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Superfusion experiments

Regulation of InsP3 receptors by cytosolic Ca2+ lessons from superfusion experiments... [Pg.92]

Using superfusion experiments, electrophysiological techniques, pithed animal preparations, and experiments in which transmitter release was determined indirectly via the end-organ response (e.g., twitch response of vas deferens preparations), numerous presynaptic opioid receptors have been identified (Table 2). For the identification of the receptors, classical drug tools were used for future studies, knockout mice (now available for each of the four opioid receptor subtypes) and special nucleotides (e.g., antisense oligodeoxynucleotides or short interfering... [Pg.412]

The results obtained from in vitro superfusion experiments are in accord with the conclusion that the cholinergic interneurons possess a D-2 dopamine receptor. Dopamine inhibits the release of [3H]-acetylcholine from neostriatal tissue however, concentrations greater than 1 are required to achieve maximal inhibition. Because dopamine is removed from the extracellular space by the dopaminergic nerve terminals, it is difficult to... [Pg.119]

The possibility that dopamine regulates neostriatal GABA-ergic function receives no support from in vitro superfusion experiments determining the release of [3HJ-GABA from slices of rat neostriatum (5 3). The D-2 receptor agonist RU 24926 is... [Pg.125]

Electrophysiological Experiments. Guinea pig myocardial cells prepared as described previously 24) were superfused at 37 C with a Tyrode solution. Electrical properties of the myocytes were examined by the patch-clamp methods (25) using fire-polished pipettes. The current was measured by means of a patch-clamp amplifier, stored on the tape through a digital PCM data recording system, and analyzed with a computer. [Pg.134]

Taylor In the experiments I showed we deliberately used a high Ca2+. This is partly a technical feature of the way that the superfusion works, but also we wanted to completely inhibit. The EC50 for this effect depends on how long the cells are left incubating in it, but it is in the order of 1.5 fiM. [Pg.103]

Fig. 5. Zn2+ enhances amphetamine induced release of [3H]MPP+. HEK-293 cells stably expressing the hDAT were preloaded with [3H]MPP+ and superfused upon reaching a stable baseline (basal efflux mean of the three fractions before drug addition hDAT wt (A) basal efflux 0.247 0.004% min T, i.e., 245.6 + 6.7 dpm min, n = 60 observations of randomly chosen experiments performed on different days hDAT-H193K (B) basal [3H]MPP+ efflux 0.433 0.08% min-1, i.e., 181.2 + 7.1 dpm min-1, n = 47. The experiment was started with the collection of 4-min fractions. After three fractions (12 min) of basal efflux, cells were exposed to Zn2+ (101iM), or left at control conditions as indicated. After six fractions (from 24 min and onward), amphetamine (10 pM) was added to all superfusion channels. After nine fractions (from 36 min and onward), all channels were switched back to control conditions. Data are presented as fractional efflux, i.e., each fraction is expressed as the percentage of radioactivity present in the cells at the beginning of that fraction. Symbols represent means + S.E. of 6-12 observations (one observation equals one superfusion chamber all experiments were performed in triplicate). Reproduced with permission from ref. (83). Fig. 5. Zn2+ enhances amphetamine induced release of [3H]MPP+. HEK-293 cells stably expressing the hDAT were preloaded with [3H]MPP+ and superfused upon reaching a stable baseline (basal efflux mean of the three fractions before drug addition hDAT wt (A) basal efflux 0.247 0.004% min T, i.e., 245.6 + 6.7 dpm min, n = 60 observations of randomly chosen experiments performed on different days hDAT-H193K (B) basal [3H]MPP+ efflux 0.433 0.08% min-1, i.e., 181.2 + 7.1 dpm min-1, n = 47. The experiment was started with the collection of 4-min fractions. After three fractions (12 min) of basal efflux, cells were exposed to Zn2+ (101iM), or left at control conditions as indicated. After six fractions (from 24 min and onward), amphetamine (10 pM) was added to all superfusion channels. After nine fractions (from 36 min and onward), all channels were switched back to control conditions. Data are presented as fractional efflux, i.e., each fraction is expressed as the percentage of radioactivity present in the cells at the beginning of that fraction. Symbols represent means + S.E. of 6-12 observations (one observation equals one superfusion chamber all experiments were performed in triplicate). Reproduced with permission from ref. (83).
We do not know whether the interactions between the presynaptic receptors occur on the level of the receptors or on a site beyond the receptor level, e.g. on the level of G proteins, ion channels or other second messengers. Such receptor interactions may explain drug interactions in vivo. They are also of importance for planning in vitro experiments. H3 receptor-mediated effects in superfused slice preparations are frequently small the inhibitory effect on NA and DA release can be increased by simultaneous blockade of the respective autoreceptor. There are even examples of H3 heteroreceptors which could only be identified if the respective autoreceptor was blocked3 12,36. [Pg.21]

Fig. 4 Effect of various peptides and nonpeptides on the electrically (3 Hz) evoked tritium overflow from superfused mouse brain cortex slices preincubated with 3H-serotonin. The evoked overflow represents quasi-physiological exocytotic serotonin release. In all experiments, serotonin autoreceptors were blocked by metitepine. The figure shows that human neuropeptide Y concentration-dependently inhibited serotonin release and that this effect was mimicked by human neuropeptide Y (13-36) (NPYi3 36), which has a high affinity for Y2 but a very low affinity for Yi receptors. These results are compatible with the view that neuropeptide Y acts via Y2 receptors in the present model. For the sake of comparison, the figure also shows the inhibitory effects of another three agonists, acting via cannabinoid CBi, histamine H3 and prostaglandin EP3 receptors and used at concentrations causing the maximum or near-maximum effect at their respective receptors. Drug concentrations in pM. P < 0.05, P < 0.003, compared to the control (from Nakazi et al. 2000 and Nakazi 2001 redrawn). Fig. 4 Effect of various peptides and nonpeptides on the electrically (3 Hz) evoked tritium overflow from superfused mouse brain cortex slices preincubated with 3H-serotonin. The evoked overflow represents quasi-physiological exocytotic serotonin release. In all experiments, serotonin autoreceptors were blocked by metitepine. The figure shows that human neuropeptide Y concentration-dependently inhibited serotonin release and that this effect was mimicked by human neuropeptide Y (13-36) (NPYi3 36), which has a high affinity for Y2 but a very low affinity for Yi receptors. These results are compatible with the view that neuropeptide Y acts via Y2 receptors in the present model. For the sake of comparison, the figure also shows the inhibitory effects of another three agonists, acting via cannabinoid CBi, histamine H3 and prostaglandin EP3 receptors and used at concentrations causing the maximum or near-maximum effect at their respective receptors. Drug concentrations in pM. P < 0.05, P < 0.003, compared to the control (from Nakazi et al. 2000 and Nakazi 2001 redrawn).
Similar results have been obtained when the effect of GABA on the release of glutamate was studied in spinal cord gliosomes. In this experiment, purified gliosomes were labeled with [3H]- D-aspartate and exposed in superfusion to GABA. [Pg.310]

The physiological relevance of most of the studies on desensitization in ovarian and testis cells is not clear because they were carried out with high unphysiological levels of hormones and over long periods of time. Experiments with superfused... [Pg.171]

Synaptosomes isolated from the central nervous system of the cockroach and maintained on filter platforms, as outlined, show no deterioration in response to the neurotoxicants examined for at least one hour after the start of superfusion. Variability within an experiment was less than 8%, and there was good agreement between experiments carried out on different days. [Pg.267]

Experiments utilizing isolated superfused and blood perfused cardiac tissue preparations and isolated rat, rabbit, and cat whole hearts all demonstrate the potent, concentration-dependent, negative inotropic activity of the calcium inhibitory compounds (45 50, 90-95, 112, 113, 114, 118, 140, 141). Studies comparing the relative negative inotropic effects of several of the calcium inhibitory compounds indicate that those compounds exhibiting the most potent calcium inhibitory effects in vitro are the most effective in reducing cardiac contractility in vivo (6). Of those compounds most frequently compared, nifedipine and niludipine exhibit the most profound negative inotropic activity followed by verapamil (levo isomer), diltiazem and perhexiline (88, 89-142). [Pg.66]

In addition to its other functions BH4 enhances the release of dopamine and serotonin in the rat striatum when administered locally through the dialysis membrane. The enhancement of dopamine release persisted even when dopamine biosynthesis or dopamine reuptake was completely blocked, but it was abolished when hlockers of voltage-dependent Na" " or Ca " " channels were administered with BH4. Further experiments using selective inhibitors of tyrosine, TH, and NOS demonstrated that BH4 stimulates dopamine release directly, independent of its cofactor action on TH and NOS, by acting from the outside of neurons. The exact mechanism is not entirely clear but it has been shown that arginine also induces a concentration-dependent increase of dopamine release in the superfusate of rat striatum slices, and that it is dependent on the presence of BH4. ... [Pg.620]

In our experiments however, strips of RbA, RbCa and RS did not respond when the fluid superfusing strips of i.p.a. was directed over the above assay tissues even when AA was infused over the i.p.a. These data suggested that, if PGs were indeed formed, the levels were too low to be detected by the assay tissues. [Pg.74]


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See also in sourсe #XX -- [ Pg.92 , Pg.95 ]

See also in sourсe #XX -- [ Pg.13 ]




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Superfusion

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