Calcium release from InsP₃‐sensitive internal stores initiates action potential in Chara

Abstract

Neomycin and U73122 are known to suppress inositol 1,4,5-trisphosphate (InsP3) production by inhibition of phospholipase C. We studied the effects of these inhibitors on the excitatory currents, Iex, in Chara corallina under voltage-clamp conditions. Computer simulations of the experimental effects by a minimum model for the excitatory reaction pathway allow the assignment of the inhibitory effects to one specific reaction step, i.e. the release of Ca2+ from InsP3-sensitive internal stores. In contrast, the inhibitory effect of La3+ on Iex suggests inactivation of Cl- channels. Furthermore, ryanodine-sensitive Ca2+ stores seem to be irrelevant for electrical excitation in Chara.

Ca2+ Dynamics during Membrane Excitation of Green Alga Chara: Model Simulations and Experimental Data

“…These findings suggested the involvement of a long-lived signaling molecule, which is produced in a voltage-dependent manner and is able to mobilize Ca 2+ internal stores. This interpretation is in good agreement with other experiments, which had already suggested from independent approaches that electrical excitation in Chara is due to a mobilization of Ca 2+ from internal stores , Thiel & Dityatev, 1998, and may be mediated by the second messenger inositol 1,4,5-trisphosphate (IP 3 ) (Thiel, MacRobbie & Henke, 1990;Biskup, Gradmann & Thiel, 1999;Wacke & Thiel, 2001).…”

“…These reveal that plants possess the key proteins and mechanisms for a stimulus-induced and IP 3 -mediated mobilization of Ca 2+ from internal stores (Sanders, Brownlee & Harper, 1999;Reddy, 2001). Also Chara cells most likely have such a signalling system, because it was shown that electrophoretic injection of IP 3 triggered membrane excitation (Thiel, MacRobbie & Hanke, 1990), while inhibition of phospholipase C abolished excitability of these cells (Biskup et al, 1999).…”

“…A large body of experimental evidence has precluded that voltage-dependent Ca 2+ influx via plasma membrane channels can be the primary source for the rise in Ca 2+ during excitation in Chara (Homann & Thiel, 1994;Thiel et al, 1997;Plieth et al 1998;Wacke & Thiel, 2001). The experimental data on the dynamics of ½Ca 2þ cyt as well as on the gating of the Ca 2+ -sensitive Cl À channels, which produce the depolarization of the action potential, can be best explained by a model in which a voltage-dependent production of a second messenger (Homann & Thiel, 1994;Thiel & Dityatev, 1998;Wacke & Thiel, 2001), most likely IP 3 (Thiel et al, 1990;Biskup et al, 1999), is triggering the release of Ca 2+ from internal stores. The above analysis of a combined model for voltagedependent production of such a second messenger and Ca 2+ mobilization from internal stores by IP 3 and Ca 2+ now allows successful simulation of the aforementioned body of experimental observations in the context of electrical excitation in plants.…”

Light- and dark-induced action potentials inPhyscomitrella patens

“…The source of Ca 2+ ions entering the cytoplasm in an early phase of the AP is still a matter of debate. Either external 41 or internal stores 42 are postulated as being responsible for Ca 2+ fluxes. Here, we show that lanthanum, a rather unspecific Ca 2+ channel blocker, completely inhibits APs in Physcomitrella cells.…”

Low-Temperature Induced Transmembrane Potential Changes in the Liverwort Conocephalum conicum

“…An essential mechanism for AP generation is the activation of the voltage-dependent ion channels. In plants, changes in ion permeability during APs are largely explained on the basis of a transient activation of Ca 2+ channel first, and Cl -channel next, both responsible for the depolarization phase of AP (Kourie 1994, Thiel and Dityatev 1998, Biskup et al 1999, Wacke and Thiel 2001.…”