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The cAMP/PKA Pathway Rapidly Activates SIRT1 to Promote Fatty Acid Oxidation Independently of Changes in NAD +. Treatment with an adenylyl cyclase activator (forskolin. PDE- resistant PKA Inhibitors; PDE. A copy of the certificate issued by the German T. Protein Kinase A-Mediated Synapsin I Phosphorylation Is a Central Modulator of Ca 2. The Calcium/CaMKKalpha/beta and the cAMP/PKA Pathways Are Essential Upstream Regulators of AMPK Activity in Boar Spermatozoa1. Compared with other dihydropyridines. DHPs), nifedipine has been reported to have relatively high incidence of neurologic adverse reactions, such as dizziness. DD/SE/Display. Drug/1,3. DVHName=Nifedipine). Nifedipine can easily cross the brain–blood barrier (1); thus, it may have a direct effect in the brain. The present report introduces a previously uncharacterized action of nifedipine. Nifedipine induces a profound increase in spontaneous glutamate release. This effect was unique to nifedipine and could not be mimicked by other DHPs; thus, its action. L- type calcium channels. Such synaptic activation in the central nervous system may underlie some. It is not yet clear what may be the role of spontaneous release for the function. Recent studies indicate that spontaneously released glutamate acts to maintain the postsynaptic dendritic. AMPA (. Spontaneous release can also have transient impact on the electrical activity of the postsynaptic cells (5). Although it has been considered to be a stochastic event, finding of possible physiological functions of spontaneous release. A number of secretagogues promote spontaneous transmitter release from. VDCCs). Although their mechanisms of action remain largely unknown, they have been found useful for investigation of transmitter. The present study suggests that nifedipine may be used as another agent for. The nifedipine effect was dose dependent, with EC5. A significant increase in spontaneous EPSC frequency could be detected with concentration as low as 1. M (2. 13. 7 . At 1. M, although the effect was statistically insignificant as a group (2. On washout of the agent, it took 5–2. Fig. Cells that showed recovery responded repeatedly to nifedipine. Most of these EPSCs were action potential- independent m. EPSCs. as shown by their insensitivity to tetrodotoxin (1 . These m. EPSCs were mediated by non- N- methyl- d- aspartate receptors because they were abolished by 6,7- dinitroquinoxaline- 2,3- dione (DNQX; 1. Nifedipine increased m. EPSCs (Middle), which were abolished by DNQX (Right). Numbers above each data point indicate number of cells. Dashed line, control; solid lines, in the presence of nifedipine or nifedipine. In addition, miniature inhibitory postsynaptic currents recorded in the SON were similarly. Contamination of nifedipine by its photodegraded product, 2- nitroso- pyridine. Nifedipine stock solution was left under. This procedure abolished the facilitatory effect of nifedipine (1. This finding may indicate both a pre- and postsynaptic effect. However, large miniature events may also occur if the spontaneous. If the amplitude increase was due to postsynaptic change, the peak of m. EPSC amplitude distribution should shift to the. The largest peak, however, remained the same with the distribution more. Fig. In control condition, m. EPSC amplitude distribution was best fitted by one to three Gaussian curves, with mean smallest. In the presence of nifedipine, two to four. Gaussian curves could be best fitted to m. EPSC amplitude distribution, with mean smallest peak amplitude of 1. Thus, the apparent increase in mean amplitude may reflect multiquantal release. Another possibility is an increase. Scaled and superimposed traces (Right) show that the time course of the events has not changed. However, no detectable change was observed in m. EPSC kinetics, i. Fig. In addition, in contrast to the amplitude increase in m. EPSCs, current induced by brief application of AMPA was decreased. Such change was considered to be due to an effect on postsynaptic L- type calcium channels, because nicardipine had. AMPA currents (7. Therefore, it is unlikely that changes in kinetics or numbers of AMPA receptors underlie the increase in m. EPSC amplitude. or could be responsible for increased frequency due to altered ability to detect more events. Because the m. EPSC frequency is a sensitive measure of presynaptic modulation, the remainder of the study. EPSCs. The following compounds that are known to bind to L- type channels were. EPSCs: nimodipine (2. A); Bay K 8. 64. 4, a DHP that activates L- type channels (1. B, none of these L- type calcium channel modulators had a significant effect on the amplitude (Fig. B) or frequency (Fig. C) of m. EPSCs (P > 0. Interestingly, when the slice was pretreated with nicardipine (1. This result suggests that nifedipine acts on a site distinct to a conventional DHP binding site to induce this unique. This effect was mimicked by BK or SK channel blockers (1. Although, in the present study, other L- type channel modulators failed to induce an effect similar to nifedipine, the possibility. SON. Subclasses. of L- type channels showing different sensitivities to different DHPs have been reported (1. However, such a mechanism cannot explain the effect observed in the SON because direct blockade of BK or SK by their specific. M, 1. 25. 2 . For example, nifedipine is known to interact with the adenosine system by acting as an antagonist to its receptor and/or. It is possible that the massive increase in m. EPSC frequency induced by nifedipine is due to disinhibition of inhibitory. In that case, blocking endogenous adenosine by an antagonist should mimic the nifedipine effect. However, an adenosine. SPT; 1. 0 . To examine whether NO mediates the effect of nifedipine, an NO synthase inhibitor, NG- nitro- l- arginine methyl ester (l- NAME) was tested. Application of l- NAME (1. In addition, a NO donor, sodium nitroprusside (1. All these results show that none of the above previously known effects of nifedipine. Thus, one possible explanation of the nifedipine effect is that intraterminal calcium concentration is elevated. Major. sources of intraterminal calcium elevation are extracellular calcium through VDCCs and release from intracellular stores. To perform a paired test, Cd. EPSCs (9. 1. 6 . 4. C) whereas it completely blocked evoked EPSCs. This result indicates that these events are independent of calcium influx through. VDCCs, and also strengthens our contention that the nifedipine action is not via L- type channels. In these cells, nifedipine was applied first. Thaps, thapsigargin; Nifed, nifedipine. Nifedipine. was capable of inducing m. EPSCs in the presence of thapsigargin (n = 3, Fig. In addition, thapsigargin had no effect in reversing nifedipine- induced m. EPSCs (1. 00. 3 . B), excluding these stores as a major source of calcium for the nifedipine effect. This result contrasts with a report describing. DHPs to induce calcium release from internal stores in skeletal muscles (2. To further elucidate the involvement of intracellular calcium, BAPTA- AM (2. It took 7–2. 6 min to reach its maximum. EPSCs by 6. 8. 3 . This result of partial reduction of evoked transmitter release by BAPTA- AM is similar to other reports (2. In contrast to its effect on evoked EPSCs, BAPTA- AM induced only a slight, statistically insignificant reduction of the. EPSCs induced by nifedipine (8. Nifedipine was also able to induce increase in m. EPSCs in the presence of BAPTA- AM (n = 2, Fig. Taken together, our result indicated that the nifedipine effect is largely calcium independent. The slices were pretreated with a PKA. H8. 9, 2. 0 . In contrast, H8. PKA activator, forskolin (1. Similarly, application of PKC inhibitors calphostin C (0. However, calphostin C was effective in blocking the facilitation of m. EPSCs by a phorbor ester, phorbol 1. M; Fig. Nifedipine was effective in inducing m. EPSCs in the. presence of these inhibitors. PMA, phorbol 1. 2- myristate 1. Cal. C. calphostin C; nifed, nifedipine. The facilitation seems to be due to a direct action on the release process, independent. L- type calcium channels. It cannot be attributed to the already known action of nifedipine. NO (2. 0), or block calcium- dependent potassium currents (1. Also, we have shown that its action is not due to activation of a PKA or PKC pathway. The finding that nifedipine effect. PKC activation may indicate that its action is not due to an increase in the size of a readily releasable. PKC has been shown to increase the refilling rate and the size of a readily releasable. We cannot expect NMDA receptor or VDCC activation in our recording condition of normal magnesium concentration and holding. In addition, blocking calcium influx through VDCCs by Cd. BAPTA- AM did not prevent the nifedipine effect. Thus, the most likely site of action. First, nifedipine has an ortho- nitro substituent on its aromatic ring whereas the other two have a meta- nitro substituent. The substitution of the aromatic ring is thought to be important in locking the compound in its active. Second, nifedipine has two identical ester side chains on the 1,4- DHP ring at positions 3 and 5. In contrast, nimodipine. Variation of the esters alters the pharmacokinetic properties. These differences may account for the selectivity for nifedipine on a yet undetermined target. It may be relevant that. Aiello et al. Such a change in the local rigidity may create distortion in the membrane that would promote fusion. Alternatively. nifedipine action may involve an intracellular site, which might account for the long latency and washout of the effect. In normal. human subjects, it has been shown that, after a single oral administration of clinical dose of nifedipine (1. M) (4. 0). Therefore, it is conceivable that nifedipine exerts its facilitatory effect on central synapses in vivo. Its effect was not specific to excitatory synapses in the SON: other excitatory synapses in other brain areas, as well as. SON, responded similarly. This result may be an indication that the nifedipine target is something. Thus, in addition to a central effect, nifedipine may have a similar effect on the peripheral. Download patch stronghold crusader 1. Click here to download patch stronghold crusader 1. D1%8. 1%D0%BA%D0%B0%D1%8. D0%B0%D1%8. 2%D1%8. C %D0%BF%D0%B0%D1%8. D1%8. 7 stronghold crusader 1. D1%8. 1%D0%BA%D0%B0%D1%8. 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