Downregulation of voltage-gated sodium channels by dexamethasone in clonal rat pituitary cells

Ávila, Guillermo; Monjaraz, Eduardo; Espinosa, Juan Luis; Cota, Gabriel

doi:10.1016/s0304-3940(02)01460-x

Cited by 6 publications

(3 citation statements)

References 19 publications

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“…Glucocorticoids have been known to affect the expression of Na + -K + ATPase (Chalaka et al, 1999) and several ion channels such as K V 1.5, a non-inactivating K + current (Takimoto et al, 1993;Takimoto and Levitan, 1994). Dexamethasone has been also reported to downregulate voltage-gated Na + channel in clonal rat pituitary cells, by using patch-clamp techniques, and saxitoxin binding assay (Avila et al, 2003). In the present study, short-term application of dexamethasone did not affect I Na significantly.…”

Section: Discussioncontrasting

confidence: 38%

Effect of dexamethasone on voltage-gated Na+ channel in cultured human bronchial smooth muscle cells

Nakajima

Meguro

et al. 2008

Life Sciences

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Section: Discussioncontrasting

confidence: 38%

Effect of dexamethasone on voltage-gated Na+ channel in cultured human bronchial smooth muscle cells

Nakajima

Meguro

et al. 2008

Life Sciences

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“…Actions of dexamethasone on pulpal growth factors (Srisawasdi and Pavasant 2007;Chidiac et al 2008), arachidonic acid (Carattino et al 2003;Smith et al 2007), or direct actions on nerve cells (Supowit et al 1995) could also be important factors. In other studies, dexamethasone has been shown to decrease Na v 1.6 in pituitary cells in vitro on the basis of their reduced Na + conductance and caused an 80% reduction in Na v 1.6 in the cell membrane (Avila et al 2003).…”

Section: Discussionmentioning

confidence: 78%

Dexamethasone effects on Nav1.6 in tooth pulp, dental nerves, and alveolar osteoclasts of adult rats

2009

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Dexamethasone causes extensive physiologic reactions including the reduction of inflammation and pain. Here, we asked whether it also affected dental or periodontal cells or dental innervation by altering voltage-gated sodium channel Na(v)1.6 immunoreactivity (IR) or neural synaptophysin. Daily dexamethasone (0.2 mg/kg) given for 1 week to rats caused 12-fold increased intensity of Na(v)1.6-IR in dendritic pulpal cells of normal molars and incisors compared with vehicle treatment. These cells also co-localized monocyte (ED-1) or dendritic cell (CD11b/Ox42) markers, and their location in molars expanded during dexamethasone treatment to include deeper pulp. Furthermore, dexamethasone caused a 10-fold decrease in the number of Na(v)1.6-immunoreactive multinucleate osteoclasts along the alveolar bone of molar root sockets. No changes occurred for neural Na(v)1.6 at axonal nodes of Ranvier, even though IR for calcitonin gene-related peptide was greatly decreased, as expected, and neural synaptophysin-IR was decreased 59% by dexamethasone. At 4 days after tooth injury, pulpal vasodilation and increased Na(v)1.6-immunoreactive pulp cells were similar for all groups. Thus, dexamethasone changes dental pulp cell and alveolar osteoclast Na(v)1.6-IR in normal teeth, but different mechanisms occur after tooth injury when tissue reactions were similar for dexamethasone- and vehicle-treated rats. Steroid-induced alterations of dental pain and inflammation coincide with altered exocytic capability in dental nerve fibers as shown by synaptophysin-IR and with altered pulp cell Na(v)1.6-IR and osteoclast number, but not with any changes in Na(v)1.6-IR for nodes of Ranvier in myelinated dental axons.

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“…The TTX‐sensitive current has also been identified in rat (98,143,145), mouse (174), ovine (175,176) and fish (147,177) gonadotrophs, as well as in αT3‐1 mouse gonadotrophs (149,178). Rat lactotrophs (179,180), somatotrophs (98), corticotrophs (143) and GH 3 cells (181), as well as fish lactotrophs (182), also express Na v channels. In a fraction of ovine gonadotrophs (175) and bovine lactotrophs (183), the Na v channels are also responsible for AP generation.…”

Section: Voltage‐gated Sodium Channelsmentioning

confidence: 99%

Dependence of the Excitability of Pituitary Cells on Cyclic Nucleotides

Stojilković

Kretschmannova

Tomić

et al. 2012

J Neuroendocrinology

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Cyclic 3′,5′-adenosine monophosphate and cyclic 3′,5′-guanosine monophosphate are intracellular (second) messengers that are produced from the nucleotide triphosphates by a family of enzymes consisting of adenylyl and guanylyl cyclases. These enzymes are involved in a broad array of signal transduction pathways mediated by the cyclic nucleotide monophosphates and their kinases, which control multiple aspects of cell function through the phosphorylation of protein substrates. Here, we review the findings and working hypotheses on the role of the cyclic nucleotides and their kinases in the control of electrical activity of the endocrine pituitary cells and the plasma membrane channels involved in this process.

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Downregulation of voltage-gated sodium channels by dexamethasone in clonal rat pituitary cells

Cited by 6 publications

References 19 publications

Effect of dexamethasone on voltage-gated Na+ channel in cultured human bronchial smooth muscle cells

Effect of dexamethasone on voltage-gated Na+ channel in cultured human bronchial smooth muscle cells

Dexamethasone effects on Nav1.6 in tooth pulp, dental nerves, and alveolar osteoclasts of adult rats

Dependence of the Excitability of Pituitary Cells on Cyclic Nucleotides

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