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A New Theory on the Acquisition of Sperm Motility During Epididymal Transit
Published in Claude Gagnon, Controls of Sperm Motility, 2020
Dale D. Hoskins, S. Vijayaraghavan
The mechanism by which cyclic AMP levels are increased in developing sperm is unknown. Since the amount of cyclic AMP must be a consequence of the relative rates of synthesis and break down the amount of the nucleotide in developing sperm must be a function of the activities of cyclic AMP-phosphodiesterase (breakdown) and adenylate cyclase (synthesis). Efforts to document a role for either enzyme for elevating cyclic AMP levels in sperm during epididymal transit, have however, produced equivocal results. For example, we characterized the phosphodiesterase31 from bovine caput and caudal sperm with respect to kinetic properties, distribution between soluble and particulate forms, presence of multiple isozymes, and changes in activity during epididymal passage. From this effort we were only able to conclude that the external, particulate form of the enzyme might be involved in elevating cyclic AMP levels in developing sperm. From literature reports we similarly conclude that it is yet to be shown that adenylate cyclase activity is regulated in sperm during epididymal transit.
Mechanisms of Taste Transduction
Published in Robert H. Cagan, Neural Mechanisms in Taste, 2020
John H. Teeter, Robert H. Cagan
Many bitter tasting compounds inhibit cyclic AMP phosphodiesterase activity, which could result in a transient accumulation of cAMP in the cell.92,117–119 This second messenger could have a variety of effects, including modulation of specific ion channels in the taste cells.60
Chemical Carcinogenesis as a Consequence of Alterations in the Structure and Function of DNA
Published in Philip L. Grover, Chemical Carcinogens and DNA, 2019
Cyclic AMP has been postulated to mediate the activity of steroid hormones.98 Dixon-Shanies and Knittle,99 as well as Lee and Reed,100 have shown that certain steroid hormones affect the regulation of the levels of cyclic AMP in human lymphocytes. As mentioned previously, steroidal agents are known to inhibit tumor promotion by phorbol esters,80 as well as the production of plasminogen activator.82 Theophylline and papaverine (cyclic AMP phosphodiesterase inhibitors) increase cyclic AMP levels and depress the production of plasminogen activator.101 More direct evidence was provided by the report that the growth of two-hormone-dependent mammary tumors was inhibited by cyclic AMP. 102
Tacrine and its 7-methoxy derivate; time-change concentration in plasma and brain tissue and basic toxicological profile in rats
Published in Drug and Chemical Toxicology, 2021
Jana Zdarova Karasova, Ondrej Soukup, Jan Korabecny, Milos Hroch, Marketa Krejciova, Martina Hrabinova, Jan Misik, Ladislav Novotny, Vendula Hepnarova, Kamil Kuca
Moreover, nicotinic brain transmission is also altered in AD patient so nicotinic agonists are considered as one of the therapeutic approaches in the treatment of AD (Zhang et al. 2002). Among other mechanisms, presynaptic nicotinic receptors are able to modulate release of other neurotransmitters, for example, glutamate that plays significant role in learning and memory (Crismon 1994). The affinity of tacrine to nicotinic receptor is higher than affinity of 7-MEOTA (Cheffer and Ulrich 2011, Soukup et al. 2013). Interestingly, tacrine was reported to increase in number of brain nicotinic receptors, their potentiation at low and inhibition at high concentration, and overall potentiation of the neuromuscular transmission (Adem 1992, Szilagyi and Lau 1993, Wagstaff and McTavish 1994, Soares and Gershon 1995). Thus, pharmacodynamic profile of tacrine seems to be rather complex. Besides that, tacrine have also been reported to modulate other biological targets, for example, it inhibits cyclic AMP phosphodiesterase in neuromuscular junctions, blocks potassium channels, inhibits sodium channel inactivation, alters phosphorylation of proteins and stimulates glucose metabolism and insulin secretion (Albin et al. 1975, Freeman and Dawson 1991, Soares and Gershon 1995). Moreover, tacrine has been shown to inhibit the uptake and increases the release of 5-hydroxytryptamine, noradrenaline, dopamine and GABA, and blocks both monoamine oxidase subtypes (MAO-A and MAO-B) and the brain histamine-N-methyltransferase (Summers et al. 1986, Wagstaff and McTavish 1994, Davis and Powchick 1995). At high concentrations, tacrine interacts with adenosine receptors, inhibits potassium-evoked release of excitatory amino acids and blocks neuronal calcium ion channels (Wagstaff and McTavish 1994, Soares and Gershon 1995). Finally, tacrine was also identified as an inhibitor of the N-methyl-D-aspartate receptors (NMDARs) which play essential role in excitatory neurotransmission, long-term potentiation as well as in etiology of many neuropsychiatric diseases (Hershkowitz and Rogawski 1991, Horak et al. 2014).