Effects of age-related loss of P/Q-type calcium channels in a mice model of peripheral nerve injury

[1]  N. Corbi,et al.  Novel Adeno-Associated Viral Vector Delivering the Utrophin Gene Regulator Jazz Counteracts Dystrophic Pathology in mdx Mice , 2014, Journal of cellular physiology.

[2]  Eiki Takahashi,et al.  Ca2+ channel currents in dorsal root ganglion neurons of P/Q-type voltage-gated Ca2+ channel mutant mouse, rolling mouse Nagoya , 2012, Neuroscience Research.

[3]  T. Foster Dissecting the age-related decline on spatial learning and memory tasks in rodent models: N-methyl-D-aspartate receptors and voltage-dependent Ca2+ channels in senescent synaptic plasticity , 2012, Progress in Neurobiology.

[4]  Lucas G Vattino,et al.  Amyotrophic lateral sclerosis‐immunoglobulins selectively interact with neuromuscular junctions expressing P/Q‐type calcium channels , 2011, Journal of neurochemistry.

[5]  Qing Liu,et al.  Complex distribution patterns of voltage-gated calcium channel α-subunits in the spiral ganglion , 2011, Hearing Research.

[6]  M. Tanabe,et al.  Role of voltage-dependent calcium channel subtypes in spinal long-term potentiation of C-fiber-evoked field potentials , 2011, PAIN®.

[7]  E. Straface,et al.  Botulinum neurotoxin type A counteracts neuropathic pain and facilitates functional recovery after peripheral nerve injury in animal models , 2010, Neuroscience.

[8]  M. Costanzi,et al.  Impaired Terminal Differentiation of Hippocampal Granule Neurons and Defective Contextual Memory in PC3/Tis21 Knockout Mice , 2009, PloS one.

[9]  I. Shibuya,et al.  Hypoalgesic behaviors of P/Q-type voltage-gated Ca2+ channel mutant mouse, rolling mouse Nagoya , 2009, Neuroscience.

[10]  P. Molenaar A relative weak leg muscle in the rolling Nagoya mouse as a model for Lambert–Eaton myasthenic syndrome , 2008, Journal of Neuroimmunology.

[11]  A. Dolphin,et al.  Vesicular apparatus, including functional calcium channels, are present in developing rodent optic nerve axons and are required for normal node of Ranvier formation , 2008, The Journal of physiology.

[12]  Rob C. G. van de Ven,et al.  Reduced ACh release at neuromuscular synapses of heterozygous leaner Cav2.1‐mutant mice , 2008, Synapse.

[13]  G. Bernardi,et al.  Age-related functional changes of high-voltage-activated calcium channels in different neuronal subtypes of mouse striatum , 2008, Neuroscience.

[14]  W. Campana Schwann cells: Activated peripheral glia and their role in neuropathic pain , 2007, Brain, Behavior, and Immunity.

[15]  X. Navarro,et al.  Neural plasticity after peripheral nerve injury and regeneration , 2007, Progress in Neurobiology.

[16]  Rob C. G. van de Ven,et al.  Severely impaired neuromuscular synaptic transmission causes muscle weakness in the Cacna1a‐mutant mouse rolling Nagoya , 2007, The European journal of neuroscience.

[17]  U. Namgung,et al.  Cdc2-mediated Schwann cell migration during peripheral nerve regeneration , 2007, Journal of Cell Science.

[18]  Yu-Qing Cao,et al.  Voltage-gated calcium channels and pain , 2006, Pain.

[19]  Gerald W. Zamponi,et al.  Presynaptic Ca2+ channels – integration centers for neuronal signaling pathways , 2006, Trends in Neurosciences.

[20]  C. Fletcher,et al.  Pain sensitivity in mice lacking the Cav2.1α1 subunit of P/Q-type Ca2+ channels , 2006, Neuroscience.

[21]  G. Comi,et al.  Loss of glial fibrillary acidic protein (GFAP) impairs Schwann cell proliferation and delays nerve regeneration after damage , 2006, Journal of Cell Science.

[22]  U. Namgung,et al.  Involvement of Cdc2 in axonal regeneration enhanced by exercise training in rats. , 2006, Medicine and science in sports and exercise.

[23]  Jeffrey Field,et al.  Schwann cells: origins and role in axonal maintenance and regeneration. , 2006, The international journal of biochemistry & cell biology.

[24]  L. Greensmith,et al.  The effect of peripheral nerve injury on disease progression in the SOD1(G93A) mouse model of amyotrophic lateral sclerosis , 2005, Neuroscience.

[25]  W. Catterall,et al.  International Union of Pharmacology. XLVIII. Nomenclature and Structure-Function Relationships of Voltage-Gated Calcium Channels , 2005, Pharmacological Reviews.

[26]  R. Mirsky,et al.  The origin and development of glial cells in peripheral nerves , 2005, Nature Reviews Neuroscience.

[27]  A. Twijnstra,et al.  P/Q-type calcium channel antibodies, Lambert–Eaton myasthenic syndrome and survival in small cell lung cancer , 2005, Journal of Neuroimmunology.

[28]  C. Stokes,et al.  Validation of computer-assisted, pixel-based analysis of multiple-colour immunofluorescence histology. , 2005, Journal of immunological methods.

[29]  D. Pietrobon Function and dysfunction of synaptic calcium channels: insights from mouse models , 2005, Current Opinion in Neurobiology.

[30]  M. Urban,et al.  Medullary N-type and P/Q-type calcium channels contribute to neuropathy-induced allodynia , 2005, Neuroreport.

[31]  Olivier Poirot,et al.  Silencing of the Cav3.2 T‐type calcium channel gene in sensory neurons demonstrates its major role in nociception , 2005, The EMBO journal.

[32]  I. Forsythe,et al.  Functional Compensation of P/Q by N-Type Channels Blocks Short-Term Plasticity at the Calyx of Held Presynaptic Terminal , 2004, The Journal of Neuroscience.

[33]  Takashi Suzuki,et al.  Antinociceptive effect of different types of calcium channel inhibitors and the distribution of various calcium channel α1 subunits in the dorsal horn of spinal cord in mice , 2004, Brain Research.

[34]  S. Ando,et al.  Age-related changes in the levels of voltage-dependent calcium channels and other synaptic proteins in rat brain cortices , 2004, Neuroscience Letters.

[35]  H. Schaible,et al.  Effects of N-, P/Q- and L-type Calcium Channel Blockers on Nociceptive Neurones of the Trigeminal Nucleus with Input from the Dura , 2004, Cephalalgia : an international journal of headache.

[36]  Kyong-Tai Kim,et al.  Activation of cyclin-dependent kinase 5 is involved in axonal regeneration , 2004, Molecular and Cellular Neuroscience.

[37]  H. Meier The neuropathology of ducky, a neurological mutation of the mouse , 1968, Acta Neuropathologica.

[38]  W. Atchison,et al.  Ca2+ Channels as Targets of Neurological Disease: Lambert–Eaton Syndrome and Other Ca2+ Channelopathies , 2003, Journal of bioenergetics and biomembranes.

[39]  Daesoo Kim,et al.  Thalamic Control of Visceral Nociception Mediated by T-Type Ca2+ Channels , 2003, Science.

[40]  A. Woodard,et al.  αvβ3 integrin expression up-regulates cdc2, which modulates cell migration , 2003, The Journal of cell biology.

[41]  B. Díaz-Esnal,et al.  S‐100 proteins in the human peripheral nervous system , 2003, Microscopy research and technique.

[42]  T. Bartsch,et al.  P/Q-Type Calcium-Channel Blockade in the Periaqueductal Gray Facilitates Trigeminal Nociception: A Functional Genetic Link for Migraine? , 2002, The Journal of Neuroscience.

[43]  S. Hatakeyama,et al.  Differential nociceptive responses in mice lacking the alpha(1B) subunit of N-type Ca(2+) channels. , 2001, Neuroreport.

[44]  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.

[45]  Takashi Suzuki,et al.  Distribution of various calcium channel α1 subunits in murine DRG neurons and antinociceptive effect of ω-conotoxin SVIB in mice , 2001, Brain Research.

[46]  Dong-Hoon Shin,et al.  Differential alterations in the distribution of voltage-gated calcium channels in aged rat cerebellum , 2001, Brain Research.

[47]  H. Saegusa,et al.  Suppression of inflammatory and neuropathic pain symptoms in mice lacking the N‐type Ca2+ channel , 2001, The EMBO journal.

[48]  C. Fletcher,et al.  Dystonia and cerebellar atrophy in Cacna1a null mice lacking P/Q calcium channel activity , 2001, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[49]  M. Kim,et al.  Age-related changes in the distribution of Kv1.1 and Kv1.2 channel subunits in the rat cerebellum , 2001, Brain Research.

[50]  S. Ando,et al.  Age-related changes in the subtypes of voltage-dependent calcium channels in rat brain cortical synapses , 2001, Neuroscience Research.

[51]  M. Takamori,et al.  Lambert-Eaton myasthenic syndrome as an autoimmune calcium-channelopathy. , 2004, Neuroscience research.

[52]  I. Mintz,et al.  Low-Affinity Blockade of Neuronal N-Type Ca Channels by the Spider Toxin ω-Agatoxin-IVA , 2000, The Journal of Neuroscience.

[53]  S. McMahon,et al.  Keeping in touch: sensory neurone regeneration in the CNS. , 2000, Trends in pharmacological sciences.

[54]  M. Osanai,et al.  Altered pain responses in mice lacking α1E subunit of the voltage-dependent Ca2+ channel , 2000 .

[55]  H. Schaible,et al.  Effects of antagonists to high-threshold calcium channels upon spinal mechanisms of pain, hyperalgesia and allodynia , 2000, Pain.

[56]  C. Sotelo,et al.  An ultrastructural study of granule cell/Purkinje cell synapses in tottering (tg/tg), leaner (tgla /tgla ) and compound heterozygous tottering/leaner (tg/tgla ) mice , 1999, Neuroscience.

[57]  T. Soong,et al.  Splicing of α1A subunit gene generates phenotypic variants of P- and Q-type calcium channels , 1999, Nature Neuroscience.

[58]  S. Oda,et al.  Morphologic investigation of rolling mouse Nagoya (tg rol /tg rol ) cerebellar Purkinje cells: an ataxic mutant, revisited , 1999, Neuroscience Letters.

[59]  W. Catterall,et al.  Localization of Ca2+ Channel Subtypes on Rat Spinal Motor Neurons, Interneurons, and Nerve Terminals , 1998, The Journal of Neuroscience.

[60]  M. Cousins,et al.  Effect of subcutaneous administration of calcium channel blockers on nerve injury-induced hyperalgesia , 1998, Brain Research.

[61]  Tatsuo Yamamoto,et al.  Differential effects of intrathecally administered N- and P-type voltage-sensitive calcium channel blockers upon two models of experimental mononeuropathy in the rat , 1998, Brain Research.

[62]  P. Ince,et al.  Differential Localization of Voltage-Dependent Calcium Channel α1 Subunits at the Human and Rat Neuromuscular Junction , 1997, The Journal of Neuroscience.

[63]  K. Page,et al.  Functional expression of rat brain cloned α1E calcium channels in COS-7 cells , 1997, Pflügers Archiv.

[64]  J. Kapfhammer,et al.  Overexpression of the neural growth-associated protein GAP-43 induces nerve sprouting in the adult nervous system of transgenic mice , 1995, Cell.

[65]  D. Triggle,et al.  Age-dependent changes in voltage-gated calcium channels and ATP-dependent potassium channels in fisher 344 rats , 1995 .

[66]  J. Luebke,et al.  Exocytotic Ca2+ channels in mammalian central neurons , 1995, Trends in Neurosciences.

[67]  M. Reynolds,et al.  GAP-43 expression in primary sensory neurons following central axotomy , 1994, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[68]  R. Nahin,et al.  Primary sensory neurons exhibit altered gene expression in a rat model of neuropathic pain , 1994, Pain.

[69]  T. Yaksh,et al.  Role of voltage-dependent calcium channel subtypes in experimental tactile allodynia. , 1994, The Journal of pharmacology and experimental therapeutics.

[70]  Michael E. Adams,et al.  P-type calcium channels in rat central and peripheral neurons , 1992, Neuron.

[71]  Gary J. Bennett,et al.  A peripheral mononeuropathy in rat that produces disorders of pain sensation like those seen in man , 1988, Pain.

[72]  M. Zimmermann,et al.  Ethical guidelines for investigations of experimental pain in conscious animals , 1983, Pain.

[73]  H. Meier,et al.  Three syndromes produced by two mutant genes in the mouse. Clinical, pathological, and ultrastructural bases of tottering, leaner, and heterozygous mice. , 1971, The Journal of heredity.