No abstract

The spontaneous rhythmic motor activity (vasomotion) of arterioles was studied in vivo in the hamster cheek pouch by means of intravital microscopy. In control conditions, arteriolar vasomotion was regularly present in healthy preparations, independent of anesthesia (pentobarbital sodium or alpha-chloralose), composition of the superfusate [tris(hydroxymethyl)aminomethane-buffered or N-2-hydroxy-ethylpiperazine-N'-2-ethanesulfonic acid-supported HCO3(-)-buffered saline solutions) or a combined nerve, alpha- and beta- receptor blockade. In arterioles with internal diameters between 13 and 52 microns, the vasomotion frequency (3-15 cycles/min) and amplitude (2-10 microns) were not significantly correlated to vessel size. The frequency and amplitude of the spontaneous arteriolar vasomotion could be modified by changes in the physical and chemical environment of the preparation. Thus, addition of pinacidil, a K+ channel activator, to the superfusate dose dependently decreased and finally suppressed vasomotion, in combination with an increase of the vessel diameter. These effects could be counteracted if glibenclamide (10(-6) M), a K+ channel blocker, was added to the superfusing solution. In the absence of any major changes in vessel diameter, vasomotion was also abolished by increasing the PO2 (from approximately 15 to 30 mmHg), varying the pH (from 7.40 to 7.22 or 7.65), and lowering the temperature to 15 degrees C in the superfusion solution. The abolition of vasomotion observed because of increased PO2 and changes in pH could be reversed by addition of glibenclamide (10(-6) M) or tetraethylammonium chloride (TEA, 5 x 10(-3) M), another K+ channel blocker, to the superfusion solution; in the case of lowered temperature only glibenclamide was effective.(ABSTRACT TRUNCATED AT 250 WORDS)

4. The post-denervation fall in the maximum rate of rise and in the amplitude of the overshoot of the muscle fibre action potential was unaffected by actinomycin D treatment.5. Actinomycin D failed to inhibit the appearance of the membrane changes if given later than 2 days after denervation.6. Chloramphenicol (6 g/kg in divided doses) and cycloheximide (40 g/ kg every 12 hr) were also able to inhibit the appearance of the membrane changes.7. It is concluded that some denervation induced changes in the muscle fibre membrane depend on the synthesis of new proteins. The results imply that the motor nerve cell normally exerts a regulatory influence on the genome of the muscle cell.

SUMMARY1. The transmembrane exchange of Na+, K+, and Cl-in slowly and rapidly adapting lobster stretch receptor neurones was studied using ion-sensitive microelectrodes in combination with conventional electrophysiological techniques.2. The investigation was founded on the assumption that the transmembrane ion exchange is accomplished by active and passive transports which add up to zero in steady state for each ion involved. The active transports are assumed to include Na+ and K+ transports driven by an electrogenic Na-K pump. To these transports are also added equimolar fluxes of K+ and Cl-leaking from the impaling micro-electrode. The passive transports are assumed to pass through membrane channels in accordance with constant field kinetics.3. For a quantitative evaluation of the transmembrane ion exchange in resting conditions measurements were made of (a) the resting concentrations of Na+, K+ and Cl-; (b) the voltage dependence of the ungated leak current; and (c) ouabain-induced changes in resting membrane current and intracellular ion concentrations. From the results it follows that both the resting pump current and the leak permeabilities for the ions investigated have values which do not seem to differ between slowly and rapidly adapting receptor neurones.4. For a quantitative evaluation of the relation between internal Na+ and pump current production, measurements were made of the outward membrane current as a function ofinternal Na+ and K+ following a shift of these ions by means ofprolonged repetitive impulse activation. It was found that the investigated relation is compatible with Garay-Garrahan kinetics (Garay & Garrahan, 1973) in both receptor neurones, but the results imply a larger maximum Na+-extrusion capacity in slowly than in rapidly adapting cells.5. From recordings of the time course of post-tetanic normalization of both the membrane current and intracellular Na+ concentration, cell volume values could be deduced which were closely similar in slowly and rapidly adapting receptors. A corresponding similarity was also found for the cell area which was derived from membrane capacitance measurements.

SUMMARY1. The gated membrane currents (a tetrodotoxin-sensitive Na+ current and a tetraethylammonium-and 4-aminopyridine-sensitive K+ current) of the rapidly adapting stretch receptor neurone of lobster were investigated with respect to their kinetic properties using electrophysiological, pharmacological, and mathematical techniques.2. The currents were found to be controlled by slow inactivations as well as by fast Hodgkin-Huxley (1952) gating processes. They could be described by kinetic expressions which differed from those inferred for the slowly adapting receptor (Gestrelius & Grampp, 1983a;Gestrelius, Grampp & Sjolin, 1983) only with respect to some of the parameter values.3. With these expressions, and additional equations for the cell's pump and leak current components (Edman, Gestrelius & Grampp, 1986), a mathematical receptor model was formulated which accurately predicts the impulse activity of the living preparation in different functional circumstances and which, therefore, was adopted as an appropriate theory of firing regulation.4. From a model analysis it appeared (a) that the 'rapid' adaptation of the receptor's impulse activity is mainly an effect of slow Na+ current inactivation starting a regenerative process of accommodation which, basically, is due to a small ratio of subthreshold Na+ to K+ currents; (b) that, because of the transmembrane Na+ influx being limited by accommodation, impulse firing is only little affected by a Na+-dependent pump current activation; and (c) that the phenomenon of increased firing frequency initially during prolonged stimulation ('negative adaptation') is an effect of the slow K+ current inactivation being faster than the slow Na+ current inactivation at comparable degrees of membrane polarization.5. From further model studies it also appeared that, during depolarizations between successive action potentials evoked by constant stimulation, the membrane behaves like a high-resistance constant-current generator feeding into a shortcircuiting capacitor. In consequence, the cell's stimulus sensitivity (change in firing frequency with stimulation strength) is, at functionally relevant stimulation intensities, mainly determined by the membrane capacitance and by the amplitude of the interspike membrane depolarization while, at higher stimulation intensities and firing frequencies, it becomes more and more a function of the spike duration itself.