Expression patterns of T-type Cav3.2 channel and insulin-like growth factor-1 receptor in dorsal root ganglion neurons of mice after sciatic nerve axotomy

Substantial evidence indicates that T-type Cav3.2 channel and insulin-like growth factor-1 (IGF-1) contribute to pain hypersensitivity within primary sensory nerves. A recent study suggested that activation of IGF-1 receptor (IGF-1R) could increase Cav3.2 channel currents and further contribute to inflammatory pain sensitivity. However, the expression patterns of Cav3.2 and IGF-1R and their colocalization in dorsal root ganglion (DRG) in chronic neuropathic pain condition remain unknown. In this study, we explored expression patterns of Cav3.2, IGF-1R and their colocalization, and whether phenotypic switch occurs in a subpopulation of Cav3.2+ or IGF-1R+ neurons in mouse DRGs after sciatic nerve axotomy with immunofluorescence, real-time reverse transcription-PCR, and western blot assays. We found that expressions of Cav3.2 and IGF-1R, and their colocalization were not increased in DRGs of mice following axotomy. In addition, Cav3.2+ or IGF-1R+ subpopulation neurons did not acquire significant switch in expression phenotype after sciatic nerve axotomy. Our findings argue for an upregulation of Cav3.2 and IGF-1R expression in lumbar DRGs post-sciatic nerve axotomy and provided an insight for understanding the functions of peripheral afferent Cav3.2 channel and IGF-1/IGF-1R signaling in chronic neuropathic pain.

[1]  B. Wang,et al.  Colocalization of insulin-like growth factor-1 receptor and T type Cav3.2 channel in dorsal root ganglia in chronic inflammatory pain mouse model , 2016, Neuroreport.

[2]  B. Wang,et al.  TLR signaling adaptor protein MyD88 in primary sensory neurons contributes to persistent inflammatory and neuropathic pain and neuroinflammation , 2016, Scientific Reports.

[3]  S. Laffray,et al.  T-type calcium channels in neuropathic pain , 2016, Pain.

[4]  Y. Zhang,et al.  Peripheral pain is enhanced by insulin-like growth factor 1 through a G protein–mediated stimulation of T-type calcium channels , 2014, Science Signaling.

[5]  C. Bladen,et al.  The Deubiquitinating Enzyme USP5 Modulates Neuropathic and Inflammatory Pain by Enhancing Cav3.2 Channel Activity , 2014, Neuron.

[6]  Zhen-Zhong Xu,et al.  Nociceptive neurons regulate innate and adaptive immunity and neuropathic pain through MyD88 adapter , 2014, Cell Research.

[7]  C. Bladen,et al.  1,4-Dihydropyridine derivatives with T-type calcium channel blocking activity attenuate inflammatory and neuropathic pain , 2014, Pflügers Archiv - European Journal of Physiology.

[8]  V. Jevtovic-Todorovic,et al.  CaV3.2 T-Type Calcium Channels in Peripheral Sensory Neurons Are Important for Mibefradil-Induced Reversal of Hyperalgesia and Allodynia in Rats with Painful Diabetic Neuropathy , 2014, PloS one.

[9]  G. Zamponi,et al.  Neuronal Voltage-Gated Calcium Channels: Structure, Function, and Dysfunction , 2014, Neuron.

[10]  V. Jevtovic-Todorovic,et al.  Targeting of CaV3.2 T-type calcium channels in peripheral sensory neurons for the treatment of painful diabetic neuropathy , 2014, Pflügers Archiv - European Journal of Physiology.

[11]  C. Altier,et al.  Calcium-permeable ion channels in pain signaling. , 2014, Physiological reviews.

[12]  Seungkyu Lee.  Pharmacological Inhibition of Voltage-gated Ca2+ Channels for Chronic Pain Relief , 2013, Current neuropharmacology.

[13]  P. Barrett,et al.  Reversal of Neuropathic Pain in Diabetes by Targeting Glycosylation of Cav3.2 T-Type Calcium Channels , 2013, Diabetes.

[14]  R. Mason,et al.  Curcumin and its Derivatives: Their Application in Neuropharmacology and Neuroscience in the 21st Century , 2013, Current neuropharmacology.

[15]  C. Bladen,et al.  Surface expression and function of Cav3.2 T-type calcium channels are controlled by asparagine-linked glycosylation , 2013, Pflügers Archiv - European Journal of Physiology.

[16]  B. Shu,et al.  Upregulation of T-type Ca2+ Channels in Primary Sensory Neurons in Spinal Nerve Injury , 2013, Spine.

[17]  Xu Zhang,et al.  Activin C expressed in nociceptive afferent neurons is required for suppressing inflammatory pain. , 2012, Brain : a journal of neurology.

[18]  三浦 真由美.  Peripheral sensitization caused by insulin-like growth factor 1 contributes to pain hypersensitivity after tissue injury , 2012 .

[19]  V. Jevtovic-Todorovic,et al.  T‐type voltage‐gated calcium channels as targets for the development of novel pain therapies , 2011, British journal of pharmacology.

[20]  M. Sekiguchi,et al.  Localization and Function of Insulin-like Growth Factor 1 in Dorsal Root Ganglia in a Rat Disc Herniation Model , 2011, Spine.

[21]  Ya-Ting Chang,et al.  Cav3.2 T-Type Ca2+ Channel-Dependent Activation of ERK in Paraventricular Thalamus Modulates Acid-Induced Chronic Muscle Pain , 2010, The Journal of Neuroscience.

[22]  Shiyuan Xu,et al.  The Roles of T-Type Calcium Channel in the Development of Neuropathic Pain following Chronic Compression of Rat Dorsal Root Ganglia , 2010, Pharmacology.

[23]  A. Eschalier,et al.  T-Type Calcium Channel Inhibition Underlies the Analgesic Effects of the Endogenous Lipoamino Acids , 2009, The Journal of Neuroscience.

[24]  M. Sekiguchi,et al.  Gene Expression Changes in Dorsal Root Ganglion of Rat Experimental Lumber Disc Herniation Models , 2008, Spine.

[25]  V. Jevtovic-Todorovic,et al.  Upregulation of the T-type calcium current in small rat sensory neurons after chronic constrictive injury of the sciatic nerve. , 2008, Journal of neurophysiology.

[26]  K. Campbell,et al.  Attenuated pain responses in mice lacking CaV3.2 T‐type channels , 2007, Genes, brain, and behavior.

[27]  D. Bayliss,et al.  Cell-Specific Alterations of T-Type Calcium Current in Painful Diabetic Neuropathy Enhance Excitability of Sensory Neurons , 2007, The Journal of Neuroscience.

[28]  Patrick Delmas,et al.  Pharmacological Dissection and Distribution of NaN/Nav1.9, T-type Ca2+ Currents, and Mechanically Activated Cation Currents in Different Populations of DRG Neurons , 2007, The Journal of general physiology.

[29]  S. Todorovic,et al.  Is there a role for T-type calcium channels in peripheral and central pain sensitization? , 2006, Molecular Neurobiology.

[30]  B. A. Forshee.  The aging brain: is function dependent on growth hormone/insulin-like growth factor-1 signaling? , 2006, AGE.

[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]  C. Pierson,et al.  Insulin Deficiency Rather than Hyperglycemia Accounts for Impaired Neurotrophic Responses and Nerve Fiber Regeneration in Type 1 Diabetic Neuropathy , 2003, Journal of neuropathology and experimental neurology.

[33]  S. Waxman,et al.  Preferential expression of IGF-I in small DRG neurons and down-regulation following injury , 2002, Neuroreport.

[34]  Michael Nilsson,et al.  Insulin-like growth factor-I and neurogenesis in the adult mammalian brain. , 2002, Brain research. Developmental brain research.