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PubMed1995

The action of thymol on oral bacteria.

Several effects of thymol, a plant-derived antimicrobial agent, on Porphyromonas gingivalis, Selenomonas artemidis and Streptococcus sobrinus were examined. The extremely rapid efflux of intracellular constituents evoked by thymol is consistent with its postulated membranotropic effects. Correlations between leakage-inducing concentrations of thymol and minimal inhibitory concentrations and minimal bactericidal concentrations suggest that membrane perforation is a principal mode of action of this substance. The thymol-induced decline in intracellular ATP in S. sobrinus appears to be entirely attributable to leakage, whereas in P. gingivalis thymol may also inhibit ATP-generating pathways. Relative changes in the transmembrane potential of resting cells of S. sobrinus pulsed with glucose are as sensitive to thymol as is leakage from this organism. The effects of thymol on transmembrane potential are probably secondary to those arising from leakage of intracellular substances.

Adenosine Triphosphate↗
PubMed1996

Swelling-activated amino acid efflux in the human neuroblastoma cell line CHP-100.

1. The effects of hypoosmotic stress on cell volume and amino acid efflux were evaluated in the human neuroblastoma cell line CHP-100 with the Coulter Counter Multisizer and radiolabeled amino acid efflux, respectively. 2. CHP-100 cells swelled by approximately 35 +/- 5% (means +/- SE) when the osmolarity of the solution was decreased from 290 to 190 mOsm/kg H2O. The rapid swelling was followed by a biphasic regulatory volume decrease (RVD). 3. In cells loaded with 14C-taurine, hypoosmotic stress induced a 300 +/- 22% (n = 23, P < 0.05) increase in taurine efflux compared with controls. This efflux was inhibited by the chloride channel blockers 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB), 4,4'-diisothio-cyanostilbene-2,2'-disulfonic acid (DIDS), niflumic acid and by the volume-activated anion channel blocker tamoxifen. In addition, the swelling-activated taurine efflux was dependent upon extracellular calcium. 4. Similarly, in cells loaded with 14C-glycine, hypoosmotic stress significantly increased glycine efflux, which was also sensitive to NPPB. In contrast, efflux of 3H-glutamate was not significantly altered after hypoosmotic stress. 5. With the use of patch clamp recording techniques, Cl- channels were activated in cell attached patches after exposure to hypoosmotic solutions. 6. In nystatin perforated patches, permeability of the hypoosmotically activated anion channel was observed to be SCN- > I- > Br- > Cl- >> Glutamate. 7. It is concluded that in CHP-100 cells, anion channels are activated during hypoosmotic stress and these channels represent a pathway for efflux of amino acids.

Amino Acids↗
PubMed1997

Five-year experience with radiofrequency catheter ablation: implications for management of arrhythmias in pediatric and young adult patients.

OBJECTIVE: A review of the results of the first 5 years of radiofrequency catheter ablation procedures performed at Children's Hospital, Boston, a large tertiary referral center for patients with congenital heart disease and arrhythmias common to the infant, child, and young adult. STUDY DESIGN: A retrospective review of 410 consecutive procedures in 346 patients who underwent at least one application of radiofrequency energy for the treatment of recurrent supraventricular or ventricular tachycardia. RESULTS: The overall final success rate for all diagnoses was 90%, with a higher success rate in patients with an accessory pathway (96%). During the 5-year study period, the success rate improved while the rates of failures and late recurrences declined. The incidence of serious complications was 1.2% (1 late death, 1 ventricular dysfunction, 1 complete heart block, 1 cardiac perforation, and 1 cerebrovascular accident). CONCLUSIONS: This report of a large series of radiofrequency catheter ablation procedures performed at an institution committed to treating congenital heart disease and pediatric arrhythmias confirms the safety and efficacy of this procedure. The pediatric cardiologist/electrophysiologist treating such patients must be aware of specific technical, anatomic, and electrophysiologic variations in the pediatric patient that are critical to the success of this therapy.

Adolescent↗
PubMed1997

Luteinizing hormone activates chloride currents in hen ovarian granulosa cells.

Luteinizing hormone (LH) induces progesterone production in hen ovarian granulosa cells, and this induction is inhibited when chloride ions are removed from the culture medium. This suggests that chloride channels may be involved in the signal transduction pathway responsible for the LH-induced progesterone production. In this report, we examined effects of LH on plasma membrane ion currents in single granulosa cells isolated from the largest preovulatory follicle (Fl) of the hen (Gallus domesticus). Using the perforated patch whole cell voltage clamp technique, we found that addition of LH rapidly activated a chloride current in these cells. This chloride current was present at all voltages tested (-90 to +50 mV), showed outward rectification and showed no obvious time or voltage dependence. Its magnitude was 3.5-fold that of the total resting membrane current measured before LH treatment. LH is known to elevate cyclic AMP in these cells. We found that addition of the cAMP analog Sp-cAMPS mimicked LH in inducing chloride currents in these cells. We conclude that LH can activate a chloride conductance in granulosa cells, and that this action may be mediated by cAMP.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed2002

Perturbation by geraniol of cell membrane permeability and signal transduction pathways in human colon cancer cells.

Geraniol, a natural component of plant essential oils, has antiproliferative effects on human colon cancer cells. To obtain more insight into its mechanism of action, we studied its effect on the resting membrane potential and on the expression of proteins involved in cell signaling pathways. Since geraniol is a well known inhibitor of mevalonate metabolism, the effect of mevalonate supplementation on geraniol-triggered growth inhibition was also determined. Geraniol (400 microM) induced membrane depolarization with a decrease of membrane resistance due to local perforation of the cell membrane. Incubation of Caco-2 cells with geraniol (400 microM) for 6 h caused a 60% reduction of protein kinase C (PKC) activity. After 16 h of incubation, geraniol decreased by 50% the amount of active forms of p44/p42 extracellular signal-regulated protein kinases (ERK). Mevalonate supplementation did not reverse inhibition of cell growth by geraniol. These results indicate that the antiproliferative effect of geraniol on Caco-2 cells was not related to a limitation of the mevalonate pool but was directly linked to the perturbation of cell membrane function leading to the reduction of PKC activity and to the decreased expression of p44/p42 ERK active forms.

Acyclic Monoterpenes↗
PubMed1987

Trophic and growth-regulating mechanisms in the central nervous system monitored by intracerebral neural transplants.

In vitro studies have demonstrated the presence of nerve growth factor (NGF) and other neurotrophic factors in the mammalian central nervous system (CNS). This paper reviews a series of experiments in which the intracerebral neural grafting technique was used to monitor the in vivo expression of such neurotrophic factors and the changes induced by denervating lesions, with the hippocampal formation as a model. Neonatal or adult sympathetic ganglionic neurons, and fetal septal cholinergic neurons, were grafted into or adjacent to the hippocampal formation in adult rats, and the effect of removal of the major afferent inputs (i.e. the septal, commissural or entorhinal inputs) on neuronal survival and fibre outgrowth was assessed histochemically or biochemically. Damage to the septohippocampal (partly cholinergic) pathway had a dramatic effect on survival and fibre outgrowth from neonatal and adult sympathetic ganglionic neurons, and increased the survival of both cholinergic and noncholinergic neurons in the fetal septal grafts. These effects were specific for lesions of the septohippocampal system (fimbria-fornix transection or medial septal lesions), and were not seen after transection of the entorhinal perforant path or the commissural system. It is proposed that neurotrophic factors in the hippocampal formation are under some type of regulation from the afferent inputs, and that removal of the septal afferents, in particular, will increase the availability of NGF or an NGF-like factor from the denervated target. This mechanism may play a normal role in the induction and regulation or regeneration and compensatory collateral sprouting from the remaining afferents in partially denervated brain regions.

Afferent Pathways↗
PubMed1975

Maze performance in rats with hippocampal perforant paths lesions: some aspects of functional recovery.

The performance of two experimental groups--one with lesions of the perforant paths projecting to the dorsal hippocampus (the D group) and one with lesions of the perforant paths to both the dorsal and ventral hippocampus (the DV group)--was compared with the performance of a lesioned control group and an intact control group during two test sessions in the Hebb-Williams maze. Both experimental groups displayed impaired maze learning in Session I. The DV group showed some recovery of function in Session II, and the D group was indistinguishable from controls. The results are discussed in terms of reduced sensory information to the hippocampal formation resulting from perforant paths lesions. It is suggested that the hippocampus is involved in relating new stimuli to previous experience.

Animals↗
PubMed2001

Insulin activates ATP-sensitive K(+) channels in pancreatic beta-cells through a phosphatidylinositol 3-kinase-dependent pathway.

Insulin is known to regulate pancreatic beta-cell function through the activation of cell surface insulin receptors, phosphorylation of insulin receptor substrate (IRS)-1 and -2, and activation of phosphatidylinositol (PI) 3-kinase. However, an acute effect of insulin in modulating beta-cell electrical activity and its underlying ionic currents has not been reported. Using the perforated patch clamp technique, we found that insulin (1-600 nmol/l) but not IGF-1 (100 nmol/l) reversibly hyperpolarized single mouse beta-cells and inhibited their electrical activity. The dose-response relationship for insulin yielded a maximal change (mean +/- SE) in membrane potential of -13.6 +/- 2.0 mV (P < 0.001) and a 50% effective dose of 25.9 +/- 0.1 nmol/l (n = 63). Exposing patched beta-cells within intact islets to 200 nmol/l insulin produced similar results, hyperpolarizing islets from -47.7 +/- 3.3 to -65.6 +/- 3.7 mV (P < 0.0001, n = 11). In single cells, insulin-induced hyperpolarization was associated with a threefold increase in whole-cell conductance from 0.6 +/- 0.1 to 1.7 +/- 0.2 nS (P < 0.001, n = 10) and a shift in the current reversal potential from -25.7 +/- 2.5 to -63.7 +/- 1.0 mV (P < 0.001 vs. control, n = 9; calculated K(+) equilibrium potential = -90 mV). The effects of insulin were reversed by tolbutamide, which decreased cell conductance to 0.5 +/- 0.1 nS and shifted the current reversal potential to -25.2 +/- 2.3 mV. Insulin-induced beta-cell hyperpolarization was sufficient to abolish intracellular calcium concentration ([Ca(2+)](i)) oscillations measured in pancreatic islets exposed to 10 mmol/l glucose. The application of 100 nmol/l wortmannin to inactivate PI 3-kinase, a key enzyme in insulin signaling, was found to reverse the effects of 100 nmol/l insulin. In cell-attached patches, single ATP-sensitive K(+) (K(ATP)) channels were activated by bath-applied insulin and subsequently inhibited by wortmannin. Our data thus demonstrate that insulin activates the K(ATP) channels of single mouse pancreatic beta-cells and islets, resulting in membrane hyperpolarization, an inhibition of electrical activity, and the abolition of [Ca(2+)](i) oscillations. We thus propose that locally released insulin might serve as a negative feedback signal within the islet under physiological conditions.

Adenosine Triphosphate↗
PubMed1994

Muscarinic regulation of Ca2+ currents in rat sensory neurons: channel and receptor types, dose-response relationships and cross-talk pathways.

We studied, in rat sensory neurons, the modulation of high voltage-activated Ca2+ currents (ICa) mediated by the pertussis toxin-sensitive activation of muscarinic receptors, which were found to be of subtypes M2 or M4. Muscarine reversibly blocked somatic Ca2+ spikes but strong predepolarizations only partially relieved the inhibited Ca2+ current. On the other hand, the putative coupling messenger could not rapidly diffuse towards channels whose activity was recorded from a macro-patch. The perforated patch technique virtually prevented the response rundown present during whole-cell experiments. Both omega-conotoxin GVIA (omega-CgTx)-sensitive channels and omega-CgTx- and dihydropyridine-resistant channels are coupled to the muscarinic receptor, but not the L-channel. When measured in the same neuron, dose-response relationships for the first and subsequent agonist applications differed; maximal inhibition, the reciprocal of half-maximal concentration and the Hill coefficient were always highest in the first trial. Muscarine and oxotremorine exhibited monotone dose-response curves, but oxotremorine-M showed non-linear relationships which became monotonic when cells were intracellularly perfused with inhibitors of protein kinase A (PKA) and C (PKC), suggesting that either PKA or receptor-induced PKC could phosphorylate and thus inactive G-proteins or other unknown proteins involved in inhibitory muscarinic actions on ICa. In summary, these data provide a preliminary pharmacological characterization of the muscarinic inhibition of the Ca2+ channels in sensory neurons, with implications about agonist specificity and the interplay between signalling pathways.

Action Potentials↗
PubMed1975

Long-term potentiation of the perforant path-granule cell synapse in the rat hippocampus.

When the entorhinal cortex is electrically stimulated, a monosynaptic evoked potential is produced in the ipsilateral hippocampus. Twenty-four hours after a 120-pulse stimulation train, the response to a single test pulse was found to be increased. Stimulation trains presented at a rate of 1/day had a cumulative effect on both the population EPSP and spike components of the evoked potential, and the potentiation so produced lasted at least 12 days. In a few cases, retested 2 months after the last stimulation train, the population EPSP was found to be still highly potentiated while the population spike had declined to initial levels. The most reliable results and largest potentiation were obtained with diphasic stimulation trains of 10 Hz or greater, though some changes were observed even with very low frequencies (0.2 Hz). The results imply that the efficiency of synaptic transmission in the perforant path-granule cell synapse can be modified.

Animals↗
PubMed1988

The role of medial and lateral hippocampal perforant path lesions and object distinctiveness in rats' reaction to novelty.

The purpose of the present study was to investigate whether damage to the medial (MPP) or lateral hippocampal perforant path (LPP) may differentially affect rats' ability to react to novelty or environmental change. Three different types of task were used based on various sets of stimuli; visual/tactile, olfactory, or visual only. The results showed that the lesions produced different responses to different novel stimuli. In contrast to control and MPP animals, LPP rats displayed excessive exploration of the test cage. The results are discussed in terms of impoverished cognitive structure following perforant path disruptions and functional differentiation between MPP and LPP.

Animals↗
PubMed2005

Evidence against reciprocal regulation of Ca2+ entry by vasopressin in A7r5 rat aortic smooth-muscle cells.

Recent studies by Moneer and Taylor [(2002) Biochem. J. 362, 13-21] have proposed a reciprocal regulation of two Ca2+-entry pathways by AVP ([Arg8]-vasopressin) in A7r5 vascular smooth-amuscle cells. Their model proposes that AVP inhibits CCE (capacitative Ca2+ entry) and predicts a rebound of CCE after the removal of AVP. In the present study, we used whole-cell perforated patch-clamp techniques to measure ISOC (store-operated current) corresponding to CCE in A7r5 cells. When 100 nM AVP is present, it activates ISOC with no apparent rebound on removal of AVP. ISOC activated by thapsigargin or cyclopiazonic acid was not inhibited by 100 nM AVP. We also used fura 2 fluorescence techniques to re-examine the model of Moneer and Taylor, specifically focusing on the proposed inhibition of CCE by AVP. We find that 100 nM AVP activates capacitative Mn2+ entry and does not inhibit thapsigargin- or cyclopiazonic acid-activated Mn2+ entry. Moreover, Ca2+ entry after depletion of intracellular Ca2+ stores is enhanced by AVP and we detect no rebound of Ca2+ or Mn2+ entry after AVP removal. On the basis of these findings, we conclude that AVP does not inhibit CCE in A7r5 cells.

Animals↗
PubMed1995

The entorhinal cortex entrains fast CA1 hippocampal oscillations in the anaesthetized guinea-pig: role of the monosynaptic component of the perforant path.

Entorhinal inputs reach the hippocampal CA1 field through a trisynaptic circuit involving dentate granule cells and CA3 pyramidal neurons, as well as through a monosynaptic path ending on the distal apical dendrites of CA1 pyramidal cells. The influence of monosynaptic entorhinal inputs onto CA1 operations is poorly understood. In this study, we characterized the involvement of the monosynaptic pathway in the generation of the fast CA1 oscillation bursts (30-60 Hz) that occur in the dorsal hippocampus of anaesthetized guinea-pigs after partial cortex removal. Using multiple-site extracellular and intracellular recording, we found that in this particular preparation, devoid of theta rhythm, fast oscillations are temporally coherent over a large portion of the CA1 region along the hippocampal septotemporal axis. Current source density analysis revealed that fast CA1 oscillations involve two dipoles reflecting synchronous synaptic activities in the stratum lacunosum-moleculare of the hippocampus proper and in the stratum moleculare of the dentate gyrus. These layers constitute the two major termination zones of entorhinal afferents, suggesting that the entorhinal cortex entrains fast CA1 oscillations. This hypothesis was corroborated by the concomitant occurrence of fast oscillation bursts in the entorhinal cortex and CA1 region. Furthermore, fast CA1 oscillations were abolished by lidocaine or tetrodotoxin injections in the entorhinal cortex. Finally, acute interruption of the hippocampal trisynaptic loop did not affect the stratum lacunosum-moleculare dipole recorded extracellularly, but also intracellularly, as high-frequency postsynaptic potentials in CA1 pyramidal cells. These results indicate that the monosynaptic pathway is involved in the genesis of fast CA1 oscillations.

Animals↗
PubMed2000

Visual processing in patients with macular hole.

Macular hole is a specific disease of the central retina that affects central visual acuity and central visual field. The purpose of this study is to investigate the alteration of visual processing in patients with macular hole who had small central scotoma. Six patients with macular hole participated in this study. We used positron emission tomography (PET) to measure task-related changes in regional cerebral blood flow to identify regions of the brain activated during visual stimulation. Three tasks were performed in each eye: control task, checkerboard task, shape-discrimination task. Checkerboard stimuli caused a greater blood flow activation response in normal eyes than in affected eyes at the occipital cortex. The area involved in the macular hole appeared to be 20 mm or more anteriorly from the occipital pole. The Shape-discrimination task in affected eyes activated angular gyrus, inferoparietal lobule, and middle frontal gyrus. Our findings demonstrated greater confidence in Horton's new retinotopic map than in Holmes' retinotopic map in cortical areas involved in macular function. The dorsal pathway of the visual system was activated more than the ventral pathway in patients with macular hole.

Aged↗
PubMed1990

Percutaneous transcatheter laser balloon ablation from the canine coronary sinus: implications for the Wolff-Parkinson-White syndrome.

Transcatheter direct current electrical shocks for ablation of left-sided accessory pathways in Wolff-Parkinson-White patients have led to serious complications. We report the feasibility of percutaneous transcatheter laser balloon ablation of left-sided accessory pathways from the coronary sinus using a 1,064-nm, continuous wave Nd:YAG laser triple lumen catheter with an optical fiber terminating in a cylindrical diffusing tip within a 2-cm-long, 3-mm-diameter balloon transparent to Nd:YAG laser radiation. In eight mongrel dogs (18 to 31 kg), the laser balloon catheter was positioned via an 8 French guide catheter in the distal and proximal coronary sinus. During balloon inflation, two to three consecutive laser doses of 30 W x 20 sec were applied to each site (cumulative energy, 1,200 to 1,800 J). Coronary angiography, left ventriculography, and coronary sinus injection were performed before and after laser exposure. After percutaneous transcatheter laser balloon ablation, there was no evidence of mitral regurgitation, left circumflex artery, coronary sinus obstruction, or perforation. Coagulation necrosis and/or polymorphonuclear infiltrates involving the atrioventricular groove and left atrial wall over a mean length of 17 mm were present in all eight dogs sacrificed 6 +/- 1 hr postablation. In conclusion, percutaneous transcatheter laser balloon ablation from the coronary sinus is free of immediate major complications and may be feasible for potential interruption of left-sided accessory pathways.

Animals↗
PubMed1996

Myoblast fusion requires cytosolic calcium elevation but not activation of voltage-dependent calcium channels.

Many studies of in vitro skeletal myogenesis have demonstrated that fusion of myoblasts into multinucleated myotubes is regulated by calcium-dependent processes. Calcium ions appear to be necessary at the outer face of the membrane, and an additional internal calcium increase seems required to promote fusion of aligned myoblasts. It has been proposed that a calcium influx could take place prior to fusion and that this may be mediated by voltage-dependent calcium channels. Previously, we showed that two types of voltage-dependent calcium currents were expressed in multinucleated myotubes but not in rat myoblasts growing in primary culture before the withdrawal of the growth medium. We also showed that the previous formation of multinucleated synticia was not a prerequisite of developmental appearance of calcium currents, suggesting that the two events were time-correlated but not sequentially dependent. These features led us to investigate changes in internal calcium activity and the possible appearance of voltage-dependent calcium influx pathways just after the promotion of fusion by the change of culture medium. The results confirm that a rise in cytosolic calcium activity occurs slightly before fusion in confluent myoblasts and remained in newly formed myotubes. Reducing this elevation by internal calcium buffering lowered myoblast fusion and, reciprocally, blocking cell fusion prevented calcium increase. Treatment with the organic calcium channel blockers nifedipine (5 microM) and PN 200-110 (1 microM) did not alter cytosolic calcium changes nor cell fusion, and voltage-dependent calcium currents were never observed by the perforated patch-clamp technique in aligned fusion-competent myoblasts. Other voltage-operated mechanisms of calcium rise were not detected since depolarization with hyperpotassium solutions failed to elicit increases in intracellular calcium. On the contrary, acetylcholine was able to promote extracellular calcium-dependent calcium transients. Our results confirm the requirement of an increase in resting calcium during fusion, but do not support the hypothesis of an influx through voltage-dependent channels or other voltage-operated pathways. The elevation of internal calcium activity may result from other mechanisms, such as a cholinergic action for example.

Animals↗
PubMed1991

Focal stimulation of the mossy fibers releases endogenous dynorphins that bind kappa 1-opioid receptors in guinea pig hippocampus.

Physiological release of endogenous opioids in guinea pig hippocampal slices was detected in an in vitro competition binding assay using [3H]U69,593, a kappa 1-selective radioligand. Veratridine-induced opioid release caused a decrease in [3H]U69,593 binding that was blocked by either tetrodotoxin addition or the removal of calcium from the incubation buffer. Focal electrical stimulation of opioid peptide-containing afferent pathways resulted in a decrease in [3H]U69,593 binding, whereas stimulation of a major afferent lacking endogenous opioid immunoreactivity had no effect. The addition of 6-cyano-7-nitroquinoxaline-2,3-dione blocked the reduction in [3H]U69,593 binding caused by perforant path stimulation, but not the reduction caused by mossy fiber stimulation, suggesting that the primary source of endogenous kappa ligands was likely to be the dentate granule cells. Antisera against dynorphin A(1-8) or dynorphin B peptides inhibited the effects of mossy fiber stimulation in the [3H]U69,593 displacement assay. Antisera against other prodynorphin- and proenkephalin-derived opioid peptides had no effect. As shown by receptor autoradiography, the distribution of kappa 1 binding sites was limited to the molecular layer of the dentate gyrus and the presubiculum region of temporal hippocampal slices. These results indicate that prodynorphin-derived opioids released under physiological conditions from the mossy fibers act at kappa 1 receptors in the guinea pig dentate gyrus.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed2005

Effects of unoprostone and endothelin 1 on L-type channel currents in human trabecular meshwork cells.

BACKGROUND: The trabecular meshwork (TM) is a smooth muscle-like tissue with contractile properties and by this mechanisms involved in the regulation of aqueous humor outflow. Isopropyl unoprostone (Rescula, Novartis Ophthalmics), a synthetic docosanoid, reduces intraocular pressure in glaucoma patients and normal subjects. In isolated TM strips, unoprostone reduces TM contractility in the presence of endothelin 1 (ET-1). However, the signal transduction pathway of unoprostone still remains unclear. Since L-type channel currents are known to influence the contractility of TM, we examined the effects of unoprostone and ET-1 on L-type channel currents of TM cells. METHODS: The effects of unoprostone, ET-1 and the tyrosine kinase inhibitor herbimycin A on L-type channel currents of cultured human TM cells were investigated using the perforated patch configuration of the patch-clamp technique. RESULTS: Application of ET-1 had no effect on L-type channel currents. Unoprostone led to a dose-dependent reduction of control currents. The effect of unoprostone is independent of ET-1. After preincubation of cells with herbimycin A, unoprostone had no effect on the L-type channel current amplitude. Human TM cells preincubated with herbimycin A showed a reduced current density compared with control cells. Both substances, unoprostone and herbimycin A, increased the inactivation time constant of L-type channel currents. CONCLUSION: We conclude that unoprostone reduces the activity of L-type Ca2+ channels. This effect seems to be independent of ET-1. The signal transduction pathway seems to be mediated by tyrosine kinases.

Benzoquinones↗