The role of divalent cations in electrically elicited release of a neurohormone from crab pericardial organs.
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Biomedical subjects
Publications and source records attributed to I M Cooke.
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THE CRAYFISH TONIC STRETCH RECEPTOR NEURON MANIFESTS THREE PHENOMENA: (a) Impulse frequency in response to a depolarizing current decays exponentially to half the initial rate with a time constant of about 4 sec. (b) One or more extra impulses superimposed on steady activity result in a lengthening of the interspike interval immediately following the last extra impulse which is proportional to the number of extra impulses. However, above a "threshold' number of impulses the proportionality constant becomes abruptly larger. (c) Following trains of impulses, the resting potential of the cell is hyperpolarized by an amount proportional to impulse number. Such posttetanic hyperpolarization (PTH) decays approximately exponentially with a time constant of 11 sec, but this varies with membrane potential. These effects are attributed to the incremental increase of an inhibitory (hyperpolarizing) current with a long (relative to interspike interval) decay constant. We suggest that this inhibitory current is the result of increased electrogenic Na pumping stimulated by Na entering with each impulse. Evidence is presented that the three effects are reversibly inhibited by conditions which depress active Na transport: (a) Li substituted for Na in the bath; (b) application of strophanthidin; (c) K removal; (d) treatment with cyanide; (e) cooling. We conclude that a single process is responsible for the three responses described above and identify that process as electrogenic Na pumping. Our observations also indicate that electrogenic pumping contributes to this neuron's resting potential.
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Given the pattern of impulses impinging on a neuron, it should be possible to predict its output firing pattern if enough is known about pre- and postsynaptic properties. A quantitative reproduction of the first part of this input-output conversion is reported, namely the translation of input pattern into a sequence of postsynaptic membrane potential variations.
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Control of secretion, by a mechanism in which membrane depolarization leads to Ca2+ entry, has been extensively studied. The small size and inaccessibility of most nerve terminals, however, have precluded direct analysis of membrane ionic currents and their influence on secretion (with some notable exceptions). Recently, patch-clamp methods have been applied to several secretory systems for both voltage-clamp and single-channel recordings. We now report the extension of this analysis to isolated peptidergic nerve terminals. We used terminals obtained from a crustacean neurohaemal organ, the sinus gland. Analyses of currents under whole-terminal voltage clamp showed inward currents carried by Na+ and by Ca2+, and outward currents carried predominantly by K+. Furthermore, we have observed two types of single-channel currents that may be unique to nerve terminals. Both show little selectivity between Na+ and K+. The first channel is activated by intracellular Na+ and the second by intracellular Ca2+. These channels have conductances of 69 and 213 pS, respectively, in symmetrical 310 mM KCl. It should now be possible to compare electrical activity recorded intracellularly from intact nerve endings, with whole-cell and single-channel currents and with the release of peptide neurohormones from isolated neuronal terminals.