to better treatments for addictions and related neuropsychiatric illnesses.
    Full-text · Article · Sep 2015 · Pharmacological reviews
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    ABSTRACT: The nucleus incertus (NI), located in the caudal brainstem, mainly consists of GABAergic neurons with widespread projections across the brain. It is the chief source of relaxin-3 in the mammalian brain and densely expresses corticotropin-releasing factor type 1 (CRF1) receptors. Several other neurotransmitters, peptides and receptors are reportedly expressed in the NI. In the present investigation, we show the expression of dopamine type-2 (D2) receptors in the NI by reverse transcriptase-polymerase chain reaction (RT-PCR), Western blotting (WB) and immunofluorescence (IF). RT-PCR did not show expression of D3 receptors. Cells of the NI co-labelled with D2 receptor short isoform (D2S)-like immunoreactivity and relaxin-3, CRF1/2 receptors and NeuN immunoreactivity. Behavioural effects of D2 receptor activation by intra-NI infusion of quinpirole (a D2/D3 agonist) were evaluated. Hypolocomotion was observed in home cage monitoring system (LABORAS) and novel environment-induced suppression of feeding behavioural paradigms. Thus the D2 receptors expressed in the NI are likely to play a role in locomotion. Based on its strong bidirectional connections to the median raphe and interpeduncular nuclei, the NI was predicted to play a role in modulating behavioural activity [21] and the present results lend support to this hypothesis. This is the first evidence of expression of a catecholamine receptor, D2-like immunoreactivity, in the NI. Copyright © 2015. Published by Elsevier Inc.
    No preview · Article · Aug 2015 · Physiology & Behavior
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    ABSTRACT: The iron siderophore binding protein lipocalin 2 (LCN2, also known as 24p3, NGAL and siderocalin) may be involved in iron homeostasis, but till date, little is known about expression of its putative receptor, brain-type organic cation transporter (BOCT, also known as BOCT1, 24p3R, NGALR and LCN2R), in the brain during neurodegeneration. The present study was carried out to elucidate the expression of LCN2 and BOCT in hippocampus after excitotoxicity induced by the glutamate analog, kainate (KA) and a possible role of LCN2 in neuronal injury. As reported previously, a rapid and sustained induction in expression of LCN2 was found in the hippocampus after intracerebroventicular injection of KA. BOCT was expressed in neurons of the saline-injected control hippocampus, and immunolabel for BOCT protein was preserved in pyramidal neurons of CA1 at 1 day post-KA injection, likely due to the delayed onset of neurodegeneration after KA injection. At 3 days and 2 weeks after KA injections, loss of immunolabel was observed due to degenerated neurons, although remaining neurons continued to express BOCT, and induction of BOCT was found in OX-42 positive microglia. This resulted in an overall decrease in BOCT mRNA and protein expression after KA treatment. Increased expression of the pro-apoptotic marker, Bim, was found in both neurons and microglia after KA injection, but TUNEL staining indicating apoptosis was found primarily in Bim- expressing neurons, but not microglia. Apo-LCN2 caused no significant differences in neuronal Bim expression or cell survival, whereas holo-LCN2 increased Bim mRNA expression and decreased cell survival. Together, the results suggest that LCN2 and BOCT may have a role in neuronal injury. Copyright © 2015. Published by Elsevier Ltd.
    No preview · Article · May 2015 · Neurochemistry International
  • R Rajkumar · J Fam · E Y M Yeo · G S Dawe
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    ABSTRACT: Depression and suicide are known to be intricately entwined but the neurobiological basis underlying this association is yet to be understood. Ketamine is an N-methyl D-aspartate (NMDA) receptor antagonist used for induction and maintenance of general anaesthesia but paradoxically its euphoric effects lead to its classification under drugs of abuse. The serendipitous finding of rapid-onset antidepressant action of subanaesthetic dose ketamine intravenous infusion has sparked many preclinical and clinical investigations. A remarkable suppression of suicidal ideation was also reported in depressed patients. This review focuses on the clinical trials on ketamine that reported remedial effects in suicidal ideation in depression and addresses also the molecular mechanisms underlying the antidepressant and psychotomimetic actions of ketamine. The neuropsychiatric profile of subanaesthetic doses of ketamine encourages its use in the management of suicidal ideation that could avert emergent self-harm or suicide. Finally, the need for neuroimaging studies in suicidal patients to identify the brain region specific and temporal effects of ketamine, and the possibility of employing ketamine as an experimental tool in rodent-based studies to study the mechanisms underlying suicidal behaviour are highlighted. Copyright © 2015. Published by Elsevier Ltd.
    No preview · Article · May 2015 · Pharmacological Research
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    ABSTRACT: Amyloid precursor protein (APP), is commonly associated with Alzheimers disease, but its physiological function remains unknown. Nav1.6 is a key determinant of neuronal excitability in vivo. Since mouse models of gain-of-function and loss-of-function of APP and Nav1.6 share some similar phenotypes, we hypothesized that APP might be a candidate molecule for sodium channel modulation. Here, we report that APP co-localized and interacted with Nav1.6 in mouse cortical neurons. Knocking down APP decreased Nav1.6 sodium channel currents and cell surface expression. APP-induced increases in Nav1.6 cell surface expression were Go protein-dependent and were enhanced by a constitutively active Go-protein mutant and blocked by a dominant negative Go-protein mutant. APP also regulated c-Jun N-terminal kinase (JNK) activity in a Go-protein-dependent manner. JNK inhibition attenuated increases in cell surface expression of Nav1.6 sodium channels induced by overexpression of APP. JNK in turn phosphorylated APP. Nav1.6 sodium channel surface expression was increased by T668E, and decreased by T668A, mutations of APP695 mimicking and preventing T668 phosphorylation, respectively. Phosphorylation of APP695 at T668 enhanced its interaction with Nav1.6. Thus, we show that APP enhances Nav1.6 sodium channel cell surface expression through a Go-coupled JNK pathway. Copyright © 2015, The American Society for Biochemistry and Molecular Biology.
    No preview · Article · Mar 2015 · Journal of Biological Chemistry
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    R Shu · W Wong · Q H Ma · Z Z Yang · H Zhu · F J Liu · P Wang · J Ma · S Yan · J M Polo · C C A Bernard · L W Stanton · G S Dawe · Z C Xiao
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    ABSTRACT: Amyloid precursor protein (APP) is best known for its involvement in the pathogenesis of Alzheimer's disease. We have previously demonstrated that APP intracellular domain (AICD) regulates neurogenesis; however, the mechanisms underlying AICD-mediated regulation of neuronal differentiation are not yet fully characterized. Using genome-wide chromatin immunoprecipitation approaches, we found that AICD is specifically recruited to the regulatory regions of several microRNA genes, and acts as a transcriptional regulator for miR-663, miR-3648 and miR-3687 in human neural stem cells. Functional assays show that AICD negatively modulates neuronal differentiation through miR-663, a primate-specific microRNA. Microarray data further demonstrate that miR-663 suppresses the expression of multiple genes implicated in neurogenesis, including FBXL18 and CDK6. Our results indicate that AICD has a novel role in suppression of neuronal differentiation via transcriptional regulation of miR-663 in human neural stem cells.
    Full-text · Article · Feb 2015 · Cell Death & Disease
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    ABSTRACT: Calcium independent phospholipase A2 (iPLA2) is an 85kDa protein that catalyzes the hydrolysis of the sn-2 acyl ester bond to liberate free fatty acids and lysophospholipids. In this study, we determined the role of constitutive iPLA2β in long term potentiation (LTP) of the hippocampal prefrontal cortex pathway in vivo. We also examined the effect of iPLA2 knockdown using the rewarded alternation in T-maze task, a test of spatial working memory which is dependent on this pathway. Intracortical injection of an inhibitor to iPLA2, bromoenol lactone (BEL) or antisense oligonucleotide to iPLA2β in the prefrontal cortex abolished induction of hippocampal prefrontal cortex LTP. Moreover, iPLA2 inhibition and antisense knockdown resulted in increased errors in the rewarded alternation in T maze task, indicating negative effects on spatial working memory. BEL or antisense injection did not produce DNA fragmentation in the cortex as demonstrated by TUNEL assay. Results confirm a role of constitutive iPLA2β in hippocampal prefrontal cortex synaptic plasticity in vivo, and add to previous observations of a role of iPLA2 in hippocampal LTP in vitro, and long-term memory retrieval. They may be relevant in Alzheimer’s disease, and other neurodegenerative conditions that are associated with changes in iPLA2.
    No preview · Article · Dec 2014 · Neurochemistry International
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    ABSTRACT: In this study, we performed gas chromatography time-of-flight mass spectrometry (GC-TOFMS)-based extracellular metabolic profiling on AβPP-transfected CHO cells (CHO-AβPP695) and its wildtype. Orthogonal partial least squares discriminant analysis (OPLS-DA) was then used to identify discriminant metabolites, which gave clues on the effects of AβPP transgene on cellular processes. To confirm the hypotheses generated based on the metabolic data, we performed biochemical assays to gather further evidence to support our findings. The OPLS-DA showed a robust differentiation following 24 h of incubation (Q2(cum) = 0.884) and 15 discriminant metabolites were identified. In contrast, extracellular Aβ42 was identified to increase significantly in CHO-AβPP695 only after incubation for 48 h. The observed 24-h metabolic fluxes were associated with increased mitochondrial AβPP and reduced mitochondrial viabilities, which occurred before extracellular Aβ accumulation. We also investigated the therapeutic potential of peroxisome proliferator-activated receptor gamma (PPARγ) agonists, namely rosiglitazone (RSG) and pioglitazone (PIO), by employing the same approach to characterize the metabolic profiles of CHO-AβPP695 treated with RSG and PIO, with or without their respective receptor blockers. Treatment with PIO was found to reduce the perturbation of the discriminant metabolites in CHO-AβPP695 to a larger extent than treatment with RSG. We also attributed the PIO effects on the lowering of Aβ42, and restoration of mitochondrial activity to PPARγ and PPARα agonism, respectively. Taken together, PIO was demonstrated to be therapeutically superior to RSG. Our findings provide further insights into early disease stages in this AβPP model, and support the advancement of PIO in AD therapy.
    No preview · Article · Sep 2014 · Journal of Alzheimer's disease: JAD
  • Yi Chen · Arindam Basu · Lei Liu · Xiaodan Zou · Ramamoorthy Rajkumar · Gavin Stewart Dawe · Minkyu Je
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    ABSTRACT: A novel signal folding and reconstruction scheme for neural recording applications that exploits the $1/f^{n}$ characteristics of neural signals is described in this paper. The amplified output is ‘folded’ into a predefined range of voltages by using comparison and reset circuits along with the core amplifier. After this output signal is digitized and transmitted, a reconstruction algorithm can be applied in the digital domain to recover the amplified signal from the folded waveform. This scheme enables the use of an analog-to-digital convertor with less number of bits for the same effective dynamic range. It also reduces the transmission data rate of the recording chip. Both of these features allow power and area savings at the system level. Other advantages of the proposed topology are increased reliability due to the removal of pseudo-resistors, lower harmonic distortion and low-voltage operation. An analysis of the reconstruction error introduced by this scheme is presented along with a behavioral model to provide a quick estimate of the post reconstruction dynamic range. Measurement results from two different core amplifier designs in 65 nm and 180 nm CMOS processes are presented to prove the generality of the proposed scheme in the neural recording applications. Operating from a 1 V power supply, the amplifier in 180 nm CMOS has a gain of 54.2 dB, bandwidth of 5.7 kHz, input referred noise of 3.8 $mu V_{rms}$ and power dissipation of 2.52 $mu {rm W}$ leading to a NEF of 3.1 in spike band. It exhibits a dynamic range of 66 dB and maximum SNDR of 43 dB in LFP band. It also reduces system level power (by reducing the number of bits in the ADC by 2) as well as data rate to 80% of a conventional design. In vivo measurements validate the ability of t- is amplifier to simultaneously record spike and LFP signals.
    No preview · Article · Aug 2014 · IEEE Transactions on Biomedical Circuits and Systems
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    ABSTRACT: Neural stem cells (NSCs) and neural progenitors (NPs) in the mammalian neocortex give rise to the main cell types of the nervous system. The biological behavior of these NSCs and NPs is regulated by extracellular niche derived autocrine-paracrine signaling factors on a developmental timeline. Our previous reports [1, 2] have shown that chondroitin sulfate proteoglycan (CSPG) and ApolipoproteinE (ApoE) are autocrine-paracrine survival factors for NSCs. NogoA, a myelin related protein, is expressed in the cortical ventricular zones where NSCs reside. However, the functional role of Nogo signaling proteins in NSC behavior is not completely understood. In this study, we show that NogoA receptors, NogoR1 and PirB, are expressed in the ventricular zone where NSCs reside between E10.5-14.5 but not at E15.5. Nogo ligands stimulate NSC survival and proliferation in a dosage dependent manner in vitro. NogoR1 and PirB, are low and high affinity Nogo receptors respectively, and are responsible for the effects of Nogo ligands on NSC behavior. Inhibition of autocrine-paracrine Nogo signaling blocks NSC survival and proliferation. In NSCs, NogoR1 functions through Rho whereas PirB uses Shp1/2 signaling pathways to control NSC behavior. Taken together, this work suggests that Nogo signaling is an important pathway for survival of NSCs. Stem Cells 2014.
    No preview · Article · Jun 2014 · Stem Cells
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    Liying Corinne Lee · Ramamoorthy Rajkumar · Gavin Stewart Dawe

    Preview · Article · Jun 2014 · Brain Research
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    ABSTRACT: Amyloid precursor protein (APP), commonly associated with Alzheimer disease, is upregulated and distributes evenly along the injured axons, and therefore, also known as a marker of demyelinating axonal injury and axonal degeneration. However, the physiological distribution and function of APP along myelinated axons was unknown. We report that APP aggregates at nodes of Ranvier (NOR) in the myelinated central nervous system (CNS) axons but not in the peripheral nervous system (PNS). At CNS NORs, APP expression co-localizes with tenascin-R and is flanked by juxtaparanodal potassium channel expression demonstrating that APP localized to NOR. In APP-knockout (KO) mice, nodal length is significantly increased, while sodium channels are still clustered at NORs. Moreover, APP KO and APP-overexpressing transgenic (APP TG) mice exhibited a decreased and an increased thickness of myelin in spinal cords, respectively, although the changes are limited in comparison to their littermate WT mice. The thickness of myelin in APP KO sciatic nerve also increased in comparison to that in WT mice. Our observations indicate that APP acts as a novel component at CNS NORs, modulating nodal formation and has minor effects in promoting myelination.
    Preview · Article · Apr 2014 · Cell adhesion & migration
  • Jared W Young · Anil Ratty · Gavin S Dawe · Mark A Geyer
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    ABSTRACT: Schizophrenia is a prevalent neurodevelopmental psychiatric disorder with poor prognosis and limited understanding of its etiology. This limited etiological understanding renders developing animal models of schizophrenia difficult. Although attempts are made to recreate putative etiologies in models, these models may only enable the generation of treatments targeted at the mechanisms manipulated. Although the chakragati mouse was not created as a result of a specific gene target, reports to date suggest these mice exhibit behavioral abnormalities that are consistent with some observed in patients with schizophrenia. As an initial screen on the relevance of these mice to schizophrenia, we tested the exploration and sensorimotor gating of male and female chakragati mice in the cross-species tests behavioral pattern monitor (BPM) and prepulse inhibition (PPI), respectively. The chakragati mice exhibited hyperactive yet more meandering/circling movements of exploration compared with wildtype (WT) littermates. Moreover, chakragati mice exhibited impaired PPI compared with WT mice, primarily at high prepulse intensity levels. Thus, chakragati mice share some of the abnormal exploratory and PPI behaviors that are observed in patients with schizophrenia. These behaviors can be used to screen for novel antipsychotics which may be based on novel mechanisms of action. The multivariate abnormal exploration of these mice may also yield further information for treatment effects. Further characterization of these mice in tasks with putative links to negative or cognitive symptoms may further advance the utility of these mice as a screen for novel treatments for schizophrenia. (PsycINFO Database Record (c) 2014 APA, all rights reserved).
    No preview · Article · Apr 2014 · Behavioral Neuroscience
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    Li Shen Loo · Ning Tang · Muthafar Al-Haddawi · Gavin Stewart Dawe · Wanjin Hong
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    ABSTRACT: Sorting nexin 27 (SNX27), a PDZ domain-containing endosomal protein, was recently shown to modulate glutamate receptor recycling in Down's syndrome. However, the precise molecular role of SNX27 in GluA1 trafficking is unclear. Here we report that SNX27 is enriched in dendrites and spines, along with recycling endosomes. Significantly, the mobilization of SNX27 along with recycling endosomes into spines was observed. Mechanistically, SNX27 interacts with K-ras GTPase via the RA domain; and following chemical LTP stimuli, K-ras is recruited to SNX27-enriched endosomes through a Ca(2+)/CaM-dependent mechanism, which in turn drives the synaptic delivery of homomeric GluA1 receptors. Impairment of SNX27 prevents LTP and associated trafficking of AMPARs. These results demonstrate a role for SNX27 in neuronal plasticity, provide a molecular explanation for the K-ras signal during LTP and identify SNX27 as the PDZ-containing molecular linker that couples the plasticity stimuli to the delivery of postsynaptic cargo.
    Full-text · Article · Jan 2014 · Nature Communications
  • Dong Han · Yuanjin Zheng · Ramamoorthy Rajkumar · Gavin Stewart Dawe · Minkyu Je
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    ABSTRACT: Neural prosthetics and personal healthcare have increasing need of high channel density low noise low power neural sensor interfaces. The input referred noise and quantization resolution are two essential factors which prevent conventional neural sensor interfaces from simultaneously achieving a good noise efficiency factor and low power consumption. In this paper, a neural recording architecture with dynamic range folding and current reuse techniques is proposed and dedicated to solving the noise and dynamic range trade-off under low voltage low power operation. Measured results from the silicon prototype show that the proposed design achieves 3.2 μVrms input referred noise and 8.27 effective number of bits at only 0.45 V supply and 0.94 μW/channel power consumption.
    No preview · Article · Dec 2013 · IEEE Transactions on Biomedical Circuits and Systems
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    Corinne Liying Lee · Ramamoorthy Rajkumar · Gavin Stewart Dawe
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    ABSTRACT: The nucleus incertus (NI), a brainstem nucleus found in the pontine periventricular grey, is the primary source of the neuropeptide relaxin-3 in the mammalian brain. The NI neurons have also been previously reported to express several receptors and neurotransmitters, including corticotropin releasing hormone receptor 1 (CRF1) and gamma-aminobutyric acid (GABA). The NI projects widely to putative neural correlates of stress, anxiety, depression, feeding behaviour, arousal and cognition leading to speculation that it might be involved in several neuropsychiatric conditions. On the premise that relaxin-3 expressing neurons in the NI predominantly co-express CRF1 receptors, a novel method for selective ablation of the rat brain NI neurons using corticotropin releasing factor (CRF)-saporin conjugate is described. In addition to a behavioural deficit in the fear conditioning paradigm, reverse transcriptase polymerase chain reaction (RT-PCR), western blotting (WB) and immunofluorescence labelling (IF) techniques were used to confirm the NI lesion. We observed a selective and significant loss of CRF1 expressing cells, together with a consistent decrease in relaxin-3 and GAD65 expression. The significant ablation of relaxin-3 positive neurons of the NI achieved by this immunolesioning approach is a promising model to explore the neuropsychopharmacological implications of NI/relaxin-3 in behavioural neuroscience.
    Preview · Article · Nov 2013 · Brain research
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    ABSTRACT: This paper presents a fully implantable 100-channel neural interface IC for neural activity monitoring. It contains 100-channel analog recording front-ends, 10 multiplexing successive approximation register ADCs, digital control modules and power management circuits. A dual sample-and-hold architecture is proposed, which extends the sampling time of the ADC and reduces the average power per channel by more than 50% compared to the conventional multiplexing neural recording system. A neural amplifier (NA) with current-reuse technique and weak inversion operation is demonstrated, consuming 800 nA under 1-V supply while achieving an input-referred noise of 4.0 μVrms in a 8-kHz bandwidth and a NEF of 1.9 for the whole analog recording chain. The measured frequency response of the analog front-end has a high-pass cutoff frequency from sub-1 Hz to 248 Hz and a low-pass cutoff frequency from 432 Hz to 5.1 kHz, which can be configured to record neural spikes and local field potentials simultaneously or separately. The whole system was fabricated in a 0.18-μm standard CMOS process and operates under 1 V for analog blocks and ADC, and 1.8 V for digital modules. The number of active recording channels is programmable and the digital output data rate changes accordingly, leading to high system power efficiency. The overall 100-channel interface IC consumes 1.16-mW total power, making it the optimum solution for multi-channel neural recording systems.
    No preview · Article · Oct 2013 · Circuits and Systems I: Regular Papers, IEEE Transactions on

Publication Stats

1k Citations
283.66 Total Impact Points


  • 2013-2015
    • National University Health System
    • Nanyang Technological University
      • School of Electrical and Electronic Engineering
      Tumasik, Singapore
  • 2007-2015
    • National University of Singapore
      Tumasik, Singapore
    • Institute of Molecular Biology
      Mayence, Rheinland-Pfalz, Germany
  • 2009
    • Clinical Research Center of Moscow
      Moskva, Moscow, Russia
  • 2004-2006
    • University of Hamburg
      Hamburg, Hamburg, Germany
  • 2001
    • University of Oxford
      Oxford, England, United Kingdom