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Biomedical subjects

P F Baker

Publications and source records attributed to P F Baker.

At least 73 records · Page 4Linked to original sources
PubMed1976

Kinetics and energetics of calcium efflux from intact squid giant axons.

The Ca efflux from intact squid axons consists of three major components: one that is activated by Cao, one that is activated by Nao and a residual flux that persists in the nominal absence of both Cao and Nao. The properties of these components have been investigated in unpoisoned axons and in axons poisoned with cyanide. 2. Under all conditions the shape of the curve relating Cao to Cao-activated Ca efflux approximates to a section of a rectangular hyperbola, consistent with simple Michaelis activation. 3. The external Ca concentration giving half-maximal activation of Cao-activated Ca efflux is about 2 muM in unpoisoned axons immersed in Na-ASW, but on poisoning changes progressively to values in the range 1-10 mM. The residual efflux from unpoisoned axons may reflect activation by traces of Ca present immediately external to the axolemma. 4. The apparent affinity for Cao of Cao-activated Ca efflux is very similar in unpoisoned axons immersed in sea waters containing Na, Li, Tris or K as major cation, whereas in poisoned axons the affinity in Na and Li is about the same but higher than that in choline and Tris. 5. In unpoisoned axons Ca influx increases linearly as Cao is increased from 2 muM to 110 mM. The absolute value of the Ca influx from 10 muM-Cao is less than 1% of the Cao-activated Ca efflux at this external Ca concentration. In poisoned axons the sizes of Cao-activated Ca efflux and Ca influx were similar at all Ca concentrations examined. 6. The shape of the curve relating Nao to Nao-activated Ca efflux approximates to a section of rectangular hyperbola in unpoisoned axons but is clearly sigmoidal in axons that have been fully poisoned with cyanide. The sigmoidal shape develops progressively during poisoning. ...

Adenosine Monophosphate↗
PubMed1975

Voltage-dependent changes in the permeability of nerve membranes to calcium and other divalent cations.

Transmitter release from depolarized nerve terminals seems to be preceded by a rise in the intracellular concentration of ionized calcium. In squid giant axons, depolarization promotes calcium entry by two routes: one that is blocked by tetrodotoxin and one that is insensitive to tetrodotoxin. The TTX-sensitive route seems to be the sodium channel of the action potential; but the TTX-insensitive route seems to be quite distinct from the sodium and potassium channels of the action potential. It is blocked by Mg-2+, Mn-2+ and Co-2+ ions and by the organic calcium antagonist D-600 and has many features in common with the mechanism that couples excitation to secretion.

Action Potentials↗
PubMed1975

A note of the mechanism by which inhibitors of the sodium pump accelerate spontaneous release of transmitter from motor nerve terminals.

1. The actions of 0-1 mM ouabain and of K-free Ringer have been examined at the frog neuromuscular junction. 2. After a delay of more than 30 min, ouabain produces an increase in the miniature end-plate potential (m.e.p.p.) frequency. This increase occurs unchanged in Ca-free Ringer containing 1 mM-EGTA and is therefore unlikely to be due to an entry of Ca into the motor nerve terminals. 3. If the nerve to the preparation is stimulated repetitively in Ca-free Ringer containing 0-1 mM ouabain and 1 mM-EGTA the response of the m.e.p.p. frequency depends on the timing of the tetanus relative to the beginning of the ouabain treatment. 4. During the first 30 min of exposure to ouabain, the tetanus produces a small, transient increase in the m.e.p.p. frequency similar to that which occurs before ouabain is present. After about 30 min the same tetanus produces large, irreversible increases in the m.e.p.p. frequency. 5. Superfusion of an end-plate with K-free Ringer causes an immediate exponential rise in the m.e.p.p. frequency that is unaffected by the presence of external Ca ions. On replacing the normal K of the Ringer (2 mM) the m.e.p.p. frequency recovers quickly to its original value. 6. Late in an exposure to 0-1 mM ouabain the m.e.p.p. frequency becomes extremely sensitive to changes in the external Na concentration, [Na]o. Reducing [Na]o increases the m.e.p.p. frequency. The sensitivity to [Na]o is independent of external Ca ions or whether the isotonic substitute for NaCl is LiCl or sucrose. 7. It is suggested that the spontaneous release of transmitter is facilitated, in some way, by the changes in the monovalent cation content of the nerve terminals that result from blocking the Na-K exchange pump. The Na sensitivity of the m.e.p.p. frequency that develops simultaneously can be explained if a Na-dependent Ca efflux system is present in the membrane of the presynaptic terminals.

Animals↗
PubMed1975

Catecholamine release from bovine adrenal medulla in response to maintained depolarization.

Prolonged exposure of venous-perfused bovine adrenal glands to high K in the presence of external Ca produces a transient increase in catecholamine output that reaches a maximum after about 1 min and then declines with a half-time of about 1-2 min. 2. The time course of the transient secretory response to high K does not depend appreciably on the total catecholamine output which indicates that depletion of releasable catecholamine is unlikely to be responsible for the transient nature of the response. 3. Application of 3-6 mM-Ba stimulates secretion from a gland after many minutes exposure to high K, when catecholamine output has declined close to resting levels. This provides further evidence that depletion does not play a major role in the transient response and shows that maintained depolarization does not inhibit the secretory mechanism. 4. Exposure to high K solutions in which Ca has been replaced isomotically by Mg does not evoke any catecholamine output. Subsequent application of Ca always elicits some secretion although the size of this response to added Ca declines rapidly during exposure to Ca-free, high K solutions. The failure of the secretory response in these experiments is more rapid, and earlier in onset than the declining phase of the normal secretory response evoked in the presence of calcium. 5. Pre-treatment with Ca-free solutions of intermediate K content reduces the response to subsequent simultaneous application of high K and Ca. There is a roughly sigmoidal relation between the reduction in response and the logarithm of the K concentration used for pre-treatment. 6. Thin slices of bovine adrenal medulla show qualitatively similar responses on exposure to high K. Examination of the flourescent signal from slices dyed with the potential-sensitive dye DiS-C(3)-(5) suggests that maintained exposure to high K produces a stable depolarization. 7. The most likely explanation for these results is that K-depolarization first activates and subsequently inactivates a potential-sensitive Ca permeability channel. This inactivation is time and possibly potential dependent. 8. The effect of high K on calcium movements in medullary slices was examined. Exposure to 72 mM-K increases (45)Ca uptake, the increase being greatest during the first 10 min. The efflux of Ca is also increased on exposure to high K in the presence of Ca. The net Ca uptake in 72 mM-K is smaller than the tracer uptake of Ca. These findings indicate that K depolarization stimulates a Ca-Ca exchange process. They are also consistent with, but do not offer strong positive support for, the idea that K-depolarization first activates and subsequently inactivates Ca entry. 9. It is suggested that Ca inactivation might play a role in the modulation of neurosecretion and neurotransmitter release by changes in membrane potential.

Adrenal Medulla↗