Time Course Of Action Potential Research Articles

Reduction in acetylcholine sensitivity of axotomized ciliary ganglion cells.

1. Isolated cell clusters from ciliary ganglia of 3- to 4-day-old chickens were used to examine the electrical characteristics and sensitivity to iontophoretically applied acetylcholine (ACh) of normal cells and cells that had been axotomized on the day of hatching. 2. Resting potentials, input resistances and capacitances were the same in axotomized cells as in normal cells. These averaged about 70 mV, 165 Momega and 35 pF respectively. 3. Sensitivity to iontophoretically applied ACh was lower in axotomized cells than in normal cells by a factor of about 8. The rise times of the ACh potentials were the same in the two groups; indicating that the reduced sensitivity was not due to a diffusion barrier. 4. The slopes of the dose-reponse curves, plotted on a double-logarithmic scale, suggested that the co-operative action of two ACh molecules was involved in activating a post-synaptic conductance channel. This relation was unaltered by axotomy. 5. The estimated reversal potential for the action of ACh was unchanged after axotomy. 6. Cells in isolated clusters were similar to those in intact ganlia with respect to threshold depolarization, amplitude and time course of action potentials and ability to generate repetitive action potentials. There were no differences in these characteristics between normal and axotomized cells. 7. Cells in the isolated clusters had input resistances which were larger by a factor of 2-3 and capacitances that were smaller by a factor of about 2 than those of cells in intact ganglia. It is suggested that these differences were due to loss of initial segments of axons from the isolated cells. 8. Normal cells in the isolated clusters displayed spontaneous miniature synaptic potentials, indicating that synaptic integrity was maintained during the isolation procedure. As in intact ganglia, no spontaneous activity was observed in axotomized cells.

Positive and negative inotropic effects of elevated extracellular potassium level on mammalian ventricular muscle.

The effect of moderate elevation in extracellular potassium concentration (up to 12 mM) on contraction of cat ventricular muscle was examined. Isometric force development was recorded from eight excised trabeculae and from six coronary-perfused in situ papillary muscle preparations. Contraction in the steady state was variably affected, sometimes decreasing monotonically, sometimes remaining unchanged, with increasing potassium level. In 11 of these 14 preparations, the steady state was preceded by a transient period in which the contraction was augmented. In addition, eight excised trabeculae were used in an experimental arrangement designed to distinguish between inotropic effects caused by potassium-induced alterations in the action potential and other, more direct, effects of this ion on contraction. The negative inotropic effect is attributable to a potassium-induced reduction in the amplitude and/or duration of the action potential plateau. The positive inotropic effect was found in experimental arrangements where effects of the potassium-rich medium on action potential time-course were effectively "buffered." The positive inotropic effect thus depends on the presence of the elevated potassium concentration and can occur independently of effects on the action potential time-course.

The effect of some quaternary ammonium compounds upon the excitability and the membrane potentials of Bombyx mori skeletal muscle fibres

Both tetrabutyl ammonium (TBA) and tetraethyl ammonium (TEA) ions produced an initial phase of increased excitability in Bombyx mori skeletal muscle fibres, followed by a phase of inexcitability which was accompanied by a decline of both the resting and action potential magnitudes. The phase of inexcitability was not reversible. TEA ions caused the action potential time course to become prolonged, and tetanic muscle fibre responses following single stimuli to the nerve were often observed. It is argued that TBA and TEA ions may initially facilitate neuromuscular transmitter release and ion transport across the muscle fibre membrane, and that the latter eventually becomes freely permeable and depolarized resulting in irreversible inexcitability.

Further study of soma, dendrite, and axon excitation in single neurons.

The present investigation continues a previous study in which the soma-dendrite system of sensory neurons was excited by stretch deformation of the peripheral dendrite portions. Recording was done with intracellular leads which were inserted into the cell soma while the neuron was activated orthodromically or antidromically. The analysis was also extended to axon conduction. Crayfish, Procambarus alleni (Faxon) and Orconectes virilis (Hagen), were used. 1. The size and time course of action potentials recorded from the soma-dendrite complex vary greatly with the level of the cell's membrane potential. The latter can be changed over a wide range by stretch deformation which sets up a "generator potential" in the distal portions of the dendrites. If a cell is at its resting unstretched equilibrium potential, antidromic stimulation through the axon causes an impulse which normally overshoots the resting potential and decays into an afternegativity of 15 to 20 msec. duration. The postspike negativity is not followed by an appreciable hyperpolarization (positive) phase. If the membrane potential is reduced to a new steady level a postspike positivity appears and increases linearly over a depolarization range of 12 to 20 mv. in various cells. At those levels the firing threshold of the cell for orthodromic discharges is generally reached. 2. The safety factor for conduction between axon and cell soma is reduced under three unrelated conditions, (a) During the recovery period (2 to 3 msec.) immediately following an impulse which has conducted fully over the cell soma, a second impulse may be delayed, may invade the soma partially, or may be blocked completely. (b) If progressive depolarization is produced by stretch, it leads to a reduction of impulse height and eventually to complete block of antidromic soma invasion, resembling cathodal block, (c) In some cells, when the normal membrane potential is within several millivolts of the relaxed resting state, an antidromic impulse may be blocked and may set up within the soma a local potential only. The local potential can sum with a second one or it may sum with potential changes set up in the dendrites, leading to complete invasion of the soma. Such antidromic invasion block can always be relieved by appropriate stretch which shifts the membrane potential out of the "blocking range" nearer to the soma firing level. During the afterpositivity of an impulse in a stretched cell the membrane potential may fall below or near the blocking range. During that period another impulse may be delayed or blocked. 3. Information regarding activity and conduction in dendrites has been obtained indirectly, mainly by analyzing the generator action under various conditions of stretch. The following conclusions have been reached: The large dendrite branches have similar properties to the cell body from which they arise and carry the same kind of impulses. In the finer distal filaments of even lightly depolarized dendrites, however, no axon type all-or-none conduction occurs since the generator potential persists to a varying degree during antidromic invasion of the cell. With the membrane potential at its resting level the dendrite terminals contribute to the prolonged impulse afternegativity of the soma. 4. Action potentials in impaled axons and in cell bodies have been compared. It is thought that normally the over-all duration of axon impulses is shorter. Local activity during reduction of the safety margin for conduction was studied. 5. An analysis was made of high frequency grouped discharges which occasionally arise in cells. They differ in many essential aspects from the regular discharges set up by the generator action. It is proposed that grouped discharges occur only when invasion of dendrites is not synchronous, due to a delay in excitation spread between soma and dendrites. Each impulse in a group is assumed to be caused by an impulse in at least one of the large dendrite branches. Depolarization of dendrites abolishes the grouped activity by facilitating invasion of the large dendrite branches.