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  Indian J Med Microbiol
 

Figure 1: Schematic representation of pathways believed of being involved in the regulation of mammalian sperm motility. Activation of a Na+/HCO3 (NBC) co-transporter and the regulation of HCO3/Cl by SLC26 transporters increase HCO3 levels.[167] The activation of the sperm Na+/H+ exchanger (sNHE) aligned with the activation of the proton channel (Hv1) leads to a raise of the pHi, which activates CatSper, a cation channel of sperm that enables the entry of Ca2+ and thus increases the internal Ca2+ concentration ([Ca2+]).[168] Progesterone, a steroid hormone synthesized by the cumulus/granulosa cells, activates CatSper either by binding to the channel itself or to an associated protein.[27] Further, albumin, the main protein of human blood plasma and oocyte glycoproteins, together with alkalinization of the sperm cytoplasm also, elevates the internal [Ca2+].[169],[170] The overall Ca2+ increase may influence glycolysis and the axoneme activity promoting hyperactivation of motility. [171] Further, HCO3 and Ca2+ regulate the atypical soluble adenylyl cyclase (sAC), which generates cAMP and that by its turn activates protein kinase A (PKA). PKA induces phosphorylation of axonemal dynein, leading to consumption of ATP and thus increases the pHi . PKA activates sperm tyrosine kinases (with serine and threonine residues) to trigger a cascade of protein phosphorylation involved in sperm motility.[24],[35],[47] Increased cAMP may activate PKA that in turn activates tyrosine kinase and seems to inhibit tyrosine phosphatase.[172] The Ca2+ levels are regulated by a plasma membrane Ca2+ -ATPase pump (PMCA4), expressed in the principal piece of the axoneme, which extrudes Ca2+ and is essential for hyperactivated motility and male fertility.[173]

Figure 1: Schematic representation of pathways believed of being involved in the regulation of mammalian sperm motility. Activation of a Na<sup>+</sup>/HCO<sub>3</sub><sup>−</sup> (NBC) co-transporter and the regulation of HCO<sub>3</sub><sup>−</sup>/Cl<sup>−</sup> by SLC26 transporters increase HCO<sub>3</sub><sup>−</sup> levels.<sup>[167]</sup> The activation of the sperm Na<sup>+</sup>/H<sup>+</sup> exchanger (sNHE) aligned with the activation of the proton channel (Hv1) leads to a raise of the pH<sub>i</sub>, which activates CatSper, a cation channel of sperm that enables the entry of Ca<sup>2+</sup> and thus increases the internal Ca<sup>2+</sup> concentration ([Ca<sup>2+</sup>]).<sup>[168]</sup> Progesterone, a steroid hormone synthesized by the cumulus/granulosa cells, activates CatSper either by binding to the channel itself or to an associated protein.<sup>[27]</sup> Further, albumin, the main protein of human blood plasma and oocyte glycoproteins, together with alkalinization of the sperm cytoplasm also, elevates the internal [Ca<sup>2+</sup>].<sup>[169],[170]</sup> The overall Ca<sup>2+</sup> increase may influence glycolysis and the axoneme activity promoting hyperactivation of motility. <sup>[171]</sup> Further, HCO<sub>3</sub><sup>−</sup> and Ca<sup>2+</sup> regulate the atypical soluble adenylyl cyclase (sAC), which generates cAMP and that by its turn activates protein kinase A (PKA). PKA induces phosphorylation of axonemal dynein, leading to consumption of ATP and thus increases the pHi</sub> . PKA activates sperm tyrosine kinases (with serine and threonine residues) to trigger a cascade of protein phosphorylation involved in sperm motility.<sup>[24],[35],[47]</sup> Increased cAMP may activate PKA that in turn activates tyrosine kinase and seems to inhibit tyrosine phosphatase.<sup>[172]</sup> The Ca<sup>2+</sup> levels are regulated by a plasma membrane Ca<sup>2+</sup> -ATPase pump (PMCA4), expressed in the principal piece of the axoneme, which extrudes Ca<sup>2+</sup> and is essential for hyperactivated motility and male fertility.<sup>[173]</sup>