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Biomedical subjects

B Hille

Publications and source records attributed to B Hille.

118 records · Page 7Linked to original sources
PubMed1969

Light scattering and birefringence changes during activity in the electric organ of electrophorus electricus.

1. In an attempt to obtain information about structural changes related to electrical activity in Electrophorus electroplates, we have determined the size and time course of the changes in light scattering and in bire-fringence that occur during and after the discharge of the electric organ.2. The changes in light intensity detected with a photomultiplier were never greater than 0.2% for a single discharge, and were often much smaller than this, but records with an acceptable ratio of signal to noise could be obtained by signal-averaging techniques.3. A single stimulus led to a decrease, then an increase, and finally another decrease in the light scattered by slices of the main electric organ. These three phases were designated E1, E2 and E3.4. E1 started at the beginning of the action potential, and its peak was reached at the same time as the completion of repolarization, even when the repolarization was delayed by cooling or hastened by drawing larger currents from the tissue.5. E2 was proportional to the integral of the current flowing through the slice of electric organ, and may arise from the swelling and shrinking of the tubules that stud the faces of the electroplates. It developed within a millisecond or two of the start of an applied current, and lasted for about 100 msec.6. E3 was a variable decrease in scattering that lasted for some seconds.7. A stimulus also led to a transient increase in the birefringence of the electric organ. The optical change followed the change in electrical potential across the innervated faces of the electroplates with a delay of somewhat under 50 musec.8. This voltage-dependent change in birefringence may arise from a Kerr effect (electric birefringence) in the membrane or from compression of the membrane.

Action Potentials↗
PubMed1968

Pharmacological modifications of the sodium channels of frog nerve.

Voltage clamp measurements on myelinated nerve fibers show that tetrodotoxin, saxitoxin, and DDT specifically affect the sodium channels of the membrane. Tetrodotoxin and saxitoxin render the sodium channels impermeable to Na ions and to Li ions and probably prevent the opening of individual sodium channels when one toxin molecule binds to a channel. The apparent dissociation constant of the inhibitory complex is about 1 nM for the cationic forms of both toxins. The zwitter ionic forms are much less potent. On the other hand, DDT causes a fraction of the sodium channels that open during a depolarization to remain open for a longer time than is normal. The effect cannot be described as a specific change in sodium inactivation or as a specific change in sodium activation, for both processes continue to govern the opening of the sodium channels and neither process is able to close the channels. The effects of DDT are very similar to those of veratrine.

Animals↗
PubMed1968

Charges and potentials at the nerve surface. Divalent ions and pH.

The voltage dependence of the voltage clamp responses of myelinated nerve fibers depends on the concentration of divalent cations and of hydrogen ions in the bathing medium. In general, increases of the [Ca], [Ni], or [H] increase the depolarization needed to elicit a given response of the nerve. An e-fold increase of the [Ca] produces the following shifts of the voltage dependence of the parameters in the Hodgkin-Huxley model: m(infinity), 8.7 mv; h(infinity), 6.5 mv; tau(n), 0.0 mv. The same increase of the [H], if done below pH 5.5, produces the following shifts: m(infinity), 13.5 mv; h(infinity), 13.5 mv; tau(n), 13.5 mv; and if done above pH 5.5: m(infinity), 1.3 mv; h(infinity), 1.3 mv; tau(n), 4.0 mv. The voltage shifts are proportional to the logarithm of the concentration of the divalent ions and of the hydrogen ion. The observed voltage shifts are interpreted as evidence for negative fixed charges near the sodium and potassium channels. The charged groups are assumed to comprise several types, of varying affinity for divalent and hydrogen ions. The charges near the sodium channels differ from those near the potassium channels. As the pH is lowered below pH 6, the maximum sodium conductance decreases quickly and reversibly in a manner that suggests that the protonation of an acidic group with a pK(a) of 5.2 blocks individual sodium channels.

Animals↗
PubMed1967

The selective inhibition of delayed potassium currents in nerve by tetraethylammonium ion.

The effect of tetraethylammonium ion (TEA) on the voltage clamp currents of nodes of Ranvier of frog myelinated nerve fibers is studied. The delayed K currents can be totally abolished by TEA without affecting the transient Na currents or the leakage current in any way. Both inward and outward currents disappear. In low TEA concentrations small K currents remain with normal time constants. The dose-response relationship suggests the formation of a complex between TEA and a receptor with a dissociation constant of 0.4 mM. Other symmetrical quaternary ammonium ions have very little effect. There is no competition between TEA and agents that affect the Na currents such as Xylocaine, tetrodotoxin, or Ca ions. The pharmacological data demonstrate that the Na, K, and leakage permeabilities are chemically independent, probably because their mechanisms occupy different sites on the nodal membrane. The data are gathered and analyzed by digital computer.

Action Potentials↗
PubMedDate not supplied

GTP-binding proteins couple cardiac muscarinic receptors to a K channel.

Binding of acetylcholine (ACh) to cardiac muscarinic ACh receptors (mAChR) activates a potassium channel that slows pacemaker activity. Although the time course of this activation suggests a multi-step process with intrinsic delays of 30-100 ms, no second-messenger system has been demonstrated to link the mAChR to the channel. Changes in cyclic nucleotide levels (cyclic AMP and cyclic GMP) do not affect this K channel or its response to muscarinic agonists. Indeed, electrophysiological experiments argue against the involvement of any second messenger that diffuses through the cytoplasm. We report here that coupling of the mAChR in embryonic chick atrial cells to this inward rectifying K channel requires intracellular GTP. Furthermore, pretreatment of cells with IAP (islet-activating protein from the bacterium Bordetella pertussis) eliminates the ACh-induced inward rectification. As IAP specifically ADP-ribosylates two GTP-binding proteins, Ni and No, that can interact with mAChRs, we conclude that a guanyl nucleotide-binding protein couples ACh binding to channel activation. This represents the first demonstration that a GTP-binding protein can regulate the function of an ionic channel without acting through cyclic nucleotide second messengers.

Acetylcholine↗