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D Christ

Publications and source records attributed to D Christ.

18 recordsLinked to original sources
PubMed1995

Effects of calmodulin and protein kinase C antagonists on muscle in the filariid, Acanthocheilonema viteae.

Drugs that act on calmodulin and protein kinase C (PKC) were investigated in the filariid Acanthocheilonema viteae. The filariid was slit open longitudinally and attached to an isotonic muscle transducer in a warmed (37 C) chamber containing physiologic solution bubbled with 95% N2-5% CO2. The calmodulin inhibitors, trifluoperazine and N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide hydrochloride (W-7), increased the spontaneous contractions of the parasite at low concentrations and induced a contraction followed by a flaccid paralysis at high concentrations. Trifluoperazine and W-7 also reduced the contractions from acetylcholine (ACh) and KCl in a concentration-dependent manner. The phorbol esters, phorbol 12-myristate 13-acetate and phorbol 12, 13-dibutyrate, which activate PKC, were either inactive or only weakly active at inducing contractions. Staurosporine (10(-6) M), a PKC inhibitor, enhanced and then blocked the spontaneous contractions of the filariid. Two other PKC inhibitors, H-7 (10(-4) M) and sphingosine (3 x 10(-5) M), induced much smaller increases in the spontaneous contractions and did not inhibit them. Staurosporine and sphingosine inhibited the ACh contractions; however, staurosporine only slightly reduced the maximal KCl contraction. These results support a role for calmodulin, but not for PKC, in filarial muscle contraction.

Acetylcholine↗
PubMed1994

Contractions of the filariid Acanthocheilonema viteae induced by potassium chloride.

The effects of K+ on muscle contractility were explored in the filarial nematode Acanthocheilonema viteae (Dipetalonema viteae). The parasite was slit open longitudinally and mounted in a smooth muscle chamber that was filled with aerated (95% N2-5% CO2) physiological solution at 37 degrees C. KCl at concentrations ranging from 20 to 100 mM induced a rapid isotonic contraction of the filarial muscle. The maximal response from KCl was similar to the maximal response to acetylcholine chloride (ACh). When KCl was applied for several minutes, tolerance frequently occurred. Contractions were also induced by K2SO4 but not by NaCl, Na2SO4 or sucrose. Nifedipine was more than 10 times as potent in reducing the KCl-induced contraction as in reducing that caused by ACh. The KCl-induced contraction was abolished in a Ca-free physiological medium containing ethyleneglycol-bis-(beta-aminoethyl ether) N, N, N', N'-tetraacetic acid (EGTA, 10(-4) M). Low [Ca2+]/[Mg2+] solutions blocked the spontaneous activity, the KCl-induced contractions, and the ACh-induced contractions. KCl also induced contractions in denervated muscle strips, supporting the hypothesis that K+ acts directly on the muscle cells. These results indicate that K+ can depolarize the muscle membrane and induce a muscle contraction that is dependent on extracellular calcium ions.

Animals↗
PubMed1992

[Characterization of Streptococcus uberis with special consideration of supposed pathogenicity factors].

Streptococcus uberis, as one of the principal causes of bovine streptococcal mastitis, has been characterized serologically and biochemically. Serological grouping of S. uberis revealed polysaccharide antigens of groups E, G, P and U. The biochemical properties of S. uberis, determined with the Strep-Zym identification system, differed clearly from those of S. agalactiae and S. dysgalactiae. Some cultures of S. uberis produced the enzymes hyaluronidase and neuraminidase. In addition S. uberis partly demonstrated CAMP-like synergistic hemolytic activities on sheep blood agar, reacted specifically with the lectins from Helix pomatia and Dolichos biflorus and produced bacteriocin-like inhibitors. This reactions, possibly of importance as virulence factors, as well as "DNA-fingerprinting" of S. uberis, might serve as individual markers of the respective cultures in epidemiological studies.

Animals↗
PubMed1992

Effects of calcium channel blockers on the contractility of the filariid Acanthocheilonema viteae.

The role of calcium in muscle contractility was explored in the filarial nematode Acanthocheilonema viteae (Dipetalonema viteae). The parasite was slit open longitudinally and mounted in a smooth-muscle chamber that had been filled with aerated (95% N2/5% CO2) physiological solution at 37 degrees C. Nifedipine (10(-6) M) and cadmium (3 x 10(-5) M) reduced the spontaneous isotonic contractions of A. viteae, whereas verapamil (10(-5) M) and diltiazem (10(-5) M) enhanced them. The effects of nifedipine and verapamil did not appear to be due to the solvent ethanol. All of the drugs reduced the maximal contraction induced by acetylcholine (ACh, 10(-5) M), although nifedipine was the most potent. After the exposure of worm preparations to a calcium-free medium containing ethyleneglycol-bis-(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA, 10(-4) M) for 1 h, application of ACh (10(-5) M) induced a small, transient contraction. Subsequent applications of ACh in this medium had no effect. Thus, the nematode muscle contraction appears to depend on extracellular calcium. Nifedipine, diltiazem, and verapamil could act by reducing the calcium influx across the muscle membrane.

Acetylcholine↗
PubMed1990

Actions of acetylcholine and GABA on spontaneous contractions of the filariid, Dipetalonema viteae.

1. Isotonic contractions were recorded from the filarial nematode, Dipetalonema viteae (Acanthocheilonema viteae), in an isolated tissue chamber. 2. Nicotine (10(-6) M) and pilocarpine (10(-5) M) increased the spontaneous contractions in the intact filariid, but acetylcholine (ACh, 10(-4) M) and muscarine (10(-5) M) were inactive. 3. When ACh was applied to an opened D. viteae, it was 10,000 times more potent. This indicates that the cuticle is an effective barrier to the penetration of ACh to the muscle cells. 4. The effects of ACh on the opened D. viteae were not affected by hexamethonium (10(-3) M) or atropine (10(-5) M) and were only partially reduced by (+)-tubocurarine (10(-4) M). 5. gamma-Aminobutyric acid (GABA, 10(-3) M) reduced the spontaneous activity of the intact D. viteae; however, the effect of GABA had a slow onset and recovery. Muscimol (10(-5) M) was more potent than GABA and had a more rapid onset and recovery. 6. GABA was 1,000 times more potent on the opened D. viteae than on the intact D. viteae. Baclofen (10(-3) M) was inactive on both preparations. 7. The effect of GABA was not antagonized by bicuculline (10(-4) M), picrotoxin (10(-5) M or penicillin G (10(-3) M). 8. It is concluded that the filariid cuticle acts like a lipid structure and blocks the penetration of polar substances, such as ACh and GABA. Also, due to the lack of efficacy of the ACh and GABA antagonists, it was concluded that the nematode receptors are somewhat different from the mammalian ACh and GABA receptors.

Acetylcholine↗
PubMed1989

Streptolytic activities of a lytic enzyme from Staphylococcus hyicus.

The LE IIIb fraction of the bacteriolytic enzyme from Staphylococcus hyicus could be isolated by ionic exchange chromatography and subsequent gel filtration. Isoelectric focusing of the highly purified enzyme preparation revealed an isoelectric point at pH 10.3. The lytic activity of LE IIIb on streptococci of various serogroups could be effectively analyzed with the help of an aggregometer and expressed as increase of transmittance at 546 nm. The streptococci differed in their LE IIIb lysis pattern, which was more pronounced with those of serological groups C and D and Streptococcus uberis. The lytic effect of the LE IIIb fraction was optimal at low molarity (0.01 mol/l) of the lysis buffer and reduced in the presence of HgCl2 and EDTA.

Animals↗
PubMed1984

Blockade of ganglionic afterdischarges by tyramine may be mediated by endogenous catecholamines.

Tyramine reduced the compound postganglionic action potential from preganglionic stimulation of the golden hamster isolated stellate ganglion at 0.2 Hz. This action of tyramine was only slightly reduced by phentolamine (10(-5)M), an alpha adrenoceptor antagonist. Tyramine also reduced the postganglionic discharges after preganglionic stimulation at 30 Hz for 2 sec in the presence of hexamethonium. The blockade of afterdischarges by tyramine was markedly reduced by phentolamine. Furthermore, tyramine was much less effective in blocking ganglia from reserpine-pretreated hamsters (6 mg/kg, 4 hr before isolation). Blockade of afterdischarges by norepinephrine was reduced by phentolamine, but not by reserpine. These results indicate that the blockade of afterdischarges with tyramine is mediated by endogenous catecholamines. The blocking action of tyramine was not reduced by cocaine (10(-5)M). Cocaine did reduce the afterdischarges, and this action of cocaine was partially antagonized by phentolamine and reserpine. These results suggest that the blockade of afterdischarges by tyramine and cocaine is due to inhibition of catecholamine uptake which potentiates the actions of endogenous catecholamines.

Action Potentials↗
PubMed1983

Ganglionic blockade by d-amphetamine.

The actions of d-amphetamine on ganglionic transmission in the isolated stellate ganglion of the hamster were observed. Blockade of the compound action potential by d-amphetamine had a slow onset with an onset half-time of 2-5 min. The concentration-blockade relationship for d-amphetamine was not shifted by phentolamine (10(-5) M) or propranolol (10(-6) M). The blockade was frequency-dependent, and the frequency-dependence was suppressed by atropine (10(-6) M). It was suggested that the frequency-dependence of d-amphetamine involved a muscarinic mechanism. In support of this suggestion, the afterdischarges from repetitive stimulation in hexamethonium were relatively insensitive to d-amphetamine. Also afterdischarges could be recorded after repetitive stimulation in 10(-4) M d-amphetamine, without hexamethonium. High concentrations of d-amphetamine (10(-3) M) induced discharges in the postganglionic nerve and potentiated the discharges from the cholinergic agonists, DMPP and McN-A-343. Tolerance rapidly developed to these stimulatory effects. These results indicate that ganglionic blockade by d-amphetamine is produced by a different mechanism than ganglionic blockade by the catecholamines.

Action Potentials↗
PubMed1982

Interactions of catecholamine uptake inhibitors and norepinephrine on autonomic ganglia.

The effect of catecholamine uptake inhibitors on blockade by norepinephrine was observed in the isolated stellate ganglion of the hamster. The preganglionic nerve was stimulated, supramaximally, at 0.2 Hz and compound action potentials were recorded from the postganglionic nerve. Norepinephrine blocked ganglionic transmission. The sensitivity of the ganglion to norepinephrine was increased by the catecholamine uptake inhibitors, desipramine (3 X 10(-7) M), d-amphetamine (10(-6) and 10(-5) M) and tyramine (10(-4) M). Ouabain (10(-5) and 3 X 10(-5) M) did not change the sensitivity of the ganglion to norepinephrine. All the drugs reduced the uptake by the [3H]norepinephrine into the ganglion. The inhibition of [3H]norepinephrine uptake by the drugs could be correlated with the increase in sensitivity of the ganglion to norepinephrine. These results support the hypothesis that catecholamine uptake is important in terminating the actions of exogenously applied norepinephrine, and that inhibition of the catecholamine uptake increases the sensitivity of the ganglion to norepinephrine.

Animals↗
PubMed1982

Potentiation of the ganglionic blocking action of norepinephrine by cocaine.

Concentration-response curves for the blocking action of norepinephrine were determined in the isolated stellate ganglion of the hamster. The blocking effect of norepinephrine on the postganglionic compound action potential from preganglionic nerve stimulation at 0.2 Hz was reduced by phentolamine (10(-5) M), but was not altered by propranolol (10(-6) M). Cocaine (10(-6) and 10(-5) M) increased the sensitivity of the ganglion to norepinephrine. These concentrations of cocaine produced less than 25% blockade when applied alone. The local anesthetic, procaine, did not change the sensitivity of the ganglion to norepinephrine. The blockade by norepinephrine in the presence of cocaine was antagonized by phentolamine and unaffected by propranolol. The time course of the blockade by norepinephrine was more rapid in onset and slower in recovery in the presence of cocaine. If it is assumed that cocaine is blocking norepinephrine uptake into cells within the ganglion, these results indicate that the catecholamine uptake mechanism is involved in terminating the blocking action of exogenously applied norepinephrine.

Animals↗
PubMed1980

Post-tetanic potentiation in ganglia which are blocked with hexamethonium.

1 Post-tetanic potentiation (p.t.p.) of the compound action potential in the presence of hexamethonium was observed in the isolated stellate ganglion of the hamster using extracellular postganglionic recordings. 2 The magnitude of the p.t.p. was small (less than a 20% increase) in the control solution, but increased as the depth of blockade with hexamethonium was increased. 3 The magnitude of the p.t.p. was frequency-dependent between 1 and 40 Hz. 4 Atropine partially blocked the p.t.p. 5 McN-A-343, a muscarinic agonist, potentiated ganglionic transmission which had been partially blocked by hexamethonium. 6 Repetitive stimulation in the presence of hexamethonium potentiated the discharges induced by DMPP, a nicotonic agonist. The potentiation was blocked by atropine. 7 It was concluded that the p.t.p. in the presence of hexamethonium has the same characteristics as p.t.p. in the control solution. There appears to be both a muscarinic component and a presynaptic component of the p.t.p.

Action Potentials↗
PubMed1979

Effects of nicotine and hexamethonium on discharges in the stellate ganglion.

The effects of nicotine and hexamethonium on postganglionic discharges elicited by tetanic preganglionic stimulation or muscarinic agonists were observed on the isolated hamster stellate ganglion. The amplitude and duration of the afterdischarges from tetanic preganglionic stimulation in hexamethonium (10-3 M) were smaller than the amplitude and duration of the afterdischarges in nicotine (10-3 M). Also, hexamethonium decreased the amplitude and duration of the afterdischarges from repetitive stimulation in the presence of nicotine. The mechanism of these effects was explored. After application of nicotine for 30 min, the discharges from McN-A-343, a muscarinic agonist, were the same as before the nicotine. Hexamethonium did not reverse the block of the single evoked potential by nicotine. The potentials during a train in the presence of hexamethonium plus atropine were the same as the potentials during a train in the presence of nicotine plus atropine. Hexamethonium did depress the McN-A-343 discharges in the presence of nicotine and also in the control solution. These results indicate that hexamethonium has a direct depressant effect on the muscarinic synaptic membrane.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1977

Effects of halothane on ganglionic discharges.

The effects of halothane on ganglionic transmission were studied by recording extracellular potentials from the postganglionic nerve of the isolated hamster stellate ganglion. Halothane, at concentrations greater than 0.1 mM, decreased the potentials evoked by preganglionic stimuli at 0.2 Hz. Halothane also blocked discharges elicited by 1,1-dimethyl-4-phenylpiperazinium, a selective nicotinic agonist, and discharges elicited by the nicotinic actions of exogenous acetylcholine. Repetitive preganglionic stimulation (30 Hz, 5 seconds) in the presence of nicotine (10(-3) M), or hexamethonium (10(-3) M), evoked asynchronous discharges in the postganglionic nerve. These discharges were suppressed by low concentrations of atropine, and were probably due to the muscarinic actions of neurotransmitter. Halothane depressed these discharges at approximately the same concentration that it depressed the compound action potential elicited by low frequency preganglionic stimulation in the untreated ganglion. Halothane had no effect on the discharges elicited by 4-(m-chlorophenylcarbamoyloxy)-2-butynyltrimethylammonium chloride (McN-A-343), a selective muscarinic agonist, or the discharges elicited by the muscarinic actions of acetylcholine. These results are most readily explained by hypothesizing that halothane acts at two sites in the ganglion. It appears to depress the postsynaptic response to the nicotinic actions of the neurotransmitter, acetylcholine. Also, it probably depresses transmitter release from the presynaptic nerve endings during repetitive stimulation.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMedDate not supplied

Neurotoxicological effects of trimethyltin on the stellate ganglion.

Hamsters treated with trimethyltin (TMT), 3 or 4 mg/kg IP, developed neurological symptoms, including tremor, within 24 hours. Postganglionic action potentials were recorded from isolated stellate ganglia of untreated hamsters (control ganglia) and TMT-treated hamsters (TMT ganglia). Compound action potentials (nicotinic transmission) of control and TMT ganglia were not significantly different. The afterdischarges induced by preganglionic stimulation at 30 Hz for 2 sec in the presence of 10(-3) M hexamethonium (muscarinic transmission) were significantly smaller in TMT ganglia than in control ganglia. The discharges induced by the muscarinic cholinoceptor agonist. McN-A-343, were also smaller in the TMT ganglia. Two other muscarinic processes, posttetanic potentiation and potentiation of the compound action potential by McN-A-343, were not significantly reduced in the TMT ganglia. Morphological studies of the ganglia revealed marked changes in the TMT ganglia with severe neuronal degeneration including vacuole formations and accumulations of lysosomes in the cytoplasm. These results demonstrate that TMT has marked anatomical effects on the stellate ganglion that may lead to the reduction in muscarinic cholinergic transmission.

Action Potentials↗
PubMedDate not supplied

Post-train depression of ganglionic transmission in the presence of d-amphetamine.

Repetitive stimulation (30 Hz, 20 sec) of the preganglionic nerve to the hamster isolated stellate ganglion in a control solution had only small effects on the compound action potentials of the postganglionic nerve (0.2 Hz) after the train. When 10(-5) M d-amphetamine was added to the superfusing solution, the repetitive stimulation induced a post-train depression of the postganglionic compound action potential. The mean reduction of the compound action potential during the post-train depression in d-amphetamine was 37 +/- 15% and the duration was from 60 to 120 sec. Post-train depression only occurred after long conditioning trains and was never observed with less than 100 stimuli in the conditioning train. A post-train depression (45 +/- 8%) was also observed in the presence of 10(-5) M cocaine. The post-train depression in d-amphetamine was significantly reduced by the alpha-adrenoceptor antagonist, phentolamine (10(-5) M) and by the alpha 2-adrenoceptor antagonist, yohimbine (10(-6) M), but not by the alpha 1-adrenoceptor antagonist, prazosin (10(-5) M). There was no post-train depression in the presence of d-amphetamine in ganglia from five hamsters that were pretreated with reserpine (6 mg/kg, i.p., 4 hr). Atropine (10(-6) M) increased and prolonged the post-train depression in the presence of d-amphetamine. These results indicate that repetitive stimulation in the presence of d-amphetamine leads to a post-train depression of the postganglionic compound action potential that is mediated by an action of endogenous catecholamines at alpha 2-adrenoceptors. Muscarinic cholinoceptors do not appear to be involved in the generation of the post-train depression.

Action Potentials↗