Search PubMed⌕ Search

Biomedical subjects

J W Moore

Publications and source records attributed to J W Moore.

At least 289 records · Page 16Linked to original sources
PubMed1967

Tetrodotoxin derivatives: chemical structure and blockage of nerve membrane conductance.

The nerve-impuilse-blocking actions of derivatives of tetrodotoxin have been tested on lobster and squid axons. The block produced by deoxytetrodotoxin was similar to that produced by tetrodotoxin and was probably caused by tetrodotoxin contamination. Tetrodaminotoxin and anhydrotetrodotoxin also produced a similar block but at such high concentrations that tetrodotoxin contamination cannot be ruled out. The hydroxyl group of C(4) and the hemilactal oxygen links play an important role for the nerve-blocking action.

Animals↗
PubMed1967

Basis of tetrodotoxin's selectivity in blockage of squid axons.

The blockage of nerve activity by tetrodotoxin is unusually potent and specific. Our experiments were designed to distinguish whether its specificity of action was based on the identification of ions, the direction of cation flow, or differences in the early transient and late steady conductance pathways. Alkali cations were substituted for sodium in the sea water, bathing an "artificial node" in a voltage-clamped squid axon. When tetrodotoxin was added to the artificial sea waters at a concentration of 100 to 150 mM, it was found to always block the flow of cations through the early transient channel, both inward and outward, but it never blocked the flow of ions using the late steady pathway. We conclude that the selectivity of tetrodotoxin is based on some difference in these two channels.

Animals↗
PubMed1967

Comparison of tetrodotoxin and procaine in internally perfused squid giant axons.

Squid giant axons were internally perfused with tetrodotoxin and procaine, and excitability and electrical properties were studied by means of current-clamp and sucrose-gap voltage-clamp methods. Internally perfused tetrodotoxin was virtually without effect on the resting potential, the action potential, the early transient membrane ionic current, and the late steady-state membrane ionic current even at very high concentrations (1,000-10,000 nM) for a long period of time (up to 36 min). Externally applied tetrodotoxin at a concentration of 100 nM blocked the action potential and the early transient current in 2-3 min. Internally perfused procaine at concentrations of 1-10 mM reversibly depressed or blocked the action potential with an accompanying hyperpolarization of 2-4 mv, and inhibited both the early transient and late steady-state currents to the same extent. The time to peak early transient current was increased. The present results and the insolubility of tetrodotoxin in lipids have led to the conclusion that the gate controlling the flow of sodium ions through channels is located on the outer surface of the nerve membrane.

Action Potentials↗
PubMed1967

An upper limit to the number of sodium channels in nerve membrane?

1. A small volume of artificial sea water containing 300 nM tetrodotoxin (TTX) was applied successively to seven lobster nerve trunks and the cumulative uptake of toxin investigated by bio-assay.2. Light and electron microscopy indicated that the nerve trunks had a total axonal area of 0.7 x 10(4) cm(2)/g.3. Sodium analysis gave a sodium space for the nerve trunks of 30%.4. The amount of toxin taken up by the cells in 1 g of nerve is less than 1.6 x 10(-11) moles.5. It is argued that there are probably fewer than 13 sodium channels/mu(2) axon in lobster nerve.

Action Potentials↗
PubMed1966

Tetrodotoxin does not block excitation from inside the nerve membrane.

Tetrodotoxin does not block the action potential or membrane sodium current when internally perfused through the giant axon of a squid at much higher concentrations than those required for blocking by external application. It is suggested that the gate for the sodium channel is located on the exterior surface of the axon, because tetrodotoxin is not lipid soluble.

Animals↗