Format
Sort by

Send to

Choose Destination

Links from PubMed

Items: 1 to 20 of 177

1.

Ca²⁺-dependent regulation of Ca²⁺ currents in rat primary afferent neurons: role of CaMKII and the effect of injury.

Tang Q, Bangaru ML, Kostic S, Pan B, Wu HE, Koopmeiners AS, Yu H, Fischer GJ, McCallum JB, Kwok WM, Hudmon A, Hogan QH.

J Neurosci. 2012 Aug 22;32(34):11737-49. doi: 10.1523/JNEUROSCI.0983-12.2012.

3.

Regulation of voltage-gated Ca(2+) currents by Ca(2+)/calmodulin-dependent protein kinase II in resting sensory neurons.

Kostic S, Pan B, Guo Y, Yu H, Sapunar D, Kwok WM, Hudmon A, Wu HE, Hogan QH.

Mol Cell Neurosci. 2014 Sep;62:10-8. doi: 10.1016/j.mcn.2014.07.004. Epub 2014 Jul 24.

4.

Contribution of calcium channel subtypes to the intracellular calcium signal in sensory neurons: the effect of injury.

Fuchs A, Rigaud M, Sarantopoulos CD, Filip P, Hogan QH.

Anesthesiology. 2007 Jul;107(1):117-27.

5.

Modulators of calcium influx regulate membrane excitability in rat dorsal root ganglion neurons.

Lirk P, Poroli M, Rigaud M, Fuchs A, Fillip P, Huang CY, Ljubkovic M, Sapunar D, Hogan Q.

Anesth Analg. 2008 Aug;107(2):673-85. doi: 10.1213/ane.0b013e31817b7a73.

6.
7.

Intracellular Ca2+ release-dependent inactivation of Ca2+ currents in thalamocortical relay neurons.

Rankovic V, Ehling P, Coulon P, Landgraf P, Kreutz MR, Munsch T, Budde T.

Eur J Neurosci. 2010 Feb;31(3):439-49. doi: 10.1111/j.1460-9568.2010.07081.x. Epub 2010 Jan 25.

PMID:
20105233
8.

Opposing effects of spinal nerve ligation on calcium-activated potassium currents in axotomized and adjacent mammalian primary afferent neurons.

Sarantopoulos CD, McCallum JB, Rigaud M, Fuchs A, Kwok WM, Hogan QH.

Brain Res. 2007 Feb 9;1132(1):84-99. Epub 2006 Dec 20.

9.

Sinoatrial node pacemaker activity requires Ca(2+)/calmodulin-dependent protein kinase II activation.

Vinogradova TM, Zhou YY, Bogdanov KY, Yang D, Kuschel M, Cheng H, Xiao RP.

Circ Res. 2000 Oct 27;87(9):760-7.

10.
11.

Distinct roles of CaM and Ca(2+)/CaM -dependent protein kinase II in Ca(2+) -dependent facilitation and inactivation of cardiac L-type Ca(2+) channels.

Nie HG, Hao LY, Xu JJ, Minobe E, Kameyama A, Kameyama M.

J Physiol Sci. 2007 Jun;57(3):167-73. Epub 2007 May 22.

PMID:
17511897
12.
13.

Suppressed Ca2+/CaM/CaMKII-dependent K(ATP) channel activity in primary afferent neurons mediates hyperalgesia after axotomy.

Kawano T, Zoga V, Gemes G, McCallum JB, Wu HE, Pravdic D, Liang MY, Kwok WM, Hogan Q, Sarantopoulos C.

Proc Natl Acad Sci U S A. 2009 May 26;106(21):8725-30. doi: 10.1073/pnas.0901815106. Epub 2009 May 13.

14.

The modulation of the excitability of primary sensory neurons by Ca²⁺-CaM-CaMKII pathway.

Liang R, Liu X, Wei L, Wang W, Zheng P, Yan X, Zhao Y, Liu L, Cao X.

Neurol Sci. 2012 Oct;33(5):1083-93. doi: 10.1007/s10072-011-0907-7. Epub 2011 Dec 29.

PMID:
22205399
15.

Gabapentin decreases membrane calcium currents in injured as well as in control mammalian primary afferent neurons.

Sarantopoulos C, McCallum B, Kwok WM, Hogan Q.

Reg Anesth Pain Med. 2002 Jan-Feb;27(1):47-57.

PMID:
11799505
16.
17.

Modulation by oxytocin of ATP-activated currents in rat dorsal root ganglion neurons.

Yang Q, Wu ZZ, Li X, Li ZW, Wei JB, Hu QS.

Neuropharmacology. 2002 Oct;43(5):910-6.

PMID:
12384176
18.

Activation of CaMKII and ERK1/2 contributes to the time-dependent potentiation of Ca2+ response elicited by repeated application of capsaicin in rat DRG neurons.

Zhang X, Daugherty SL, de Groat WC.

Am J Physiol Regul Integr Comp Physiol. 2011 Mar;300(3):R644-54. doi: 10.1152/ajpregu.00672.2010. Epub 2010 Dec 22.

19.

Modulation of IA currents by capsaicin in rat trigeminal ganglion neurons.

Liu L, Simon SA.

J Neurophysiol. 2003 Mar;89(3):1387-401.

20.

Distinct inhibition of voltage-activated Ca2+ channels by delta-opioid agonists in dorsal root ganglion neurons devoid of functional T-type Ca2+ currents.

Wu ZZ, Chen SR, Pan HL.

Neuroscience. 2008 Jun 2;153(4):1256-67. doi: 10.1016/j.neuroscience.2008.03.031. Epub 2008 Mar 22.

PMID:
18434033
Items per page

Supplemental Content

Write to the Help Desk