BK Channels Function in Nematocyst Discharge from Vibration-Sensitive Cnidocyte Supporting Cell Complexes of the Sea Anemone .

AbstractIntegrated chemo- and mechanosensory pathways, along with activated calcium influxes, regulate nematocyst discharge from sea anemone tentacles. Discharge from vibration-sensitive Type A cnidocyte supporting cell complexes use calcium-conducting transient receptor potential V4-like channels. Because calcium influxes often couple with calcium-activated, large-conductance potassium (BK) channels, we hypothesized that BK channels function in nematocyst discharge.

Resting Membrane Potential Modulates Chemoreceptor Sensitivity in Nematocyst Discharge of the Sea Anemone .

AbstractExtracellular calcium has been known to be required for nematocyst discharge for more than 60 years, yet calcium's role in nematocyst discharge is poorly understood. Currently, we know that extracellular calcium plays at least two distinct roles in nematocyst discharge. First, calcium plays a role in the triggering of discharge by physical contact, most likely involving transient receptor potential channels.

Functional Characterization of TRPV-Like Ion Channels Involved in Nematocyst Discharge from the Sea Anemone .

AbstractCnidarians require mechanical stimuli to trigger nematocyst discharge and initiate feeding behaviors. The interval from triggering stimulus to response is tens of microseconds, making it likely that mechanically gated ion channels trigger nematocyst discharge. Because many transient receptor potential channels are mechanically gated, we hypothesized that nematocyst discharge involves transient receptor potential channels.

-Acetyl Neuraminic Acid (NANA) Activates L-Type Calcium Channels on Isolated Tentacle Supporting Cells of the Sea Anemone ().

AbstractSensory receptors control nematocyst discharge on sea anemone tentacles. Micromolar -acetylated sugars (, -acetyl neuraminic acid [NANA]) bind chemoreceptors on ectodermal supporting cells and predispose adjacent nematocyst discharge in response to mechanical contact a cyclic adenosine monophosphate (cAMP)-dependent sensitization pathway, while higher NANA levels dose-dependently desensitize. Recent evidence implicates L-type calcium channels in desensitizing the pathway in aconitate sea anemones (also known as ).

Cnidocyte Supporting Cell Complexes Regulate Nematocyst-Mediated Feeding Behaviors in the Sea Anemone .

AbstractCnidarians, as model animals for studying conserved feeding behavior, possess the simplest nervous and digestive systems. Feeding behavior in cnidarians begins with nematocyst-mediated prey retention, proceeds to coordinated tentacle movements and mouth opening, and then proceeds to release of retained prey for ingestion. Understanding the basis of nematocyst discharge, retention, and release is central to explaining cnidarian feeding.

Activated L-Type Calcium Channels Inhibit Chemosensitized Nematocyst Discharge from Sea Anemone Tentacles.

Because nematocyst discharge requires extracellular Ca, Ca channels have been suspected to be involved; but their identity and role have not been revealed. The majority of nematocysts that discharge from sea anemone tentacles are under the control of sensitizing chemoreceptors for -acetylated sugars (, -acetylneuraminic acid). Activated chemoreceptors predispose contact-sensitive mechanoreceptors to trigger discharge.

Long-term hypoxia increases calcium affinity of BK channels in ovine fetal and adult cerebral artery smooth muscle.

Acclimatization to high-altitude, long-term hypoxia (LTH) reportedly alters cerebral artery contraction-relaxation responses associated with changes in K(+) channel activity. We hypothesized that to maintain oxygenation during LTH, basilar arteries (BA) in the ovine adult and near-term fetus would show increased large-conductance Ca(2+) activated potassium (BK) channel activity. We measured BK channel activity, expression, and cell surface distribution by use of patch-clamp electrophysiology, flow cytometry, and confocal microscopy, respectively, in myocytes from normoxic control and LTH adult and near-term fetus BA.

Long-term, progressive, aerobic training increases adiponectin in middle-aged, overweight, untrained males and females.

Adipose tissue secretes the adipokine, adiponectin (ADPN), which increases insulin sensitivity. Because some of the metabolic effects of exercise and ADPN are similar, exercise has been proposed to increase ADPN. However, most short-term (≤3 mos) and constant-effort exercise protocols have not produced increases in ADPN.

Effects of satiation and starvation on nematocyst discharge, prey killing, and ingestion in two species of sea anemone.

Studies spanning 60 years with several cnidarian species show that satiation inhibits prey capture and ingestion and that starvation increases prey capture and ingestion. Most have attributed the effects of satiation to inhibition of nematocyst discharge. We hypothesized that satiation inhibits prey capture and ingestion in sea anemones (Haliplanella luciae and Aiptasia pallida) primarily by inhibiting the intrinsic adherence (i.

The role of nitric oxide in skin blood flow increases due to vibration in healthy adults and adults with type 2 diabetes.

Background: We recently demonstrated concomitant increases in skin blood flow and nitric oxide (NO) production in young healthy adults in response to externally applied vibration of the forearm. Research has shown that adults with type 2 diabetes exhibit depressed NO production and vascular responses to NO. We hypothesized that subjects with type 2 diabetes would display lower than normal increases in skin blood flow to externally applied vibration.

Modulation of BK channel calcium affinity by differential phosphorylation in developing ovine basilar artery myocytes.

Large-conductance Ca2+-sensitive K+ (BK) channel activity is greater in basilar artery smooth muscle cells (SMCs) of the fetus than the adult, and this increased activity is associated with a lower BK channel Ca2+ set point (Ca0). Associated PKG activity is three times greater in BK channels from fetal than adult myocytes, whereas associated PKA activity is three times greater in channels from adult than fetal myocytes. We hypothesized that the change in Ca0 during development results from different levels of channel phosphorylation.

Ca2+-activated K+ channel-associated phosphatase and kinase activities during development.

In ovine basilar arterial smooth muscle cells (SMCs), the fetal "big" Ca2+-activated K+ (BK) channel activity is significantly greater and has a lower Ca2+ setpoint than BK channels from adult cells. In the present study, we tested the hypothesis that these differences result from developmentally regulated phosphorylation of these channels. Using the patch-clamp technique and a novel in situ enzymological approach, we measured the rates and extents of changes in BK channel voltage activation from SMC inside-out patch preparations in response to selective activation and inhibition of channel-associated protein phosphatases and kinases (CAPAKs).

Developmental differences in Ca2+-activated K+ channel activity in ovine basilar artery.

A primary determinant of vascular smooth muscle (VSM) tone and contractility is the resting membrane potential, which, in turn, is influenced heavily by K+ channel activity. Previous studies from our laboratory and others have demonstrated differences in the contractility of cerebral arteries from near-term fetal and adult animals. To test the hypothesis that these contractility differences result from maturational changes in voltage-gated K+ channel function, we compared this function in VSM myocytes from adult and fetal sheep cerebral arteries.

Apparent membrane pore-formation by Portuguese Man-of-war (Physalia physalis) venom in intact cultured cells.

Intracellular, ratiometric microfluorimetry with fura-2 reveals that low doses of Portuguese Man-of-war (Physalia physalis) venom cause a linear increase in intracellular calcium accumulation by cultured L-929 cells. The influx of calcium is preceded by a lag period that is relatively independent of venom concentration, except at very low concentrations. Electron micrographs of negatively stained preparations of membranes from venom-treated L-929 and GH(4)C(1) cells exhibit 10-80 nm diameter lesions.