ABSTRACT
Blind cave fish use the lateral line sensory system to detect nearby objects. The fish responds to sudden perturbations in the water column by initiating startle responses in which they swim more rapidly. Normal startle responses disappear after trauma caused by a single 15 s immersion in calcium free water, but return within 5 days if the traumatized fish are treated with 'repair proteins' isolated from sea anemones. Polyclonal antibodies raised to fraction beta, a specific chromatographic fraction of repair proteins, bind to hair cells within superficial neuromasts. Likewise, biotinylated fraction beta binds to hair cells in neuromasts. Neuromast hair cells exposed to calcium free water followed by repair proteins have more compact hair bundles than do hair cells exposed only to calcium free water. We propose that anemone repair proteins replace linkages between stereocilia destroyed by exposure to calcium free water.
Subject(s)
Fishes/physiology , Mechanoreceptors/drug effects , Mechanoreceptors/physiology , Proteins/isolation & purification , Proteins/pharmacology , Sea Anemones/chemistry , Animals , Avidin/metabolism , Blindness/physiopathology , Hair Cells, Auditory/drug effects , Hair Cells, Auditory/physiology , Hair Cells, Auditory/ultrastructure , Immunohistochemistry , Mechanoreceptors/ultrastructure , Microscopy, Electron, Scanning , Reflex, Startle/drug effects , Reflex, Startle/physiology , Regeneration/drug effectsABSTRACT
Hair bundle mechanoreceptors of sea anemones are similar to those of the acousticolateralis system of vertebrates (Watson, Mire and Hudson, 1997, Hear. Res. 107, 53-63). Anemone hair bundles are repaired by 'repair proteins' secreted following a complete loss of structural integrity and loss of function caused by 1 h exposure to calcium free seawater. Exogenously supplied repair proteins (RP) restore structural integrity to hair bundles and restore vibration sensitivity in 7-8 min (Watson, Mire and Hudson, 1998, Hear. Res. 115, 119-128). We here report that exogenously supplied ATP enhances the rate by which RP restore vibration sensitivity. A bimodal dose response to ATP indicates maximal enhancement at picomolar and micromolar concentrations of ATP. At these concentrations of ATP, vibration sensitivity is restored in 2 min. These data suggest that at least two ATPases exhibiting different binding affinities for ATP are involved in the repair process. Whereas the higher affinity site is specific for ATP, the lower affinity site does not discriminate between ATP and ADP. Nucleotidase cytochemistry localizes ATPase activity in isolated repair proteins. In the absence of exogenously added RP, sea anemones secrete and consume ATP during the 4 h recovery period after 1 h exposure to calcium free seawater. In the presence of exogenously added RP, ATP is secreted and then consumed within 10 min. Quinacrine cytochemistry localizes possible stores of ATP in the apical cytoplasm of sensory neurons located at the center of the hair bundle. According to our model, ATP is secreted by the sensory neuron after its hair bundle loses structural integrity. Hydrolysis of ATP by repair proteins is essential to the repair process.
