Prion protein is necessary for normal synaptic function

[1]  D. Price,et al.  Motor neurone disease and animal models , 1994, Neurobiology of Disease.

[2]  S. Prusiner,et al.  Scrapie infection of transgenic mice leads to network and intrinsic dysfunction of cortical and hippocampal neurones , 1994, Neurobiology of Disease.

[3]  J. Jefferys,et al.  Synaptic inhibition in primary and secondary chronic epileptic foci induced by intrahippocampal tetanus toxin in the rat. , 1993, The Journal of physiology.

[4]  T. Teyler,et al.  Role of HCO3- ions in depolarizing GABAA receptor-mediated responses in pyramidal cells of rat hippocampus. , 1993, Journal of neurophysiology.

[5]  T. Bliss,et al.  A synaptic model of memory: long-term potentiation in the hippocampus , 1993, Nature.

[6]  S. Prusiner,et al.  Normal development and behaviour of mice lacking the neuronal cell-surface PrP protein , 1992, Nature.

[7]  R. Malenka,et al.  The influence of prior synaptic activity on the induction of long-term potentiation. , 1992, Science.

[8]  N. Cashman,et al.  Nearly ubiquitous tissue distribution of the scrapie agent precursor protein , 1992, Neurology.

[9]  John Collinge,et al.  Homozygous prion protein genotype predisposes to sporadic Creutzfeldt–Jakob disease , 1991, Nature.

[10]  S. Prusiner,et al.  Molecular biology of prion diseases , 1991, Science.

[11]  C. Weissmann The prion's progress , 1991, Nature.

[12]  Stephen J. DeArmond,et al.  Transgenetic studies implicate interactions between homologous PrP isoforms in scrapie prion replication , 1990, Cell.

[13]  T. Crow,et al.  Prion dementia without characteristic pathology , 1990, The Lancet.

[14]  S N Davies,et al.  Paired‐pulse depression of monosynaptic GABA‐mediated inhibitory postsynaptic responses in rat hippocampus. , 1990, The Journal of physiology.

[15]  G. Collingridge,et al.  Low-frequency activation of the NMDA receptor system can prevent the induction of LTP , 1989, Neuroscience Letters.

[16]  B. Gähwiler,et al.  Activity-dependent disinhibition. I. Repetitive stimulation reduces IPSP driving force and conductance in the hippocampus in vitro. , 1989, Journal of neurophysiology.

[17]  S. Prusiner,et al.  Changes in the localization of brain prion proteins during scrapie infection , 1987, Neurology.

[18]  G. Collingridge,et al.  A selective N-methyl-d-aspartate antagonist depresses epileptiform activity in rat hippocampal slices , 1985, Neuroscience Letters.

[19]  J. Mellanby,et al.  Long‐term changes in hippocampal physiology and learning ability of rats after intrahippocampal tetanus toxin. , 1985, The Journal of physiology.

[20]  T. Smith Synaptosomal cholesterol and phospholipid levels in several mouse strains differentially sensitive to ethanol. , 1985, The Journal of pharmacology and experimental therapeutics.

[21]  R. Nicoll,et al.  Pharmacological evidence for two kinds of GABA receptors on rat hippocampal pyramidal cells studied in vitro , 1982, The Journal of physiology.

[22]  R. H. Evans,et al.  γ‐AMINOBUTYRIC ACID AGONISTS: AN in vitro COMPARISON BETWEEN DEPRESSION OF SPINAL SYNAPTIC ACTIVITY AND DEPOLARIZATION OF SPINAL ROOT FIBRES IN THE RAT , 1980, British journal of pharmacology.

[23]  M. Royston,et al.  Synaptic degeneration is the primary neuropathological feature in prion disease: a preliminary study. , 1993, Neuroreport.