Effects of age-related loss of P/Q-type calcium channels in a mice model of peripheral nerve injury
暂无分享,去创建一个
C. Severini | V. Vacca | G. Strimpakos | S. Marinelli | F. Pavone | E. Mattei | S. Luvisetto | C. Eleuteri
[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.