Ether anesthetics prevents touch‐induced trigger hair calcium‐electrical signals excite the Venus flytrap

Ether anesthetics prevents touch‐induced trigger hair calcium‐electrical signals excite the Venus flytrap

Sönke Scherzer, Shouguang Huang, Anda Iosip, Ines Kreuzer, Ken Yokawa, Khaled A. S. AL‐Rasheid, Manfred Heckmann and Rainer Hedrich

Scientific Reports volume 12, Article number: 2851 (2022) 

Plants do not have neurons but operate transmembrane ion channels and can get electrical excited by physical and chemical clues. Among them the Venus flytrap is characterized by its peculiar hapto-electric signaling. When insects collide with trigger hairs emerging the trap inner surface, the mechanical stimulus within the mechanosensory organ is translated into a calcium signal and an action potential (AP). Here we asked how the Ca²⁺ wave and AP is initiated in the trigger hair and how it is feed into systemic trap calcium-electrical networks. When Dionaea muscipula trigger hairs matures and develop hapto-electric excitability the mechanosensitive anion channel DmMSL10/FLYC1 and voltage dependent SKOR type Shaker K⁺ channel are expressed in the sheering stress sensitive podium. The podium of the trigger hair is interface to the flytrap’s prey capture and processing networks. In the excitable state touch stimulation of the trigger hair evokes a rise in the podium Ca²⁺ first and before the calcium signal together with an action potential travel all over the trap surface. In search for podium ion channels and pumps mediating touch induced Ca²⁺ transients, we, in mature trigger hairs firing fast Ca²⁺ signals and APs, found OSCA1.7 and GLR3.6 type Ca²⁺ channels and ACA2/10 Ca²⁺ pumps specifically expressed in the podium. Like trigger hair stimulation, glutamate application to the trap directly evoked a propagating Ca²⁺ and electrical event. Given that anesthetics affect K⁺ channels and glutamate receptors in the animal system we exposed flytraps to an ether atmosphere. As result propagation of touch and glutamate induced Ca²⁺ and AP long-distance signaling got suppressed, while the trap completely recovered excitability when ether was replaced by fresh air. In line with ether targeting a calcium channel addressing a Ca²⁺ activated anion channel the AP amplitude declined before the electrical signal ceased completely. Ether in the mechanosensory organ did neither prevent the touch induction of a calcium signal nor this post stimulus decay. This finding indicates that ether prevents the touch activated, glr3.6 expressing base of the trigger hair to excite the capture organ.

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