Behavioral and neurochemical characterization of mice deficient in the N-type Ca2+ channel α1B subunit

[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.