Publications

Scholarly Journals--Published

  • N-Acetyl Neuraminic Acid (NANA) Activates L-Type Calcium Channels on Isolated Tentacle Supporting Cells of the Sea Anemone (Aiptasia pallida). Ozacmak VH, Arrieta AR, Thorington GU, Hessinger DA.Biol Bull. 2021 Oct;241(2):196-207. doi: 10.1086/715844. Epub 2021 Sep 22.PMID: 34706210 Abstract: Sensory receptors control nematocyst discharge on sea anemone tentacles. Micromolar N-acetylated sugars (e.g., N-acetyl neuraminic acid [NANA]) bind chemoreceptors on ectodermal supporting cells and predispose adjacent nematocyst discharge in response to mechanical contact via 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 Aiptasia pallida (also known as Exaiptasia diaphana). We, therefore, hypothesize that NANA activates calcium influx via L-type calcium channels. We demonstrate a dose-dependent, NANA-activated 45Ca influx into dissociated ectodermal cells isolated from A. pallida tentacles, with maximal influx occurring at desensitizing concentrations of NANA. The L-type calcium channel inhibitors nifedipine, diltiazem, methoxyverapamil, and cadmium blocked NANA-stimulated 45Ca influx. Elevated extracellular KCl levels dose-dependently increased nifedipine-sensitive 45Ca influx to implicate voltage-gated calcium channels. Forskolin, 8-bromo-cAMP, and the protein kinase A inhibitor H-8 affect NANA-stimulated calcium influx in a manner consistent with activated cAMP-dependent pathway involvement. Because NANA chemoreceptors localize to supporting cells of cnidocyte supporting cell complexes, NANA activation of 45Ca influx into isolated tentacle ectodermal cells suggests that L-type calcium channels and NANA chemoreceptors co-localize to supporting cells. Indeed, a fluorescent marker of L-type calcium channels localizes to the apical ectoderm adjacent to nematocysts of live tentacles. We conclude that supporting cell chemoreceptors activate co-localized L-type calcium channels via a cAMP-dependent mechanism in order to initiate desensitization. We suggest that pathway desensitization may conserve nematocysts from excessive discharge during prey capture. (11/2022)
  • V. Haktan Ozacmak, Aida Riccrdo Arrieta, Glyne U. Thorington, and David A. Hessinger. 2021. N-acetyl neuraminic acid (NANA) activates L-type calcium channels on isolated tentacle supporting cells of the sea anemone (Aiptasia pallida). The Biological Bulletin 241:196-207. Abstract.  Sensory receptors control nematocyst discharge on sea anemone tentacles.  Micromolar N-acetylated sugars (e.g. N-acetyl neuraminic acid, NANA) bind chemoreceptors on ectodermal supporting cells and predispose adjacent nematocyst discharge in response to mechanical contact via a 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, Aiptasia pallida (aka Exaiptasia diaphana). We, therefore, hypothesize that NANA activates calcium influx via L-type calcium channels.  We demonstrate a dose-dependent, NANA-activated 45Ca influx into dissociated ectodermal cells isolated from A. pallida tentacles with maximal influx occurring at desensitizing concentrations of NANA.  L-type calcium channel inhibitors, nifedipine, diltiazem, methoxyverapamil, and cadmium, blocked NANA-stimulated 45Ca influx.  Elevated extracellular KCl levels dose-dependently increased nifedipine-sensitive 45Ca influx to implicate voltage-gated, calcium channels. Forskolin, 8-bromo-cAMP, and the protein kinase A inhibitor, H-8, affect NANA-stimulated calcium influx in a manner consistent with activated cAMP-dependent pathway involvement. Because NANA chemoreceptors localize to supporting cells of cnidocyte supporting cell complexes, NANA activation of 45Ca influx into isolated tentacle ectodermal cells suggests that L-type calcium channels and NANA chemoreceptors co-localize to supporting cells.  Indeed, a fluorescent marker of L-type calcium channels localizes to the apical ectoderm adjacent to nematocysts of live tentacles. We conclude that supporting cell chemoreceptors activate co-localized L-type calcium channels via a cAMP-dependent mechanism in order to initiate desensitization. We suggest that pathway desensitization may conserve nematocyst from excessive discharge during prey capture. (11/2022) (link)
  • Alice Nam, Selorm Quarshe, Matthew Kimble, and David A. Hessinger (2022). Functional characterization of TRPV-like ion channels involved in nematocyst discharge from the sea anemone, Diadumene lineata. Biol Bull. 2021 Oct;241(2):196-207. doi: 10.1086/715844. Epub 2021 Sep 22. PMID: 34706210 Abstract: Cnidarians 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. We therefore tested various transient receptor potential channel inhibitors to determine whether they inhibit nematocyst discharge and prey killing in the acontiate sea anemone (Actinaria) Diadumene lineata (a.k.a. Haliplanella luciae). Three types of cnidocyte supporting cell complexes regulate nematocyst discharge in anemones: Types C, B, and A. Discharge from Type Cs is directly triggered by stimulation of contact-sensitive mechanoreceptors, while Type Bs require activation of chemoreceptors from prey-derived N-acetylated sugars to sensitize contact-sensitive mechanoreceptors. In Type As, activated chemoreceptors tune vibration-sensitive mechanoreceptors that predispose contact-sensitive mechanoreceptors for triggering. The non-selective transient receptor potential channel blockers lanthanum and gadolinium dose-dependently inhibited about 80% of prey killing and all nematocyst discharge from Type Bs and Type Cs, but not Type As. The selective transient receptor potential vanilloid 4 (TRPV4) blocker GSK2193874 inhibited Type As and Type Bs. However, the selective TRPV4 blockers HC-067047 and RN-1734 inhibited only Type As. Thus, three TRPV4-selective blockers implicate TRPV-like involvement in discharge from Type As, whereas GSK2193874 also affected Type Bs. Our results suggest that a TRPV-like homolog plays an essential role in nematocyst-mediated prey killing from Type As, whereas other transient receptor potential channels are likely involved in discharge from Type B and C cnidocyte supporting cell complexes. (06/2022) (link)
  • Lin, M.T., D. A. Hessinger, W. J. Pearce, and L. D. Longo, . "Modulation of BK channel calcium affinity by differential phosphorylation in developing ovine basilar artery myocytes. ." Am. J. Physiol., Heart Circ. Physiol. 291. (2006): H732-H740. (01/2006)
  • M.T. Lin, L.D. Longo, W.J. Pearce, and D.A. Hesisnger. "Ca2+-activated K+ channel-associated phosphatase and kinase activities during development." Am J Physiol Heart Circ Physiol 289. (2005): H414-H425. (02/2005)
  • Lin, M.T., L. D. Longo, W. J. Pearce, and D. A. Hessinger. . "Ca2+-activated K+ channel-associated phosphatase and kinase activites during development. ." Am. J. Physiol., Heart Circ. Physiol. 289. (2005): H1-H12. (01/2005)
  • Lin, M.T., D. A. Hessinger, W. J. Pearce, and L. D. Longo. "Modulation of BK channel calcium affinity by differential phosphorylation in developing ovine basilar artery myocytes. ." Am. J. Physiol., Heart Circ. Physiol. . (): -.

Scholarly Journals--Accepted

  • Alice Nam, Selorm Quarshe, Matthew Kimble, and David A. Hessinger. 2022. Functional characterixation of TRPV-like ion channels involved in nematocyst discharge from the sea anemone, Diadumene lineata. The Biological Bulletin, accepted ms# 21057. Abstract. Cnidarians require mechanical stimuli to trigger nematocyst discharge and initiate feeding behaviors. The interval from triggering stimulus to response is tens of msec, making it likely that mechanically-gated ion channels trigger nematocyst discharge. Because many transient receptor potential (TRP) channels are mechanically gated, we hypothesized that nematocyst discharge involves TRP channels. We, therefore, tested various TRP channel inhibitors to determine if they inhibit nematocyst discharge and prey killing in aconitate sea anemones (Actinaria), Diadumene lineata (aka Haliplanella luciae).  Three types of cnidocyte supporting cell complexes (CSCCs) regulate nematocyst discharge in anemones: Types C, B, and A. Discharge from Type Cs is directly triggered by stimulation of contact-sensitive mechanoreceptors (CSMs), while Type Bs require activation of chemoreceptors from prey-derived N-acetylated sugars to sensitize CSMs. In Type As, activated chemoreceptors tune vibration-sensitive mechanoreceptors (VSMs) that predispose CSMs for triggering. The non-selective TRP channel blockers, lanthanum (La3+) and gadolinium (Gd3+) dose-dependently inhibited about 80% of prey killing and all nematocyst discharge from Type Bs and Type Cs, but not Type As. The selective TRPV4 blocker, GSK2193874, inhibited Type As and Type Bs.  However, selective TRPV4 blockers, HC-067047 and RN-1734, inhibited only Type As. Thus, three TRPV4-selective blockers implicate TRPV4-like involvement in discharge from Type As, whereas GSK2193874 also affected Type Bs.  Our results suggest that a TRPV4 homolog plays an essential role in nematocyst-mediated prey killing from Type As, whereas other TRP channels are likely involved in discharge from Type B and C CSCCs. (11/2022)
  • Alice Nam, Selorm Quarshe, Matthew Kimble, and David A. Hessinger. 2022. Functional characterixation of TRPV-like ion channels involved in nematocyst discharge from the sea anemone, Diadumene lineata. The Biological Bulletin, accepted ms# 21057. Abstract. Cnidarians require mechanical stimuli to trigger nematocyst discharge and initiate feeding behaviors. The interval from triggering stimulus to response is tens of msec, making it likely that mechanically-gated ion channels trigger nematocyst discharge. Because many transient receptor potential (TRP) channels are mechanically gated, we hypothesized that nematocyst discharge involves TRP channels. We, therefore, tested various TRP channel inhibitors to determine if they inhibit nematocyst discharge and prey killing in aconitate sea anemones (Actinaria), Diadumene lineata (aka Haliplanella luciae).  Three types of cnidocyte supporting cell complexes (CSCCs) regulate nematocyst discharge in anemones: Types C, B, and A. Discharge from Type Cs is directly triggered by stimulation of contact-sensitive mechanoreceptors (CSMs), while Type Bs require activation of chemoreceptors from prey-derived N-acetylated sugars to sensitize CSMs. In Type As, activated chemoreceptors tune vibration-sensitive mechanoreceptors (VSMs) that predispose CSMs for triggering. The non-selective TRP channel blockers, lanthanum (La3+) and gadolinium (Gd3+) dose-dependently inhibited about 80% of prey killing and all nematocyst discharge from Type Bs and Type Cs, but not Type As. The selective TRPV4 blocker, GSK2193874, inhibited Type As and Type Bs.  However, selective TRPV4 blockers, HC-067047 and RN-1734, inhibited only Type As. Thus, three TRPV4-selective blockers implicate TRPV4-like involvement in discharge from Type As, whereas GSK2193874 also affected Type Bs.  Our results suggest that a TRPV4 homolog plays an essential role in nematocyst-mediated prey killing from Type As, whereas other TRP channels are likely involved in discharge from Type B and C CSCCs. (06/2021)

Abstract

  • David Hessinger (02/2022)
  • (PEER REVIEWED) Pooja Mujumdar1, Anthony Firek~, Penelope Duerksen-Hughes*, David Hessinger? . "Effect of Endurance Exercise on Blood Lipids and Adipokines." Basic Sciences Research Symposium . (2006): -. (09/2006)
  • (PEER REVIEWED) G Thorington1, X Tao2, W Fletcher3, L Longo1,4, and D Hessinger1. . "Expression of BK channel subunits during development in ovine pulmonary artery smooth muscle." Basic Science Research Symposium . (2006): -. (09/2006)
  • (PEER REVIEWED) M.T. Lin, L.D. Longo, and D.A. Hesisnger. "Developmental regulation of BK channel activity during long-term ." FASEB Journal . (1900): -. (01/1900)