David H Small

Summary

Affiliation: University of Tasmania
Country: Australia

Publications

  1. doi request reprint Dysregulation of Ca2+ homeostasis in Alzheimer's disease: role in acetylcholinesterase production and AMPA receptor internalization
    David H Small
    Menzies Research Institute Tasmania, University of Tasmania, Hobart, TAS, Australia
    Neurodegener Dis 10:76-9. 2012
  2. doi request reprint Dysregulation of calcium homeostasis in Alzheimer's disease
    David H Small
    Menzies Research Institute, University of Tasmania, Private Bag 24, Hobart, TAS 7001, Australia
    Neurochem Res 34:1824-9. 2009
  3. doi request reprint The role of Abeta-induced calcium dysregulation in the pathogenesis of Alzheimer's disease
    David H Small
    Menzies Research Institute, University of Tasmania, Hobart, Tasmania, Australia
    J Alzheimers Dis 16:225-33. 2009
  4. doi request reprint Regulation of proBACE1 by glycosaminoglycans
    David H Small
    Department of Biochemistry and Molecular Biology, Monash University, Clayton, Vic, Australia
    Neurodegener Dis 5:206-8. 2008
  5. doi request reprint Network dysfunction in Alzheimer's disease: does synaptic scaling drive disease progression?
    David H Small
    Menzies Research Institute, University of Tasmania, Hobart 7000, Tasmania, Australia
    Trends Mol Med 14:103-8. 2008
  6. doi request reprint Neural network dysfunction in Alzheimer's disease: a drug development perspective
    David H Small
    Menzies Research Institute, University of Tasmania, Australia
    Drug News Perspect 20:557-63. 2007
  7. pmc Presenilins and the gamma-secretase: still a complex problem
    David H Small
    Menzies Research Institute, University of Tasmania, Hobart, Tasmania 7001, Australia
    Mol Brain 3:7. 2010
  8. doi request reprint Glycosaminoglycan-induced activation of the beta-secretase (BACE1) of Alzheimer's disease
    David W Klaver
    Menzies Research Institute, University of Tasmania, Hobart, Tasmania, Australia
    J Neurochem 112:1552-61. 2010
  9. ncbi request reprint Transthyretin oligomers induce calcium influx via voltage-gated calcium channels
    Xu Hou
    Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria 3800, Australia
    J Neurochem 100:446-57. 2007
  10. doi request reprint Inhibition of Abeta aggregation and neurotoxicity by the 39-kDa receptor-associated protein
    Megan L Kerr
    Department of Biochemistry and Molecular Biology, School of Biomedical Sciences, Monash University, Victoria, Australia
    J Neurochem 112:1199-209. 2010

Collaborators

Detail Information

Publications54

  1. doi request reprint Dysregulation of Ca2+ homeostasis in Alzheimer's disease: role in acetylcholinesterase production and AMPA receptor internalization
    David H Small
    Menzies Research Institute Tasmania, University of Tasmania, Hobart, TAS, Australia
    Neurodegener Dis 10:76-9. 2012
    ....
  2. doi request reprint Dysregulation of calcium homeostasis in Alzheimer's disease
    David H Small
    Menzies Research Institute, University of Tasmania, Private Bag 24, Hobart, TAS 7001, Australia
    Neurochem Res 34:1824-9. 2009
    ....
  3. doi request reprint The role of Abeta-induced calcium dysregulation in the pathogenesis of Alzheimer's disease
    David H Small
    Menzies Research Institute, University of Tasmania, Hobart, Tasmania, Australia
    J Alzheimers Dis 16:225-33. 2009
    ..It is likely that elucidation of the mechanism by which Abeta and presenilin cause Ca(2+) dysregulation in neurons will help to identify new drug targets for the treatment of AD...
  4. doi request reprint Regulation of proBACE1 by glycosaminoglycans
    David H Small
    Department of Biochemistry and Molecular Biology, Monash University, Clayton, Vic, Australia
    Neurodegener Dis 5:206-8. 2008
    ..We speculate that proBACE1 can be regulated by endogenous heparan sulfate proteoglycans and that drugs which target this interaction may have value in the treatment of Alzheimer's disease...
  5. doi request reprint Network dysfunction in Alzheimer's disease: does synaptic scaling drive disease progression?
    David H Small
    Menzies Research Institute, University of Tasmania, Hobart 7000, Tasmania, Australia
    Trends Mol Med 14:103-8. 2008
    ..It is suggested that further studies on synaptic scaling in AD could reveal new targets for therapeutic drug development...
  6. doi request reprint Neural network dysfunction in Alzheimer's disease: a drug development perspective
    David H Small
    Menzies Research Institute, University of Tasmania, Australia
    Drug News Perspect 20:557-63. 2007
    ..This review examines mechanisms of synaptic scaling in the brain and explores prospects for future drug development based on a neural network perspective...
  7. pmc Presenilins and the gamma-secretase: still a complex problem
    David H Small
    Menzies Research Institute, University of Tasmania, Hobart, Tasmania 7001, Australia
    Mol Brain 3:7. 2010
    ..Unanswered questions about their biochemical mechanism of action and their effects on Ca2+ homeostasis are examined...
  8. doi request reprint Glycosaminoglycan-induced activation of the beta-secretase (BACE1) of Alzheimer's disease
    David W Klaver
    Menzies Research Institute, University of Tasmania, Hobart, Tasmania, Australia
    J Neurochem 112:1552-61. 2010
    ..The results suggest a model in which conformational changes close to the prodomain may be involved in the mechanism of heparin-induced activation of proBACE1...
  9. ncbi request reprint Transthyretin oligomers induce calcium influx via voltage-gated calcium channels
    Xu Hou
    Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria 3800, Australia
    J Neurochem 100:446-57. 2007
    ..These results suggest that increasing [Ca(2+)](i) via VGCCs may be an important early event which contributes to TTR-induced cytotoxicity, and that TTR oligomers, rather than mature fibrils, may be the major cytotoxic form of TTR...
  10. doi request reprint Inhibition of Abeta aggregation and neurotoxicity by the 39-kDa receptor-associated protein
    Megan L Kerr
    Department of Biochemistry and Molecular Biology, School of Biomedical Sciences, Monash University, Victoria, Australia
    J Neurochem 112:1199-209. 2010
    ..RAP also blocked an Abeta-induced inhibition of long-term memory consolidation in 1-day-old chicks. This study demonstrates that RAP binds to Abeta and is an inhibitor of the neurotoxic effects of Abeta...
  11. doi request reprint Effect of heparin on APP metabolism and Abeta production in cortical neurons
    David Klaver
    Menzies Research Institute, University of Tasmania, Hobart, TAS, Australia
    Neurodegener Dis 7:187-9. 2010
    ..Several studies suggest that heparin or heparan sulfate analogues may have value as therapeutic agents for the treatment of AD...
  12. ncbi request reprint The beta-amyloid protein of Alzheimer's disease binds to membrane lipids but does not bind to the alpha7 nicotinic acetylcholine receptor
    David H Small
    Department of Biochemistry and Molecular Biology, Monash University, Melbourne, Victoria, Australia
    J Neurochem 101:1527-38. 2007
    ..Instead, we speculate that Abeta may exert its effects by altering the packing of lipids within the plasma membrane, which could, in turn, influence the function of a variety of receptors and channels on the cell surface...
  13. doi request reprint Size and sulfation are critical for the effect of heparin on APP processing and Aβ production
    Hao Cui
    Menzies Research Institute Tasmania, University of Tasmania, Hobart, Tasmania, Australia
    J Neurochem 123:447-57. 2012
    ..This suggests that it might be possible to alter the structure of GAGs to achieve more specific inhibitors of APP processing that can cross the blood-brain barrier...
  14. pmc Effects of heparin and enoxaparin on APP processing and Aβ production in primary cortical neurons from Tg2576 mice
    Hao Cui
    Menzies Research Institute Tasmania, University of Tasmania, Hobart, Tasmania, Australia
    PLoS ONE 6:e23007. 2011
    ..Enoxaparin, a low molecular weight form of the glycosaminoglycan (GAG) heparin, has been reported to lower Aβ plaque deposition and improve cognitive function in AD transgenic mice...
  15. doi request reprint Is BACE1 a suitable therapeutic target for the treatment of Alzheimer's disease? Current strategies and future directions
    David W Klaver
    Menzies Research Institute, University of Tasmania, Hobart, Tasmania, Australia
    Biol Chem 391:849-59. 2010
    ..This review focuses on the structure BACE1, current therapeutic strategies based on developing active-site inhibitors, and new approaches to therapy involving targeting the expression or post-translational regulation of BACE1...
  16. doi request reprint Characterization of early stage intermediates in the nucleation phase of Aβ aggregation
    Jiali Zhai
    Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria 3800, Australia
    Biochemistry 51:1070-8. 2012
    ..These results are the first reported measurements of the real-time changes in Aβ molecular structure during the early stages of amyloid formation at the nanometer level...
  17. doi request reprint Astrocytes in Alzheimer's disease: emerging roles in calcium dysregulation and synaptic plasticity
    Adele J Vincent
    Menzies Research Institute, University of Tasmania, Hobart, Tasmania, Australia
    J Alzheimers Dis 22:699-714. 2010
    ..Therefore, astrocyte dysfunction may contribute to the earliest neuronal deficits in AD. Here we discuss emerging concepts in glial biology and the implications of astrocyte dysfunction on neurodegeneration in AD...
  18. doi request reprint Memory loss caused by beta-amyloid protein is rescued by a beta(3)-adrenoceptor agonist
    Marie E Gibbs
    Department of Anatomy and Developmental Biology, Monash University, Clayton Campus, Wellington Road, Clayton, Victoria 3800, Australia
    Neurobiol Aging 31:614-24. 2010
    ..A beta(3)-AR agonist (CL316243), but not a beta(2)-AR agonist, rescued Abeta-induced memory loss, suggesting the need for further studies on the role of beta(3)-ARs in AD...
  19. doi request reprint Surface plasmon resonance spectroscopy: a new lead in studying the membrane binding of amyloidogenic transthyretin
    Xu Hou
    Department of Biochemistry and Molecular Biology, Monash University, Clayton, Vic, Australia
    Methods Mol Biol 752:215-28. 2011
    ..In this chapter, we describe the application of SPR to the study of amyloidogenic transthyretin binding to the plasma membrane and artificial lipid bilayers...
  20. doi request reprint Mechanisms of transthyretin aggregation and toxicity
    Robert J Gasperini
    Menzies Research Institute, University of Tasmania, Liverpool Street, 7001, Hobart, TAS, Australia
    Subcell Biochem 65:211-24. 2012
    ..It is clear that many amyloidoses share common features of fibrillogenesis and toxicity. This chapter examines the mechanisms of TTR aggregation with a view to understanding the possible therapeutic interventions in amyloid disease...
  21. ncbi request reprint Cholesterol and anionic phospholipids increase the binding of amyloidogenic transthyretin to lipid membranes
    Xu Hou
    Department of Biochemistry and Molecular Biology, Monash University, Clayton, VIC 3800, Australia
    Biochim Biophys Acta 1778:198-205. 2008
    ..These results suggest that cholesterol and anionic phospholipids may be important for TTR aggregation and TTR-induced cytotoxicity...
  22. ncbi request reprint The beta-amyloid protein of Alzheimer's disease increases neuronal CRMP-2 phosphorylation by a Rho-GTP mechanism
    Steven Petratos
    Molecular Neurobiology Laboratory, Department of Biochemistry and Molecular Biology, Monash University, Clayton 3800, Victoria, Australia
    Brain 131:90-108. 2008
    ....
  23. doi request reprint Proteoglycans in the central nervous system: role in development, neural repair, and Alzheimer's disease
    Hao Cui
    Menzies Research Institute Tasmania, University of Tasmania, Hobart, Tasmania, Australia
    IUBMB Life 65:108-20. 2013
    ..The main functions of PGs in the CNS are reviewed as are the roles of PGs in brain injury and in the development or treatment of AD...
  24. ncbi request reprint Mechanisms of synaptic homeostasis in Alzheimer's disease
    David H Small
    Dept of Biochemistry and Molecular Biology, Monash University, Victoria 3800, Australia
    Curr Alzheimer Res 1:27-32. 2004
    ..In this review, several possible mechanisms of synaptic scaling are described...
  25. ncbi request reprint High resolution scanning tunnelling microscopy of the beta-amyloid protein (Abeta1-40) of Alzheimer's disease suggests a novel mechanism of oligomer assembly
    Dusan Losic
    Department of Biochemistry and Molecular Biology, Monash University, VIC 3800, Australia
    J Struct Biol 155:104-10. 2006
    ..The results suggest that the oligomer formation can proceed through a mechanism involving the linear association of monomers...
  26. doi request reprint Surface plasmon resonance spectroscopy in determination of the interactions between amyloid beta proteins (Abeta) and lipid membranes
    Xu Hou
    Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria, Australia
    Methods Mol Biol 627:225-35. 2010
    ..In this chapter, we describe the application of SPR spectroscopy to the determination of the binding of Abeta to lipid membranes...
  27. doi request reprint β-Amyloid precursor protein: function in stem cell development and Alzheimer's disease brain
    David H Small
    Menzies Research Institute Tasmania and School of Medicine, University of Tasmania, Hobart, TAS, Australia
    Neurodegener Dis 13:96-8. 2014
    ..As cystatin C expression is also reported to inhibit the development of amyloid pathology in APP transgenic mice, our finding has implications for the possible use of cystatin C for the therapy of AD...
  28. pmc Role of cystatin C in amyloid precursor protein-induced proliferation of neural stem/progenitor cells
    Yanling Hu
    Menzies Research Institute Tasmania, University of Tasmania, Hobart, Tasmania 7001, Australia
    J Biol Chem 288:18853-62. 2013
    ..The results demonstrate that APP expression stimulates NSPC proliferation and that this effect is mediated via an increase in cystatin C secretion. ..
  29. ncbi request reprint Beta-amyloid fibril formation is promoted by step edges of highly oriented pyrolytic graphite
    Dusan Losic
    Department of Biochemistry and Molecular Biology, Monash University, Victoria 3800, Australia
    Biopolymers 84:519-26. 2006
    ..The results demonstrate that surface interactions can promote the aggregation of Abeta into amyloid fibrils and they suggest that similar interactions could promote amyloid aggregation in vivo...
  30. ncbi request reprint Heparin activates beta-secretase (BACE1) of Alzheimer's disease and increases autocatalysis of the enzyme
    Marie Beckman
    Department of Biochemistry and Molecular Biology, Monash University, Victoria 3800, Australia
    Biochemistry 45:6703-14. 2006
    ..Our study provides evidence that heparan sulfate proteoglycans could regulate the rate of Alphabeta production in vivo...
  31. doi request reprint Activation of cathepsin D by glycosaminoglycans
    Marie Beckman
    Department of Biochemistry and Molecular Biology, Monash University, Clayton, Australia
    FEBS J 276:7343-52. 2009
    ..However, it is possible that heparin may also activate the proenzyme directly. On the basis of this study, we propose that GAGs may regulate CD activity in vivo...
  32. ncbi request reprint Insights into the physiological function of the β-amyloid precursor protein: beyond Alzheimer's disease
    Edgar Dawkins
    Menzies Research Institute Tasmania, University of Tasmania, Hobart, Tasmania, Australia
    J Neurochem 129:756-69. 2014
    ..However, the mechanisms by which APP exerts its actions remain to be elucidated. The available evidence suggests that APP interacts both intracellularly and extracellularly to regulate various signal transduction mechanisms. ..
  33. ncbi request reprint Transthyretin and familial amyloidotic polyneuropathy. Recent progress in understanding the molecular mechanism of neurodegeneration
    Xu Hou
    Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria, Australia
    FEBS J 274:1637-50. 2007
    ....
  34. ncbi request reprint STIM1 is necessary for store-operated calcium entry in turning growth cones
    Camilla B Mitchell
    Menzies Research Institute Tasmania, University of Tasmania, Hobart, Tasmania, Australia
    J Neurochem 122:1155-66. 2012
    ..Our data suggest that STIM1 is essential for correct growth cone navigation, playing multiple roles in growth cone motility, including the activation of SOCE...
  35. ncbi request reprint Cytoplasmic domain of the beta-amyloid protein precursor of Alzheimer's disease: function, regulation of proteolysis, and implications for drug development
    Megan L Kerr
    Laboratory of Molecular Neurobiology, Department of Biochemistry and Molecular Biology, and Monash University Centre for Brain and Behaviour, Monash University, Victoria, Australia
    J Neurosci Res 80:151-9. 2005
    ..In this Mini-Review, the role of the cytoplasmic domain of APP in APP trafficking and proteolysis is described. These studies suggest that proteins that bind to the cytoplasmic domain may be important targets for drug development in AD...
  36. ncbi request reprint Surface plasmon resonance for the analysis of beta-amyloid interactions and fibril formation in Alzheimer's disease research
    Marie Isabel Aguilar
    Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria, 3800, Australia
    Neurotox Res 7:17-27. 2005
    ..This article reviews the application of SPR to the study of the molecular interactions associated with AD and how this information enhances our molecular understanding of ABeta -mediated toxicity...
  37. doi request reprint Neurodegeneration in familial amyloidotic polyneuropathy
    Robert J Gasperini
    Laboratory of Molecular Neurobiology, Menzies Research Institute Tasmania, University of Tasmania, Hobart, Tasmania, Australia
    Clin Exp Pharmacol Physiol 39:680-3. 2012
    ....
  38. pmc TRPM8 and Nav1.8 sodium channels are required for transthyretin-induced calcium influx in growth cones of small-diameter TrkA-positive sensory neurons
    Robert J Gasperini
    Menzies Research Institute, University of Tasmania, Tasmania, 7001, Australia
    Mol Neurodegener 6:19. 2011
    ..abstract:..
  39. ncbi request reprint Acetylcholinesterase inhibitors for the treatment of dementia in Alzheimer's disease: do we need new inhibitors?
    David H Small
    Department of Biochemistry and Molecular Biology, Monash University, Clayton Campus, Wellington Road, Clayton VIC 3800, Australia
    Expert Opin Emerg Drugs 10:817-25. 2005
    ..These new treatments could make AChEI therapy less relevant for treatment of Alzheimer's disease...
  40. ncbi request reprint Binding of amyloidogenic transthyretin to the plasma membrane alters membrane fluidity and induces neurotoxicity
    Xu Hou
    Department of Biochemistry and Molecular Biology, Monash University, Clayton, VIC 3800, Australia
    Biochemistry 44:11618-27. 2005
    ..These results demonstrate that TTR can bind to the plasma membrane and cause a change in membrane fluidity. Altered membrane fluidity may be the cause of the neurotoxicity...
  41. ncbi request reprint Alzheimer's disease therapeutics: new approaches to an ageing problem
    David H Small
    Department of Biochemistry and Molecular Biology, Monash University, Victoria 3800, Australia
    IUBMB Life 56:203-8. 2004
    ..This review examines the potential of immunization strategies, cholesterol-lowering drugs, protease inhibitors and nicotinic drugs for the treatment of AD...
  42. ncbi request reprint Alois Alzheimer and Alzheimer's disease: a centennial perspective
    David H Small
    Department of Biochemistry and Molecular Biology, Monash University, Victoria 3800, Australia
    J Neurochem 99:708-10. 2006
    ..In this article, we review the current status of the amyloid hypothesis of AD and its role in the development of future therapy...
  43. ncbi request reprint Do acetylcholinesterase inhibitors boost synaptic scaling in Alzheimer's disease?
    David H Small
    Laboratory of Molecular Neurobiology, Department of Biochemistry and Molecular Biology, Monash University, Victoria 3800, Australia
    Trends Neurosci 27:245-9. 2004
    ..It is suggested that increased cholinergic activity during the early stages of AD contributes to synaptic scaling and that acetylcholinesterase inhibitors improve cognition in AD patients by boosting this mechanism...
  44. ncbi request reprint Cholinergic regulation of synaptic plasticity as a therapeutic target in Alzheimer's disease
    David H Small
    Laboratory of Molecular Neurobiology, University of Melbourne, Victoria 3010, Australia
    J Alzheimers Dis 4:349-55. 2002
    ..Nicotinic agonists may also protect cells from Abeta toxicity. Drugs which interact with the nAChR or which inhibit Abeta binding to nAChRs may be of value for the treatment of AD...
  45. ncbi request reprint Altered glycosylation of acetylcholinesterase in APP (SW) Tg2576 transgenic mice occurs prior to amyloid plaque deposition
    Lisa R Fodero
    Laboratory of Molecular Neurobiology, Department of Pathology, The University of Melbourne, Melbourne, Australia
    J Neurochem 81:441-8. 2002
    ..The study supports the possibility that glycosylation may also be a useful biomarker of AD...
  46. ncbi request reprint Proteasome-mediated degradation of the C-terminus of the Alzheimer's disease beta-amyloid protein precursor: effect of C-terminal truncation on production of beta-amyloid protein
    Janelle Nunan
    Department of Pathology, University of Melbourne, Victoria, Australia
    J Neurosci Res 74:378-85. 2003
    ..Therefore, the proteasome-dependent trafficking pathway of APP may be a valid therapeutic target for altering Abeta production in the Alzheimer's disease brain...
  47. ncbi request reprint Alzheimer's disease biomarkers: their value in diagnosis and clinical trials
    David H Small
    Laboratory of Molecular Neurobiology, Department of Pathology, University of Melbourne, Victoria 3010, Australia
    Front Biosci 7:d986-8. 2002
    ..Nevertheless, it may eventually be possible to use several markers in combination to obtain sufficient diagnostic accuracy. However, for this to be the case, new specific biomarkers may need to be identified...
  48. ncbi request reprint Changes in molecular isoform distribution of acetylcholinesterase in rat cortex and cerebrospinal fluid after intracerebroventricular administration of amyloid beta-peptide
    Javier Saez-Valero
    Instituto de Neurociencias, Universidad Miguel Hernandez CSIC, 03550 San Juan de Alicante, Spain
    Neurosci Lett 325:199-202. 2002
    ..The results support the view that changes in AChE isoform pattern in the AD brain are a direct consequence of A beta accumulation...
  49. ncbi request reprint Toxicity of substrate-bound amyloid peptides on vascular smooth muscle cells is enhanced by homocysteine
    Su San Mok
    Department of Pathology, The University of Melbourne, Parkville, Victoria, Australia
    Eur J Biochem 269:3014-22. 2002
    ..Our studies also suggest that homocysteine, a known risk factor for other cardiovascular diseases, could also be a risk factor for hemorrhagic stroke associated with CAA...
  50. ncbi request reprint Is gamma-secretase a multienzyme complex for membrane protein degradation? Models and speculations
    David H Small
    Laboratory of Molecular Neurobiology, Department of Pathology, University of Melbourne, Victoria 3010, Australia
    Peptides 23:1317-21. 2002
    ..This article presents some models of gamma-secretase and suggests that the simplest interpretation of current data is that gamma-secretase is a complex of several proteases located in the lumen of secretory vesicles...
  51. ncbi request reprint Proteolytic processing of the amyloid-beta protein precursor of Alzheimer's disease
    Janelle Nunan
    Department of Pathology, University of Melbourne, Parkville, Victoria 3010, Australia
    Essays Biochem 38:37-49. 2002
    ..In this review, we describe the progress that has been made in identifying the secretases and their potential as therapeutic targets in the treatment or prevention of Alzheimer's disease...
  52. ncbi request reprint Cholesterol is necessary both for the toxic effect of Abeta peptides on vascular smooth muscle cells and for Abeta binding to vascular smooth muscle cell membranes
    Supundi Subasinghe
    Department of Pathology, University of Melbourne, Victoria, Australia
    J Neurochem 84:471-9. 2003
    ..Reduction of membrane cholesterol using cholesterol-lowering drugs may be of therapeutic benefit because it reduces Abeta-membrane binding...
  53. ncbi request reprint Beta-amyloid protein oligomers induced by metal ions and acid pH are distinct from those generated by slow spontaneous ageing at neutral pH
    Genevieve M J A Klug
    Department of Pathology, University of Melbourne, Victoria, Australia
    Eur J Biochem 270:4282-93. 2003
    ..4 was more cytotoxic than Abeta aged at pH 5.0. Taken together, the results suggest that Abeta oligomerizes via two mutually exclusive mechanisms to form two different types of aggregates, which differ in their cytotoxic properties...
  54. ncbi request reprint Acetylcholinesterase is increased in mouse neuronal and astrocyte cultures after treatment with beta-amyloid peptides
    Javier Saez-Valero
    Instituto de Neurociencias, Universidad Miguel Hernandez CSIC, 03550, San Juan de Alicante, Spain
    Brain Res 965:283-6. 2003
    ....