Nonselective Cation Channels

Modulation of calcium‐activated non‐selective cation channel activity by nitric oxide in rat brown adipose tissue.

“…In the intact brown fat cells, the degree of channel blockade would depend on the balance between the amount of nitric oxide present and the redox potential of the cytosol. As nitric oxide is produced in a variety of tissues from L-arginine by nitric oxide synthases (Moncada, Palmer & Higgs, 1991;Knowles & Moncada, 1994), and as calcium-activated nonselective cation channels have been demonstrated in several different tissues (Partridge & Swandulla, 1988;Siemen & Hescheler, 1993), including smooth muscle (Wang, Hogg & Large, 1993), our results could have more general significance.…”

“…Since then, non-selective cation channels have been described in a wide variety of species and cells (Partridge & Swandulla, 1988;Siemen & Hescheler, 1993), including brown fat cells (Siemen & Reuhl, 1987). The function of this channel in brown adipose tissue is not well known but it may explain (Siemen & Reuhl, 1987) the longlasting depolarization observed during adrenergic stimulation of the tissue (Girardier, Seydoux & Clausen, 1968;Lucero & Pappone, 1990).…”

Somato-dendritic mechanisms underlying the electrophysiological properties of hypothalamic magnocellular neuroendocrine cells: A multicompartmental model study

“…On the other hand, there are several lines of evidence that support the role of a CAN current in mediating the DAP. CAN channels exist in the membranes of a variety of mammalian cells, both excitable and non-excitable, and support important cellular responses such as neuronal bursting, secretion, and cardiac rhythmicity (Siemen 1993;Thorn and Petersen 1993;Partridge et al 1994;Teulon 2000). For example, CAN channels take part in plateau potential generation and persistent spiking in entorhinal cortex neurons (Egorov et al 2002), in DAPs in myenteric neurons (Vogalis et al 2002), and in after-depolarization and burst after discharge in rat neocortical neurons (Kang et al 1998;Aoyagi et al 2002).…”

Corticotropin-releasing hormone excites adrenocorticotropin-secreting human pituitary adenoma cells by activating a nonselective cation current.

“…Because CRH increased [Ca 2ϩ ] i of these ACTH-secreting adenoma cells, it is possible that the CRH-induced cation current is one of the Ca 2ϩ -activated cation currents. To investigate this, we loaded the cell with cell-permeable Ca 2ϩ chelator, BAPTA/AM, to clamp the [Ca 2ϩ ] i lower than 100 nm, at which Ca 2ϩ -activated cation currents are activated (18). Finally, it reached ‫ف‬ 30 nM at 100 min.…”