Children with brain MRI abnormalities at the time of the diagnosis of optic neuritis have an increased risk of multiple sclerosis. Larger collaborative studies are needed to further define the prognosis for childhood optic neuritis.

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In cells expressing Ca 2؉ -mobilizing receptors, InsP 3 -induced Ca 2؉ release from intracellular stores is commonly associated with extracellular Ca 2؉ influx. Operation of these two Ca 2؉ signaling pathways mediates thyrotropin-releasing hormone (TRH) and angiotensin II (AII)-induced prolactin secretion from rat pituitary lactotrophs. After an initial hyperpolarization induced by Ca 2؉ mobilization from the endoplasmic reticulum (ER), these agonists generated an increase in the steadystate firing of action potentials, further facilitating extracellular Ca 2؉ influx and prolactin release. Like TRH and AII, endothelin-1 (ET-1) also induced a rapid release of Ca 2؉ from the ER and a concomitant spike prolactin secretion during the first 3-5 min of stimulation. However, unlike TRH and AII actions, Ca Typically, in anterior pituitary cells operated by calciummobilizing agonists, release of Ca 2ϩ from intracellular Ca 2ϩ stores is associated with extracellular Ca 2ϩ influx. The coordinate actions of these two pathways provide long-lasting Ca 2ϩ signals and secretion during sustained agonist stimulation (1).Endothelins (ETs) 1 are common calcium-mobilizing agonists for secretory pituitary cells and operate through ET A receptors (2, 3) coupled to phospholipase C-(4) but not phospholipase D-dependent signaling pathways (5). In lactotrophs, the ET-1-induced release of Ca 2ϩ from intracellular pools is associated with a rapid and transient increase in prolactin secretion (6, 7) followed by a prolonged inhibition to below basal levels (8). This bidirectional effect of a calcium-mobilizing agonist on secretion is uncommon among cells expressing phospholipase C-coupled receptors and is unique for cells expressing ET A receptors. The mechanism underlying the paradoxical action of ETs on hormone secretion is still unknown. It is unlikely that a rapid desensitization of ET A receptors could explain the inhibition of secretion observed in lactotrophs. Therefore, as the sustained phase in hormone secretion is affected in ET-1-stimulated lactotrophs, we addressed the alternate hypothesis that Ca 2ϩ influx is uncoupled from Ca 2ϩ mobilization in ET-1-stimulated lactotrophs, leading to depletion of the ER calcium pool and inhibition of hormone secretion.To test this hypothesis, rat pituitary lactotrophs were employed. These cells exhibit spontaneous, extracellular Ca 2ϩ -dependent action potential (AP) activity (9), which is tightly coupled to basal prolactin secretion (10). In addition to ET A receptors, lactotrophs express thyrotropin-releasing hormone (TRH) receptors (11), the calcium-mobilizing actions of which have been well characterized (12). Angiotensin II (AII) also stimulates prolactin release, presumably through activation of AT 1B receptors (13). Two calcium entry pathways are proposed to operate in lactotrophs: voltage-gated (VGCC) and store-operated (SOCC) calcium channels (12). Our results indicate that Ca 2ϩ influx through VGCC rather than through SOCC is essential for the sustained secretagogue actions of TRH and ...