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Reduced influx is a factor in accounting for reduced vincristine accumulation in certain verapamil-hypersensitive multidrug-resistant CHO cell lines.

The rates of accumulation, influx and efflux of vincristine have been examined in a series of multidrug-resistant Chinese hamster ovary cell lines which show exceptionally high levels of hypersensitivity (collateral sensitivity) to several resistance modifiers. The more highly resistant members of the series show significantly reduced levels of vincristine influx compared to the control cell line from which they were derived. It is possible that resistance modifier hypersensitivity and reduced vincristine influx may be due to a common change in membrane composition which has arisen during prolonged selection for vincristine resistance in these cell lines.

Animals↗

De novo cisplatinum resistance does not influence cellular radiosensitivity.

The intrinsic sensitivity to 4 MeV photons, and 62.5 MeV (p-->Be+) neutrons has been examined in a panel of 11 cultured human cell lines exhibiting a wide spectrum of inherent cisplatinum sensitivity. Irrespective of whether cellular sensitivities to these therapeutic agents were compared at the 10% survival level, relative to the initial portion of the cell survival curves, or to their relative rank order of response, there were no significant correlations between inherent cisplatinum sensitivity and sensitivity to either 4 MeV photon, or 62.5 MeV neutron irradiation. This data raises the possibility that the previously reported decreased radiosensitivity of human tumour cell lines with acquired cisplatinum resistance may be due to the induction of cellular processes which confer resistance to both cisplatinum and ionising radiation, rather than the selection of innately cisplatinum-resistant cells, which are collaterally radioresistant.

Cell Line↗

Synergistic enhancement of cisplatin cytotoxicity by SN-38, an active metabolite of CPT-11, for cisplatin-resistant HeLa cells.

A cisplatin (cis-diamminedichloroplatinum(II); CDDP)-resistant HeLa cell line (HeLa/CDDP cells), which showed more than 8-fold resistance to CDDP compared to the parent cells, was newly established for this study. HeLa/CDDP cells accumulated 50% less platinum than the parent cells. There was no difference in intracellular glutathione (GSH) content between the parent and HeLa/CDDP cells. The dose modification factor by DL-buthionine-S,R-sulfoximine (BSO) pretreatment was similar in both cell lines. HeLa/CDDP cells had cross-resistance to diammine(1,1-cyclobutanedicarboxylato)platinum(II) (CBDCA), (cis-diammine(glycolato)platinum (254-S), but not to (-)-(R)-2-aminomethylpyrrolidine(1,1-cyclobutanedicarboxylato++ +)platinum(II) (DWA2114R), adriamycin, or VP-16. HeLa/CDDP cells showed a collateral sensitivity to 7-ethyl-10-hydroxycamptothecin (SN-38), an active metabolite of 7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxycamptothecin (CPT-11). Furthermore, isobologram analysis indicated synergistic interaction of CDDP and SN-38 only for HeLa/CDDP cells. The present study suggests that combination therapy with CDDP and CPT-11 may be potentially useful in the treatment of some patients with CDDP-resistant cancer.

Camptothecin↗

Role of collateral flow in a pharmacological stress test (a combination of low-dose dobutamine and a vasodilator) as a predictor of wall motion reversibility.

The role of collateral flow was evaluated in a pharmacological stress test [a combination of low-dose dobutamine (DOB) and a vasodilator] as a predictor of wall motion reversibility at rest after percutaneous transluminal coronary angioplasty (PTCA) using ultrafast computed tomography (UFCT). Segments with wall motion abnormalities before PTCA were divided into two groups; ie, either with or without collateral flow. Patients were scanned at rest for baseline and again after 5 min of intravenous administration of 4 micrograms/kg per min of DOB after nitroglycerin (0.3 mg sublingually) or isosorbide dinitrate (2.5 mg bolus intravenous injection). Three months after PTCA, patients were scanned again and wall motion was compared with the previous findings. In collateral-dependent segments, the sensitivity of the pharmacological stress test as a predictor of wall motion reversibility was 87.5% and the specificity was 83.3%. In collateral-independent segments, the sensitivity was only 41.7%, while the specificity was 95.2%. Our findings demonstrate that the pharmacological stress test we used satisfactorily predicted wall motion reversibility in collateral-dependent segments, but tended to underestimate wall motion reversibility in collateral-independent segments. Therefore, collateral flow may be an important factor in accurately predicting wall motion reversibility by this pharmacological stress test.

Adolescent↗

[Examination of myocardial perfusion with positron emission tomography: a clinically useful and valid method?].

Positron emission tomography (PET) of the heart has gained widespread scientific and clinical acceptance with regard to 2 indications: 1. the detection of perfusion abnormalities by qualitative and semiquantitative analyses of perfusion images at rest and during physical or pharmacological stress using well validated perfusion tracers such as N-13 ammonia, Rb-82 rubidiumchloride, or O-15 labeled water, 2. Viability imaging of myocardial regions with reduced contractility by combining perfusion measurements with substrate metabolism as assessed from F-18 deoxyglucose utilization. This overview summarizes the use of PET as a perfusion imaging method. With a sensitivity > 90% in combination with a high specificity, PET is today the best available nuclear imaging technique for the diagnosis of coronary artery disease (CAD). The short half-life of the perfusion tracers in combination with highly sophisticated hard- and software enables rapid PET studies with high patient throughput. The high diagnostic accuracy and the methological advantages as compared to conventional scintigraphy allows to use PET perfusion imaging for detection of subtle changes of the perfusion reserve for detection of CAD in high risk but asymptomatic patients as well as in patients with proven CAD undergoing various treatment forms such as risk factor reduction or coronary revascularization. In patients following orthotopic heart transplantation, evolving transplant vasculopathy can be detected at an early stage. Quantitative PET imaging at rest allows for detection of myocardial viability since cellular survival is based on maintenance of a minimal perfusion and structural changes correlate to the degree of perfusion reduction. Furthermore, quantitative assessment of the myocardial perfusion reserve detects the magnitude and competence of collaterals in regions with occluded epicardial arteries and thus, imaging of several coronary distribution territories in one noninvasive study. The cost of PET in combination with the cost of a cyclotron facility together with the demanding methological problems have limited the availability of PET to a few but sophisticated centers. Therefore, quantitative PET investigations have been performed predominantly for scientific purposes and the cost-effectiveness of PET in the everyday clinical setting is not yet finally proven. However, the unique possibilities of PET to study noninvasively and quantitatively myocardial perfusion and metabolism as well as cardiac innervation and pharmacokinetics of cardiac drugs have established cardiac PET as a scientific tool of highest quality for the future.

Coronary Circulation↗

Color-flow duplex scanning of the leg arteries by use of a new echo-enhancing agent.

OBJECTIVE: This was a dose-finding and effectiveness study of a newly developed contrast-enhancing agent, sulphur hexafluoride (SF(6)), in patients with peripheral arterial disease in whom the therapeutic policy could not be established on the basis of standard color-flow duplex scanning of the leg arteries. METHODS: In this open-label, randomized, dose-ranging, crossover design, 14 patients in whom the assessment of vessel patency was difficult because of poor visibility (low-flow state) or extensive wall calcifications were studied. Contrast-enhanced duplex scanning was performed on the upper leg (n = 4), lower leg (n = 6), or pedal (n = 4) arteries after intravenous injection of four different dosages of SF(6). The results were compared with those from selective angiography of the vessel of interest. Contrast duration and agreement about the diagnosis and the confidence in the diagnosis were obtained before and after administration of the contrast agent. RESULTS: No adverse effects of the contrast agent were seen. Overall agreement was reasonable with regard to vessel patency between contrast-enhanced duplex scanning and angiography (71%). Nine of 14 vessels (64%) appeared open when contrast was applied. In four cases this could not be confirmed by angiography; in two of these cases this was due to the presence of collateral vessels. All vessels that appeared occluded with the contrast agent were also occluded on the angiogram. The confidence in the diagnosis increased from 56% to 91% after contrast administration (P <.0001). CONCLUSION: SF(6)-enhanced color-flow duplex scanning is a safe method that may improve the assessment of the patency of leg arteries, particularly in low-flow states. The visualization of collateral vessles during (enhanced) duplex scanning may be misleading because they may be regarded as the vessel of interest.

Aged↗

Pleiotropic phenotype of colchicine-resistant CHO cells: cross-resistance and collateral sensitivity.

Colchicine resistant (CHR) mutants of CHO cells with reduced permeability to colchicine display extensive cross-resistance to a number of apparently unrelated compounds including puromycin, daunomycin, emetine, ethidium bromide and gramicidin D. A positive correlation was observed between the level of cross-resistance and the relative hydrophobicity of these compounds. The mutants also showed increased (collateral) sensitivity to local anaesthetics (procaine, tetracaine, xylocaine and propanolol), steroid hormones (1-dehydrotestosterone, corticosterone and 5beta-pregnan-3,20-dione) and some Triton X compounds. In general, the degree of the pleiotropic response (cross-resistance or collateral sensitivity) correlated with the degree of colchicine resistance in mutant lines. These results are consistent with the pleiotropic phenotype being the result of the same mutation(s) which confer colchicine resistance and support a model for resistance in which the reduced permeability is assumed to be the result of an alteration in the modulation of the fluidity of the surface membrane.

Anesthetics, Local↗

Effects of intracoronary cromakalim on postischaemic contractile function and action potential duration.

OBJECTIVE: The effects of intracoronary cromakalim (1 microgram.kg-1 x min-1) on postischaemic contractile function and monophasic action potential duration at the 95% repolarisation level (APD95) were assessed in a canine model of stunned myocardium. METHODS: Animals (n = 24) were anaesthetised, subjected to a left thoracotomy, and the left anterior descending coronary artery was isolated. Measurements of segmental shortening and monophasic action potential were taken before drug, after drug, during a 15 min occlusion, and at times following reperfusion. RESULTS: Cromakalim significantly improved reperfusion recovery of function. Both preischaemic and postischaemic myocardial blood flows were increased with cromakalim, although there was no significant change in collateral blood flow during ischaemia relative to vehicle. In the absence of ischaemia, cromakalim reduced APD95 by 8%. There was no change in APD95 with vehicle alone. During coronary occlusion, cromakalim significantly reduced APD95 by 27% as compared with 8% in the vehicle group. APD95 values returned to preocclusion levels within minutes of reperfusion and remained there throughout reperfusion (30 min). Glyburide (3.0 mg.kg-1 intravenously), a blocker of ATP sensitive potassium channels, abolished the APD95 effects of cromakalim. One out of six animals given glyburide survived through reperfusion. In contrast, four out of five of the glyburide+cromakalim treated animals survived through reperfusion. CONCLUSIONS: Cardioprotection with cromakalim is likely to be mediated through activation of ATP sensitive potassium channels, measured as a decrease in action potential duration. Shortening of action potential duration with cromakalim was shown to be augmented in the presence of ischaemia. It is suggested that a possible interrelationship between cardioprotection and action potential duration shortening may exist such that the cardioprotective effects of cromakalim may be selective for ischaemic conditions.

Action Potentials↗

Prolonged administration of imipramine and (+)-oxaprotiline, but not citalopram, results in sensitization of the rat hippocampal CA1 neurons to serotonin ex vivo.

Prolonged (14 days, twice daily), but not acute, application of imipramine and (+)-oxaprotiline (10 mg/kg) induced sensitization of hippocampal CA1 neurons to the inhibitory effect of 5-hydroxytryptamine (5-HT), as studied ex vivo in the rat hippocampal slice preparation. Attenuation of the population spike, recorded in the CA1 pyramidal cell layer in response to stimulation of the Schaffer collateral-commisural pathway, was used to asses the sensitivity of neurons to 5-HT. Prolonged and acute administration of the selective 5-HT reuptake blocker citalopram did not change the responsiveness of hippocampal neurons to 5-HT. Since imipramine and (+)-oxaprotiline share the inhibitory effect on the norepinephrine reuptake, our results may indicate that long-term alterations in the noradrenergic system lead to modifications in postsynaptic serotonergic receptors.

Animals↗

[Assessing myocardial perfusion with positron emission tomography].

Positron emission tomography (PET) of the heart has gained widespread scientific and clinical acceptance with regard to two indications: 1) The detection of perfusion abnormalities by qualitative and semiquantitative analyses of perfusion images at rest and during physical or pharmacological stress using well-validated perfusion tracers, such as N-13 ammonia, Rb-82 rubidium chloride, or O-15 labeled water. 2) Viability imaging of myocardial regions with reduced contractility by combining perfusion measurements with substrate metabolism as assessed from F-18 deoxyglucose utilization. This overview summarizes the use of PET as a perfusion imaging method. With a sensitivity > 90% in combination with high specificity, PET is today the best-validated available nuclear imaging technique for the diagnosis of coronary artery disease (CAD). The short half-life of the perfusion tracers in combination with highly sophisticated hard- and software enables rapid PET studies with high patient throughput. The high diagnostic accuracy and the methological advantages as compared to conventional scintigraphy allows one to use PET perfusion imaging to detect subtle changes in the perfusion reserve for the detection of CAD in high risk but asymptomatic patients as well as in patients with proven CAD undergoing various treatment forms such as risk factor reduction or coronary revascularization. In patients following orthotopic heart transplantation, evolving transplant vasculopathy can be detected at an early stage. Quantitative PET imaging at rest allows for detection of myocardial viability since cellular survival is based on maintenance of a minimal perfusion and structural changes correlate to the degree of perfusion reduction. Furthermore, quantitative assessment of the myocardial perfusion reserve detects the magnitude and competence of collaterals in regions with occluded epicardial collaterals and, thus, imaging of several coronary distribution territories in one noninvasive study. The cost of PET in combination with the cost of a cyclotron facility together with the demanding methological problems have limited the availability of perfusion PET to a few sophisticated centers. Therefore, quantitative PET investigations of myocardial perfusion have been performed predominantly for scientific purposes, and the cost-effectiveness of PET in the everyday clinical setting is not yet finally proven. However, the unique possibilities of PET to study non-invasively and quantitatively myocardial perfusion and metabolism as well as cardiac innervation and pharmacokinetics of cardiac drugs have established cardiac PET as a scientific tool of the highest quality for the future.

Coronary Circulation↗

Excitation of central and peripheral terminals of primary afferent neurons by capsaicin in vivo.

In three groups of rats discharge activity was recorded (i) from the peripheral stump of the cut saphenous nerve (saphenous-receptor preparation); (ii) from the central stump of the cut L4 or L5 dorsal root (dorsal root preparation); or (iii) from the peripheral stump of the saphenous nerve segment cut at both ends (axon preparation) during slow intraarterial infusion of capsaicin (30-300 micrograms/kg/min for 5 min) into the carotid artery. Capsaicin produced excitation, i.e. an increase in frequency of action potentials in the same dose range (100-300 micrograms/kg/min) in both the saphenous-receptor and dorsal root preparations, while the axon preparations remained unresponsive. In the cat, close arterial injection of capsaicin (up to 20 micrograms) into a collateral branch of the saphenous artery failed to evoke discharges in the saphenous axon preparation, although similar injection of 4-aminopyridine (60 micrograms), a K+ channel blocking agent was readily effective. These results indicate that after systemic application of capsaicin the peripheral and central endings of primary afferent neurons are equally important sites for activation and are much more sensitive to capsaicin than the axons of the nerve trunk.

Animals↗

Bacillus licheniformis bacitracin-resistance ABC transporter: relationship to mammalian multidrug resistance.

The nucleotide sequence of the Bacillus licheniformis bacitracin-resistance locus was determined. The presence of three open reading frames, bcrA, bcrB and bcrC, was revealed. The BcrA protein shares a high degree of homology with the hydrophilic ATP-binding components of the ABC family of transport proteins. The bcrB and bcrC genes were found to encode hydrophobic proteins, which may function as membrane components of the permease. Apart from Bacillus subtilis, these genes also confer resistance upon the Gram-negative Escherichia coli. The presumed function of the Bcr transporter is to remove the bacitracin molecule from its membrane target. In addition to the homology of the nucleotide-binding sites, BcrA protein and mammalian multidrug transporter or P-glycoprotein share collateral detergent sensitivity of resistant cells and possibly the mode of Bcr transport activity within the membrane. The advantage of the resistance phenotype of the Bcr transporter was used to construct deletions within the nucleotide-binding protein to determine the importance of various regions in transport.

ATP-Binding Cassette Transporters↗

The activation and distribution of GABA and L-glutamate receptors on goldfish Mauthner neurones: an analysis of dendritic remote inhibition.

1. The sensitivity of the membrane of the cell-body and lateral dendrite of the Mauthner neurone to iontophoretically applied GABA and L-glutamic acid has been investigated in goldfish. The cells were afterwards examined histologically. The results, taken together with physiological observations, help to explain some functional properties of dendritic synapses.2. GABA inhibits by increasing the membrane conductance, and has little effect on resting potential. L-Glutamate depolarizes, and its effects could sum with subthreshold excitatory post-synaptic potentials (e.p.s.p.s) to cause impulse firing. Neither substance was effective when released intracellularly, but only when applied to the outside of the membrane.3. Using a roving double-barrelled micropipette to apply brief iontophoretic pulses very close to the cell, and recording from the cell-body, the sensitivity to GABA was found to be uniform over a region extending from the axon-hillock to about half-way along the lateral dendrite; it then appeared to fall progressively as the drug was pipetted further and further out on the dendrite. The sensitivity to L-glutamate however seemed relatively unaffected by varying the site of application.4. In contrast to this, when the recording electrode was inserted into the same region of the cell where the drugs were applied, then the sensitivity to GABA, like that to L-glutamate, was found to be similar everywhere, including the distal part of the lateral dendrite.5. The antidromic spike, which does not actively invade the lateral dendrite, was used as a convenient test signal for detecting electrotonic decrement as well as changes in membrane conductance. The conductance changes due to small doses of GABA applied to the dendrite could be detected only over relatively short distances (tens of microns). But over these same distances very little decrement of potential change took place.6. The concept of dendritic remote inhibition has been put on a firm experimental basis. It occurs in the Mauthner cell, and is shown to be capable of providing a high spatial selectivity of action. The e.p.s.p.s most affected by it are those generated out on the same dendrite, and it follows that many of the e.p.s.p.s produced far out on other dendrites could well be influenced by it, though to a lesser extent. Least affected are large e.p.s.p.s generated in the cell-body and axon-hillock regions. The synaptic grouping provided by the distal parts of dendrites and their associated nerve endings is discussed.7. The results of a theoretical treatment (Appendix) of the effects of a localized membrane resistance change on electrotonic potentials recorded nearer to the source have been applied to results obtained on the Mauthner cell. The experimentally observed properties of the ;remote inhibition' caused by localized GABA application to the lateral dendrite, accord well with those predicted both for an infinitely long uniform cable and for a cable having a closed end at the region of the conductance change. The possible implications of these results for other central neurones are considered.8. Evidence is adduced showing that the synapses responsible for collateral inhibition in the Mauthner cell include at least part of the group of small nerve endings found on the axon-hillock, cell-body, proximal and distal lateral dendrite. (The latter distally-located endings cause dendritic remote inhibition.) All these regions, some of which certainly have excitatory synapses, thus receive an inhibitory input as well, and are sensitive to both GABA and L-glutamate.9. E.p.s.p.s recorded in the cell-body were reduced by about the same amount as was the antidromic spike when GABA was applied there, but considerably more than the spike when the GABA application was to the lateral dendrite near the origin of the e.p.s.p. Even when the recording was made from the affected region of the dendrite, the e.p.s.p. seemed more sensitive to GABA than was the electrotonically conducted spike. This, and other observations, suggests that GABA may act presynaptically on the excitatory endings as well as post-synaptically.10. The detection of effects, and the recognition of site of action, of drugs applied iontophoretically in the central nervous system is discussed on the basis of the present findings.

Action Potentials↗

Increased expression of DNA topoisomerase I gene and collateral sensitivity to camptothecin in human cisplatin-resistant bladder cancer cells.

We established three cis-diamminedichloroplatinum(II) (cisplatin)-resistant cell lines, T24/DDP5, T24/DDP7, and T24/DDP10, by the stepwise exposure of T24 human bladder cancer cells to increasing concentrations of cisplatin. The resistance to cisplatin of T24/DDP5, T24/DDP7, and T24/DDP10 cells was 2.2-, 5.2-, and 8.4-fold that of the parental T24 cells, respectively. The cisplatin-resistant cell lines also showed an increased resistance to vincristine, although their sensitivities to Adriamycin and etoposide resembled that of T24. In contrast, the cisplatin-resistant cells developed a collateral sensitivity to (4s)-4,11-diethyl-4-hydroxy-9-[(4-piperidinopiperidino)carbonyl oxy]dione hydrochloride trithydrate, a camptothecin derivative, and its active metabolite, 7-ethyl-10-hydroxy-camptothecin, that targets DNA topoisomerase I. Both a Northern blot analysis and an immunoblot analysis demonstrated increased cellular levels of DNA topoisomerase I mRNA in the resistant cell lines. However, the expression of DNA topoisomerase II in the three resistant cell lines did not differ significantly from that in the T24 cells. No significant differences in the glutathione S-transferase pi levels were observed, although the intracellular content of glutathione in the T24/DDP7 cells was slightly but significantly increased. In addition, the intracellular platinum concentration correlated negatively with the degree of cisplatin resistance and was found to be significantly decreased in T24/DDP10 at an external cisplatin concentration of 20 micrograms/ml. These results suggest that the increased levels of DNA topoisomerase I mRNA thus play an important role in cisplatin resistance and produce a collateral sensitivity to (4s)-4,11-diethyl-4-hydroxy-9[(4-piperidinopiperidino)carbonylo xy]dione hydrochloride trithydrate and 7-ethyl-10-hydroxycamptothecin in these cisplatin-resistant bladder cancer cell lines. In addition, the presence of decreased intracellular cisplatin accumulation may also contribute to the acquisition of resistance to cisplatin in these cell lines.

Blotting, Northern↗

Retinoid therapy of childhood cancer.

In vitro studies that showed RA could cause growth arrest and differentiation of myelogenous leukemia and neuroblastoma led to clinical trials of retinoids in APL and neuroblastoma that increased survival for both of those diseases. In the case of APL, ATRA has been the drug of choice, and preclinical and clinical data support direct combinations of ATRA with cytotoxic chemotherapy. For neuroblastoma, a phase I study defined a dose of 13-cis-RA, which was tolerable in patients after myeloablative therapy, and a phase III trial that showed postconsolidation therapy with 13-cis-RA improved EFS for patients with high-risk neuroblastoma. Preclinical studies in neuroblastoma indicate that ATRA or 13-cis-RA can antagonize cytotoxic chemotherapy and radiation, so use of 13-cis-RA in neuroblastoma is limited to maintenance after completion of cytotoxic chemotherapy and radiation. A limitation on the antitumor benefit of ATRA in APL is the marked decrease in drug levels that occurs during therapy as a result of induction of drug metabolism, resulting in a shorter drug half-life and decreased plasma levels. Although early studies sought to overcome the pharmacologic limitations of ATRA therapy in APL, the demonstration that ATO is active against APL in RA-refractory patients has led to a focus on studies employing ATO. Use of 13-cis-RA in neuroblastoma has avoided the decreased plasma levels seen with ATRA. It is likely that recurrent disease seen during or after 13-cis-RA therapy in neuroblastoma is due to tumor cell resistance to retinoid-mediated differentiation induction. Studies in neuroblastoma cell lines resistant to 13-cis-RA and ATRA have shown that they can be sensitive, and in some cases collaterally hypersensitive, to the cytotoxic retinoid fenretinide. Fenretinide induces tumor cell cytotoxicity rather than differentiation, acts independently from RA receptors, and in initial phase I trials has been well tolerated. Clinical trials of fenretinide, alone and in combination with ceramide modulators, are in development.

Antineoplastic Agents↗

Alteration of type II regulatory subunit of cAMP-dependent protein kinase in human cisplatin-resistant cells as a basis of collateral sensitivity to 8-chloro-cAMP.

A cyclic adenosine 3',5'-monophosphate (cAMP) analogue, 8-chloro-cAMP (8-Cl-cAMP), had a collateral growth-inhibitory effect on a cis-diamminedichloroplatinum(II) (CDDP)-resistant human cancer cell lines (PC-14/CDDP). The non-selective analogues dibutyryl-cAMP, 8-bromo-cAMP and forskolin, which are cAMP agonists, showed far less cytotoxicity than 8-Cl-cAMP in both cell lines. There was no significant difference in cAMP content between PC-14 and PC-14/CDDP. Because 8-Cl-cAMP has been shown to bind selectively to the site I receptor of the type II regulatory subunit (RII) of cAMP-dependent protein kinase, we determined the level of expression of regulatory subunits in PC-14 and PC-14/CDDP cells by photoaffinity labeling. PC-14/CDDP cells had a higher RII level, low site I receptor of type I regulatory subunit (RI) level, and a lower RI/RII ratio than the parental PC-14 cells. Exposure to 8-Cl-cAMP increased the RI and RII level in PC-14/CDDP cells in dose- and time-dependent manners. On the other hand, in parental PC-14 cells, RII was not detected and the levels of RI and RII were not increased by exposure to 8-Cl-cAMP. These results suggested that the change in RI and/or RII levels caused by 8-Cl-cAMP was correlated with 8-Cl-cAMP-induced growth inhibition and that the collateral sensitivity to 8-Cl-cAMP in CDDP-resistant cells was due to the increased RII level. Our results suggest that 8-Cl-cAMP can be used in combination with CDDP and that measurement of RI and RII levels and/or the RI/RII ratio is a useful tool to predict CDDP sensitivity.

8-Bromo Cyclic Adenosine Monophosphate↗

Baclofen induces spontaneous, rhythmic sharp waves in the rat hippocampal slice.

In rat hippocampal slices, low concentrations of (+/-) baclofen (0.1 to 1.5 microM) elicited spontaneous, rhythmic sharp waves (SRSWs). These low amplitude (0.1 to 0.3 mV) SRSWs were visible with high amplification in the extracellular recordings from the CA1, CA2, and CA3 regions and were roughly synchronous in all areas. SRSW amplitude increased and frequency decreased as baclofen concentration increased up to 1.5 microM, but SRSWs were suppressed at concentrations of 5 microM and higher. The amplitude of the SRSWs was greater in the strata radiatum and the lacunosum moleculare than in the stratum pyramidale. (-)-Baclofen was much more potent in eliciting SRSWs than (+)-baclofen. Low concentrations of baclofen also caused the extracellular excitatory postsynaptic potential in the stratum radiatum of CA3b evoked by stimulation of the Schaffer collaterals to broaden and develop a secondary peak. Slices pretreated with pertussis toxin required much higher concentrations of baclofen to elicit the SRSWs, indicating that the baclofen may be eliciting the SRSWs through a G protein-sensitive mechanism. Baclofen has both inhibitory and disinhibitory effects on neurons. The appearance of these spontaneous population events suggests that, at low concentrations, the disinhibitory effects may be more powerful than the inhibitory effects.

Action Potentials↗

[The depressing effect of GABA on synaptic excitation in isolated rat hippocampal slices].

The action of various gamma-aminobutyric (GABA) concentrations on the amplitude of population EPSPs (PEPSPs) recorded from dendrites was examined in hippocampal slices. GABA produced reversible dose-dependent diminishing of the amplitude of PEPSPs without features of desensitization. CA1 hippocampal PEPSPs were much more sensitive to GABA (threshold concentrations--3.10(-5)-2.10(-4)mol/l; IC50--5.10(-4)-1.10(-3) mol/l) the action of GABA on PEPSPs was not depressed by bicuculline, picrotoxin or penicillin. The inhibitory action of GABA on dendritic antidromic population spike (DAPS) (post-synaptic inhibitory effect) was greatly reduced by these drugs. Baclofen was more potent inhibitor of CA1 PEPSPs than GABA (threshold concentration--1.10(-6)mol/l; IC50--3.10(-6)mol/l), but even in high concentration it induced only slight reduction of DAPS amplitude. It is concluded that GABA inhibitory effects on CA1 hippocampal PEPSPs are caused in the main by its presynaptic action mediated by GABA(B)-receptors located probably on axon terminals of the Schaffer collaterals.

Animals↗