Behavioral and neurochemical characterization of mice deficient in the N-type Ca2+ channel α1B subunit
暂无分享,去创建一个
K. Tan-No | M. Murakami | H. Onogi | E. Takahashi | S. Mitazaki | H. Saito | S. Murai | T. Tadano | O. Nakagawasai | Atsushi Sato | Kenya Watanabe | Kota Nakaya
[1] R. Andrew Chambers,et al. The neonatal ventral hippocampal lesion as a heuristic neurodevelopmental model of schizophrenia , 2009, Behavioural Brain Research.
[2] R. Sprengel,et al. Suitability of tamoxifen-induced mutagenesis for behavioral phenotyping , 2008, Experimental Neurology.
[3] H. Rhim,et al. Impaired long‐term memory and long‐term potentiation in N‐type Ca2+ channel‐deficient mice , 2007, Genes, brain, and behavior.
[4] N. Swerdlow,et al. Forebrain D1 function and sensorimotor gating in rats: Effects of D1 blockade, frontal lesions and dopamine denervation , 2006, Neuroscience Letters.
[5] Meizan Lai,et al. Essential role of the LIM domain in the formation of the PKCɛ–ENH–N-type Ca2+ channel complex , 2006 .
[6] E. Roubos,et al. Quantification of synapse formation and maintenance in vivo in the absence of synaptic release , 2004, Neuroscience.
[7] P. Dudchenko. An overview of the tasks used to test working memory in rodents , 2004, Neuroscience & Biobehavioral Reviews.
[8] Takahisa Taguchi,et al. Evidence of novel neuronal functions of dysbindin, a susceptibility gene for schizophrenia. , 2004, Human molecular genetics.
[9] R. Hughes. The value of spontaneous alternation behavior (SAB) as a test of retention in pharmacological investigations of memory , 2004, Neuroscience & Biobehavioral Reviews.
[10] Richard Axel,et al. Spontaneous Neural Activity Is Required for the Establishment and Maintenance of the Olfactory Sensory Map , 2004, Neuron.
[11] Raquel E Gur,et al. Dysbindin-1 is reduced in intrinsic, glutamatergic terminals of the hippocampal formation in schizophrenia. , 2004, The Journal of clinical investigation.
[12] Kazuya Iwamoto,et al. Expression of HSPF1 and LIM in the lymphoblastoid cells derived from patients with bipolar disorder and schizophrenia , 2004, Journal of Human Genetics.
[13] K. Iwamoto,et al. Molecular characterization of bipolar disorder by comparing gene expression profiles of postmortem brains of major mental disorders , 2004, Molecular Psychiatry.
[14] J. Olney,et al. Drugs of abuse that cause developing neurons to commit suicide. , 2003, Brain research. Developmental brain research.
[15] Z. Mao,et al. Calcium Channel and NMDA Receptor Activities Differentially Regulate Nuclear C/EBPβ Levels to Control Neuronal Survival , 2003, Neuron.
[16] M. Yanagisawa,et al. N-Type Calcium Channel α1B Subunit (CaV2.2) Knock-Out Mice Display Hyperactivity and Vigilance State Differences , 2003, The Journal of Neuroscience.
[17] S. Greenfield,et al. Expression of voltage-dependent calcium channels in the embryonic rat midbrain. , 2002, Brain research. Developmental brain research.
[18] J. Hounsgaard,et al. CNTF inhibits high voltage activated Ca2+ currents in fetal mouse cortical neurones , 2002, Journal of neurochemistry.
[19] H. Ueda,et al. The cognition-enhancer nefiracetam is protective in BDNF-independent neuronal cell death under the serum-free condition , 2002, Neurochemistry International.
[20] Robert Lalonde,et al. The neurobiological basis of spontaneous alternation , 2002, Neuroscience & Biobehavioral Reviews.
[21] S. Hatakeyama,et al. Differential nociceptive responses in mice lacking the alpha(1B) subunit of N-type Ca(2+) channels. , 2001, Neuroreport.
[22] Richard Paylor,et al. The use of behavioral test batteries: Effects of training history , 2001, Physiology & Behavior.
[23] Dong Kwan Kim,et al. Altered Nociceptive Response in Mice Deficient in the α1B Subunit of the Voltage-Dependent Calcium Channel , 2001, Molecular and Cellular Neuroscience.
[24] H. Saegusa,et al. Suppression of inflammatory and neuropathic pain symptoms in mice lacking the N‐type Ca2+ channel , 2001, The EMBO journal.
[25] Sheryl E. Koch,et al. Functional disorders of the sympathetic nervous system in mice lacking the α1B subunit (Cav 2.2) of N-type calcium channels , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[26] P. Fletcher,et al. Reduced Brain Serotonin Activity Disrupts Prepulse Inhibition of the Acoustic Startle Reflex: Effects of 5,7-dihydroxytryptamine and p-chlorophenylalanine , 2001, Neuropsychopharmacology.
[27] C. Sotelo,et al. Neuronal Activity and Brain-Derived Neurotrophic Factor Regulate the Density of Inhibitory Synapses in Organotypic Slice Cultures of Postnatal Hippocampus , 2000, The Journal of Neuroscience.
[28] Pat Levitt,et al. Molecular Characterization of Schizophrenia Viewed by Microarray Analysis of Gene Expression in Prefrontal Cortex , 2000, Neuron.
[29] Gail Mandel,et al. Nomenclature of Voltage-Gated Sodium Channels , 2000, Neuron.
[30] A. Gratton,et al. Enhanced nucleus accumbens dopamine and plasma corticosterone stress responses in adult rats with neonatal excitotoxic lesions to the medial prefrontal cortex , 2000, Neuroscience.
[31] P. Fletcher,et al. Selective destruction of brain serotonin neurons by 5,7-dihydroxytryptamine increases responding for a conditioned reward , 1999, Psychopharmacology.
[32] M. Koch,et al. The neurobiology of startle , 1999, Progress in Neurobiology.
[33] C. Shatz,et al. Synaptic Activity and the Construction of Cortical Circuits , 1996, Science.
[34] A. Cools,et al. Prepulse inhibition and latent inhibition: the role of dopamine in the medial prefrontal cortex , 1996, Neuroscience.
[35] I. Ferrer,et al. Thalamic and Basal Forebrain Afferents Modulate the Development of Parvalbumin and Calbindin D28k Immunoreactivity in the Barrel Cortex of the Rat , 1996, The European journal of neuroscience.
[36] J. Kehne,et al. 5-HT modulation of auditory and visual sensorimotor gating: I. Effects of 5-HT releasers on sound and light prepulse inhibition in Wistar rats , 1996, Psychopharmacology.
[37] R. Padich,et al. 5-HT modulation of auditory and visual sensorimotor gating: II. Effects of the 5-HT2A antagonist MDL 100,907 on disruption of sound and light prepulse inhibition produced by 5-HT agonists in Wistar rats , 1996, Psychopharmacology.
[38] R. Foehring,et al. Serotonin modulates N- and P-type calcium currents in neocortical pyramidal neurons via a membrane-delimited pathway. , 1996, Journal of neurophysiology.
[39] S. Rose,et al. ω-Conotoxin GVIA Disrupts Memory Formation in the Day-Old Chick , 1995, Neurobiology of Learning and Memory.
[40] B. Bean,et al. Voltage-dependent calcium channels in rat midbrain dopamine neurons: modulation by dopamine and GABAB receptors. , 1995, Journal of neurophysiology.
[41] M. Matteoli,et al. Calcium-dependent glutamate release during neuronal development and synaptogenesis: different involvement of omega-agatoxin IVA- and omega-conotoxin GVIA-sensitive channels. , 1995, Proceedings of the National Academy of Sciences of the United States of America.
[42] R.J. Miller,et al. Developmental changes in presynaptic calcium channels coupled to glutamate release in cultured rat hippocampal neurons , 1995, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[43] H. Sakagami,et al. Localization of mRNAs of voltage-dependent Ca2+-channels: four subtypes of α1- and β-subunits in developing and mature rat brain , 1995 .
[44] J. Luebke,et al. Exocytotic Ca2+ channels in mammalian central neurons , 1995, Trends in Neurosciences.
[45] M. Koch,et al. Deficient Sensorimotor Gating After 6‐Hydroxydopamine Lesion of the Rat medial Prefrontal Cortex is Reversed by Haloperidol , 1994, The European journal of neuroscience.
[46] A. J. Scheetz,et al. Modulation of NMDA receptor function: implications for vertebrate neural development , 1994, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[47] J. McIntosh,et al. Complex patterns of [125I]omega-conotoxin GVIA binding site expression during postnatal rat brain development. , 1994, Brain research. Developmental brain research.
[48] M. Geyer,et al. Multiple serotonin receptor subtypes modulate prepulse inhibition of the startle response in rats , 1994, Neuropharmacology.
[49] J. Luebke,et al. Multiple calcium channel types control glutamatergic synaptic transmission in the hippocampus , 1993, Neuron.
[50] M. Adams,et al. Multiple Ca2+ channel types coexist to regulate synaptosomal neurotransmitter release. , 1993, Proceedings of the National Academy of Sciences of the United States of America.
[51] P. Rakic,et al. Selective role of N-type calcium channels in neuronal migration. , 1992, Science.
[52] M. Geyer,et al. Failure of haloperidol to block the effects of phencyclidine and dizocilpine on prepulse inhibition of startle , 1991, Biological Psychiatry.
[53] J. Kemp,et al. The effect of ω‐conotoxin GVIA on synaptic transmission within the nucleus accumbens and hippocampus of the rat in vitro , 1991, British journal of pharmacology.
[54] C. Regan,et al. Intraventricular infusions of antibodies to amyloid-β-protein precursor impair the acquisition of a passive avoidance response in the rat , 1990, Neuroscience Letters.
[55] I. Wessler,et al. Differential effects of calcium channel antagonists (ω-conotoxin GVIA, nifedipine, verapamil) on the electrically-evoked release of [3H]acetylcholine from the myenteric plexus, phrenic nerve and neocortex of rats , 1990, Naunyn-Schmiedeberg's Archives of Pharmacology.
[56] H. Herdon,et al. Investigations of the roles of dihydropyridine and ω-conotoxin-sensitive calcium channels in mediating depolarisation-evoked endogenous dopamine release from striatal slices , 1989, Naunyn-Schmiedeberg's Archives of Pharmacology.
[57] J. Woodward,et al. Differential sensitivity of synaptosomal calcium entry and endogenous dopamine release to ω-conotoxin , 1988, Brain Research.
[58] H. Osswald,et al. Omega-conotoxin GVIA and pharmacological modulation of hippocampal noradrenaline release. , 1988, European journal of pharmacology.
[59] N. Swerdlow,et al. Central dopamine hyperactivity in rats mimics abnormal acoustic startle response in schizophrenics , 1986, Biological Psychiatry.
[60] W R Gray,et al. Peptide neurotoxins from fish-hunting cone snails. , 1985, Science.
[61] R. Wilcox,et al. Apomorphine-induced stereotypic cage climbing in mice as a model for studying changes in dopamine receptor sensitivity , 1980, Pharmacology Biochemistry and Behavior.
[62] J. Schwartz,et al. A gradual score to evaluate the climbing behaviour elicited by apomorphine in mice , 1978, Psychopharmacology.
[63] T. Nagasu,et al. Pattern of Compensatory Expression of Voltage-Dependent Ca2+ Channel α1 and β Subunits in Brain of N-type Ca2+ Channel α1B Subunit Gene-Deficient Mice with a CBA/JN Genetic Background , 2005 .
[64] M. Koch,et al. Prepulse inhibition of the acoustic startle response of rats is reduced by 6-hydroxydopamine lesions of the medial prefrontal cortex , 2005, Psychopharmacology.
[65] S. Iversen,et al. The role of forebrain dopamine systems in amphetamine induced stereotyped behavior in the rat , 2004, Psychopharmacologia.
[66] S. Iversen,et al. Dissociable effects of 6-OHDA-induced lesions of neostriatum on anorexia, locomotor activity and stereotypy: The role of behavioural competition , 2004, Psychopharmacology.
[67] M. Colonnese,et al. Chronic NMDA receptor blockade from birth delays the maturation of NMDA currents, but does not affect AMPA/kainate currents. , 2003, Journal of neurophysiology.
[68] J. Olney,et al. Blockade of NMDA receptors and apoptotic neurodegeneration in the developing brain. , 1999, Science.