Articles in Scholarly Journals [Incomplete List]

1. Ts65Dn, a Mouse Model of Down Syndrome, Exhibits Increased GABAB-Induced Potassium Current
   Journal of Neurophysiology, vol. 97, no. 1, pp. 892–900, 2007
2. Trisomy for the Down syndrome 'critical region' is necessary but not sufficient for brain phenotypes of trisomic mice
   Human Molecular Genetics, vol. 16, no. 7, pp. 774–782, 2007
3. Altered signaling pathways underlying abnormal hippocampal synaptic plasticity in the Ts65Dn mouse model of Down syndrome
   Journal of Neurochemistry, vol. 98, no. 4, pp. 1266–1277, 2006
4. Altered signaling pathways underlying abnormal hippocampal synaptic plasticity in the Ts65Dn mouse model of Down syndrome
   Journal of Neurochemistry, vol. 99, no. 4, pp. 1320–1320, 2006
5. Abnormal expression of the G-protein-activated inwardly rectifying potassium channel 2 (GIRK2) in hippocampus, frontal cortex, and substantia nigra of Ts65Dn mouse: A model of Down syndrome
   The Journal of Comparative Neurology, vol. 494, no. 5, pp. 815–833, 2005
6. Abnormal synaptic plasticity in the Ts1Cje segmental trisomy 16 mouse model of Down syndrome
   Neuropharmacology, vol. 49, no. 1, pp. 122–128, 2005
7. Understanding mental retardation in Down's syndrome using trisomy 16 mouse models
   Genes, Brain and Behavior, vol. 2, no. 3, pp. 167–178, 2003
8. Biochemistry, vol. 40, no. 37, pp. 11114–11120, 2001
9. Increased expression of NR2A subunit does not alter NMDA-evoked responses in cultured fetal trisomy 16 mouse hippocampal neurons
   Journal of Neurochemistry, vol. 76, no. 6, pp. 1663–1669, 2001
10. Kinetic and mechanistic characterization of NMDA receptor antagonism by replacement and truncation variants of the conantokin peptides
    Neuropharmacology, vol. 41, no. 7, pp. 801–810, 2001
11. The Amino Acid Residue at Sequence Position 5 in the Conantokin Peptides Partially Governs Subunit-selective Antagonism of Recombinant N-Methyl-D-aspartate Receptors
    Journal of Biological Chemistry, vol. 276, no. 29, pp. 26860–26867, 2001
12. On the cause of mental retardation in Down syndrome: extrapolation from full and segmental trisomy 16 mouse models
    Brain Research Reviews, vol. 35, no. 2, pp. 115–145, 2001
13. Neurochemical Research, vol. 25, no. 4, pp. 431–435, 2000
14. Abnormal chloride and potassium conductances in cultured embryonic tongue muscle from trisomy 16 mouse
    Developmental Brain Research, vol. 122, no. 2, pp. 193–197, 2000
15. Increased synaptic depression in the Ts65Dn mouse, a model for mental retardation in Down syndrome
    Neuropharmacology, vol. 38, no. 12, pp. 1917–1920, 1999
16. Inhibition of NMDA-induced currents by conantokin-G and conantokin-T in cultured embryonic murine hippocampal neurons
    Neuropharmacology, vol. 38, no. 12, pp. 1819–1829, 1999
17. Activator protein-1 DNA binding activation by hydrogen peroxide in neuronal and astrocytic primary cultures of trisomy-16 and diploid mice
    Molecular Brain Research, vol. 73, no. 1-2, pp. 144–150, 1999
18. In cortical cultures of trisomy 16 mouse brain the upregulated metallothionein-I/II fails to respond to H2O2 exposure or glutamate receptor stimulation
    Brain Research, vol. 787, no. 2, pp. 292–298, 1998
19. Journal of Neurocytology, vol. 27, no. 10, pp. 707–718, 1998
20. Increased expression of voltage-activated calcium channels in cultured hippocampal neurons from mouse trisomy 16, a model for Down syndrome
    Molecular Brain Research, vol. 56, no. 1-2, pp. 200–206, 1998
21. Cerebral cortical astroglia from the trisomy 16 mouse, a model for Down syndrome, produce neuronal cholinergic deficits in cell culture
    Proceedings of the National Academy of Sciences, vol. 94, no. 23, pp. 12644–12648, 1997
22. Altered long-term potentiation in the young and old Ts65Dn mouse, a model for down syndrome
    Neuropharmacology, vol. 36, no. 11-12, pp. 1549–1554, 1997
23. Beta-amyloid induced increase in choline flux across PC12 cell membranes
    Neuroscience Letters, vol. 234, no. 1, pp. 71–73, 1997
24. Responses to NMDA in cultured hippocampal neurons from trisomy 16 embryonic mice
    Neuroscience Letters, vol. 232, no. 3, pp. 131–134, 1997
25. Reduced expression of voltage-gated sodium channels in neurons cultured from trisomy 16 mouse hippocampus
    International Journal of Developmental Neuroscience, vol. 14, no. 6, pp. 749–760, 1996
26. Increased inward current in septal neurons from the trisomy 16 mouse, a model for Down's syndrome
    Brain Research, vol. 701, no. 1-2, pp. 89–98, 1995
27. Decreased sensitivity to nerve growth factor of dorsal root ganglion neurons cultured from mouse trisomy 16, a model of Down's syndrome
    Brain Research, vol. 680, no. 1-2, pp. 108–116, 1995
28. ß-amyloid increases choline conductance of PC12 cells: possible mechanism of toxicity in Alzheimer's disease
    Brain Research, vol. 646, no. 2, pp. 332–336, 1994
29. ß-Amyloid polypeptide increases calcium-uptake in PC12 cells: a possible mechanism for its cellular toxicity in Alzheimer's disease
    Brain Research, vol. 667, no. 2, pp. 269–272, 1994
30. Effects of nerve growth factor on whole-cell currents and other electrical membrane properties in cultured dorsal root ganglion neurons from normal and trisomy 16 mice
    Brain Research, vol. 650, no. 1, pp. 161–165, 1994
31. Cultured hippocampal neurons from trisomy 16 mouse, a model for Down's syndrome, have an abnormal action potential due to a reduced inward sodium current
    Brain Research, vol. 604, no. 1-2, pp. 69–78, 1993
32. Low Ca2+-sensitive maxi-K+ channels in human cultured fibroblasts
    Pfl�gers Archiv European Journal of Physiology, vol. 413, no. 1, pp. 99–101, 1988