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Biomedical subjects

E Neher

Publications and source records attributed to E Neher.

159 records · Page 9Linked to original sources
PubMed1973

Rapid changes of potassium concentration at the outer surface of exposed single neurons during membrane current flow.

K(+)-sensitive liquid ion-exchanger microelectrodes are shown to be capable of measuring concentration changes which occur on a millisecond time scale. However, some quaternary ammonium ions, such as tetraethylammonium and acetylcholine, are able to block electrode function when present in concentrations as low as 10(-4) to 10(-3) M. Changes in extracellular potassium concentration caused by spike activity or voltage clamp pulses of exposed single neurons of the snail Helix pomatia may be measured by these electrodes. Quantitative analysis shows that the total amount of excess potassium found in the vicinity of the cell a short time after a clamp pulse, is in relatively good agreement with the amount of potassium carried by the membrane current.

Acetylcholine↗
PubMed1971

Two fast transient current components during voltage clamp on snail neurons.

Voltage clamp currents from medium sized ganglion cells of Helix pomatia have a fast transient outward current component in addition to the usually observed inward and outward currents. This component is inactivated at normal resting potential. The current, which is carried by K+ ions, may surpass leakage currents by a factor of 100 after inactivation has been removed by hyperpolarizing conditioning pulses. Its kinetics are similar to those of the inward current, except that it has a longer time constant of inactivation. It has a threshold close to resting potential. This additional component is also present in giant cells, where however, it is less prominent. Pacemaker activity is controlled by this current. It was found that inward currents have a slow inactivating process in addition to a fast, Hodgkin-Huxley type inactivation. The time constants of the slow process are similar to those of slow outward current inactivation.

Action Potentials↗
PubMedDate not supplied

Usefulness and limitations of linear approximations to the understanding of Ca++ signals.

Simple approximations to some limiting cases of Ca++ signalling provide insight into the complex problems of buffered diffusion and of Ca++ homeostasis in the presence of buffers. Three cases are presented, where the influence of Ca++ buffers can readily be understood in the limit of small signals: the return of global cellular [Ca++] following a short stimulus in a 'Single Compartment', buffered diffusion along a cylindrical axon in the 'Rapid Buffer Approximation', and nonequilibrium microdomains of elevated [Ca++] in the immediate vicinity of open Ca++ channels.

Animals↗
PubMedDate not supplied

Capacitance measurements reveal stepwise fusion events in degranulating mast cells.

Mast cells undergo an extensive and violent morphological transformation on stimulation. Here we describe the dynamics of fusion of the secretory granules in individual mast cells during exocytosis. The cell membrane capacitance (proportional to the cell surface area) was measured using the whole-cell patch-pipette technique, in which the intracellular space is dialysed with the solutions used to fill the patch pipette. Our results show that degranulation occurs spontaneously and reproducibly if the GTP analogue, GTP-gamma-S, and Mg-ATP are present in the pipette filling solution. Contrary to previous reports, in these conditions Ca2+ (and/or Ca2+ buffers) is not required for degranulation. Although electrogenic Ca2+ entry was not detected before or during degranulation and membrane conductance remained low, the capacitance, and by implication the area of the membrane of degranulating cells, increased sigmoidally and stepwise. We conclude that stepwise increases of capacitance are due to the fusion of individual secretory granules with the plasma membrane, and that guanine nucleotide regulatory proteins are involved in the control of this process.

Animals↗
PubMedDate not supplied

Intracellularly injected tetanus toxin inhibits exocytosis in bovine adrenal chromaffin cells.

The clostridial neurotoxins tetanus and botulinum toxin type A are known to block transmitter release from nerve terminals, probably by interfering with some essential process controlling exocytosis after the entry of Ca2+ ions. Although exocytosis occurs in many secretory cells, these toxins show a high specificity for neurones and the secretory response of cultured bovine adrenal medullary cells is not inhibited by exposure to medium containing tetanus or botulinum toxin type A (although it is by botulinum toxin type D). Here we report that when tetanus toxin and botulinum neurotoxin type A are injected intracellularly into chromaffin cells they strongly inhibit secretion, as revealed by the measurement of cell capacitance. These results indicate that these toxins are normally ineffective in chromaffin cells because they are not bound and internalized, so do not reach their site of action. Furthermore, we have localized the secretion-blocking effects of the toxin to a fragment comprising the light chain covalently linked to part of the heavy chain, suggesting that this part of the molecule contains the active site.

Adrenal Medulla↗