Sodium channel Nav1.6 is up-regulated in the dorsal root ganglia in a mouse model of type 2 diabetes

Highlights ► Nav1.6 is highly expressed in DRG large neurons. ► Type 2 diabetes induces persistent increase of Nav1.6 in the DRG. ► Mechanical allodynia in diabetic mice correlates with Nav1.6 increase.

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Bibliographische Detailangaben
Veröffentlicht in:	Brain research bulletin 2012-02, Vol.87 (2), p.244-249
Hauptverfasser:	Ren, Yan-Shun, Qian, Nian-Song, Tang, Yu, Liao, Yong-Hui, Yang, Yan-Ling, Dou, Ke-Feng, Toi, Masakazu
Format:	Artikel
Sprache:	eng
Schlagworte:	Age Factors Analysis of Variance Animals Blood Glucose - physiology Body Weight - physiology Diabetes Diabetes Mellitus, Type 2 - genetics Diabetes Mellitus, Type 2 - pathology Diabetes Mellitus, Type 2 - physiopathology Disease Models, Animal Dorsal root ganglion Ganglia, Spinal - metabolism Hyperalgesia - physiopathology Locomotion - physiology Mice Mice, Inbred C57BL Mice, Mutant Strains NAV1.6 Voltage-Gated Sodium Channel Nerve Tissue Proteins - genetics Nerve Tissue Proteins - metabolism Neurology Neuropathic pain Receptors, Mitogen - genetics RNA, Messenger - metabolism Sodium channel Nav1.6 Sodium Channels - genetics Sodium Channels - metabolism Up-Regulation - genetics Up-Regulation - physiology
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Beschreibung
Zusammenfassung:	Highlights ► Nav1.6 is highly expressed in DRG large neurons. ► Type 2 diabetes induces persistent increase of Nav1.6 in the DRG. ► Mechanical allodynia in diabetic mice correlates with Nav1.6 increase.
ISSN:	0361-9230 1873-2747
DOI:	10.1016/j.brainresbull.2011.10.015