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  • The enzyme mediated ATP sensing mechanism in zebrafish can b

    2024-04-02

    The enzyme-mediated ATP-sensing mechanism in zebrafish can be compared with previous studies in other animal species reporting that enzymatic conversion of chemicals in the peripheral olfactory organ results in either “activation” or “inactivation” of odorants and pheromones. In male silkmoth, the antenna-specific esterase is essential for rapid degradation and inactivation of pheromones during flight navigation through a pheromone plume [42, 43]. Similarly, in spiny lobsters, ATP and related nucleotides, but not adenosine, activate a subpopulation of OSNs, and those nucleotides are locally and rapidly inactivated by ecto-nucleotidase in the olfactory sensilla, which may facilitate the recovery and maintenance of sensitivity of OSNs [44]. In contrast, carbon dioxide, an aversive odorant, is converted into bicarbonate ion by carbonic anhydrase II in a specific subpopulation of mouse OSNs, which in turn activates a peculiar olfactory receptor, guanylyl cyclase-D [45, 46]. Although the conversion of carbon dioxide takes place within the Ethyl 3-Aminobenzoate methanesulfonate of OSNs, this enzyme-receptor machinery shares a common feature with the ATP-sensing mechanism in zebrafish. Thus, the active enzymatic conversion of odorants could be an evolutionarily conserved strategy for detecting particular odor cues that elicit innate behaviors crucial for their survival.
    STAR★Methods
    Author Contributions
    Acknowledgments We thank Y. Niimura (The University of Tokyo), H. Suzuki, and M. Nikaido (Tokyo Institute of Technology) for sharing the data of olfactory receptor sequences and helpful advice on phylogenetic tree construction; K. Mori (The University of Tokyo) for helpful discussion; K. Touhara (The University of Tokyo), K. Kawakami (National Institute of Genetics, Japan), and J. Nakai (Saitama University) for reagents; RIKEN BSI Research Resource Center for technical assistance; RIKEN BioResource Center for CHO-K1 cell line (RCB025); and members of Y.Y. laboratory for fish care and discussion. This work was supported in part by grants-in-aid for Scientific Research (20300117 to Y.Y.; 25430025 and 16K07018 to N.M.) and for Scientific Research on Innovative Areas “Memory Dynamism” (25115005 to Y.Y.) and “Fluorescence Live Imaging” (23113520 and 25113724 to N.M.) from the Ministry of Education, Culture, Sports, Science and Technology of Japan and by grants from the Human Frontier Science Program (HFSP RGP0015/2010 to Y.Y.), the Uehara Memorial Foundation (to Y.Y.), the Naito Foundation (to Y.Y.), the KAO Corporation (to Y.Y. and N.W.), and the JST ERATO Touhara Chemosensory Signal Project (JPMJER1202 to Y.Y. and M.M.).
    Introduction Cordycepin (3′-deoxyadenosine), first isolated from the fermented broth of medicinal mushroom Cordyceps militaris, is widely used as a traditional Chinese medicine and exhibits a variety of clinical effects such as immunomodulatory, antioxidant, anti-inflammatory and anti-microbial activities [1], [2], [3]. Cordycepin is deaminated quickly by adenosine deaminase and metabolized rapidly to an inactive metabolite, 3′-deoxyhypoxanthinosine in vivo. The half-life and bioavailability of cordycepin by oral administration are 2.1h and 19.2μmolh/L (area under concentration-time curve), respectively [4]. In recent studies, cordycepin has been reported to improve cognitive function in mice and protect against cell death induced by cerebral ischemia injury [5], [6]. Adenosine is mainly through its action on adenosine A1 receptor (A1R) and adenosine A2A receptor (A2AR) to control and integrate cognition and memory [7]. Adenosine deficiency is able to result in the impairment of synaptic plasticity [8], [9]. In the brain, A1R and A2AR are mainly located in synapses, controlling the release of neurotransmitters, such as glutamate (Glu) and acetylcholine (ACh) that are involved in memory and other cognitive processes [10]. Adenosine usually relies on a balance on the activation of inhibitory A1R and facilitatory A2AR [11]. The activation of A1R prevents neuronal damage [12], while the activation of A2AR plays an important effect on the associative learning process and its relevant hippocampal circuits [13]. Previous studies have shown that synaptic levels of adenosine could control synaptic transmission and plasticity by acting on synaptic A1R and A2AR [14], [15].