Biomedical subjects

D Christ

Publications and source records attributed to D Christ.

21 records · Page 2Linked to original sources

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↗