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L D Partridge

Publications and source records attributed to L D Partridge.

At least 37 records · Page 2Linked to original sources
PubMed1987

Single Ca-activated cation channels in bursting neurons of Helix.

The depolarizing drive that maintains bursting in Helix neurons is carried by a long-lasting calcium-activated inward current. This current was studied using cell-attached and inside-out patches from the right parietal fast burster neuron of Helix pomatia. One population of unitary currents was inward at -50 mV and showed an increased probability of opening when Ca2+ was injected or when excised patches were bathed in solutions with 10(-7) to 10(-5) M free Ca2+ levels. Cell-attached patches (patch electrodes filled with 10(-7) M Ca2+ Ringer) had single channel conductances near 30 pS with reversal potentials near -20 mV; excised patches had similar conductances in symmetrical Na+ solutions and reversal potentials within a few millivolts of zero. Calculations, assuming a simple spherical cell, yield a channel density of only about 1/6 micron2. The increased channel opening probability characteristically persisted well beyond the duration of transient whole-cell inward current. We conclude from this that the later phase of Ca-activated inward currents is normally masked by outward currents.

Action Potentials↗
PubMed1987

Phenobarbital: a locus of action on spike broadening and potassium inactivation.

1. The effect of phenobarbital on frequency-dependent spike broadening and potassium inactivation was studied in snail neurons. 2. The amount of spike broadening was significantly depressed by the application of 10(-3) M phenobarbital but the time course of broadening was unaffected. 3. In voltage clamped neurons, this concentration of phenobarbital significantly depressed the amount of potassium current inactivation without altering its time constant. 4. A possible locus of phenobarbital's anticonvulsant action is through a decrease in synaptic efficacy resulting from a depression of presynaptic spike broadening.

Animals↗
PubMed1984

The effect of pentylenetetrazol on inward currents of non-bursting neurons and its role in plateau formation.

The epileptogenic drug, pentylenetetrazol (PTZ) produces paroxysmal depolarization shifts in molluscan neurons that are similar to PDSs seen at a mammalian epileptic focus. Most research on molluscan neurons indicates that PTZ acts by altering ionic somatic conductances. This study was carried out to investigate the effect of PTZ on inward currents in isolated neurons of the pond snail, Lymnaea stagnalis, and to investigate how these altered currents might lead to the production of PDSs. In concentrations from 10 to 60 mM, PTZ decreased maximum inward current conductance and shifted the inactivation and activation curves to the left with the former shift being consistently greater. There was no change in reversal potential or time constants for activation and inactivation of inward currents. The effects of the PTZ-induced alterations in the inward currents were studied by incorporating them along with alterations of outward currents seen in this and other studies in a computer model for molluscan neuronal firing. The composite model reproduced in large part the intermediate changes in electrical activity seen before the development of the PDS as well as the PDS.

Animals↗
PubMed1984

The effect of pentylenetetrazol on spike broadening and potassium inactivation.

The effect of the convulsant drug, pentylenetetrazol (PTZ) on spike broadening and potassium current inactivation was studied. PTZ was found to decrease the time taken for a cell to reach maximal broadening as well as causing a decrease in the total amount of broadening. Voltage clamp studies showed that in the presence of PTZ potassium current inactivated less but exhibited a faster time constant of inactivation. By exerting an effect on potassium inactivation and thereby spike broadening, PTZ may alter synaptic efficacy. Such an effect on synaptic efficacy may partially underlie the drug's convulsive activity.

Action Potentials↗
PubMed1982

The good enough calculi of evolving control systems: evolution is not engineering.

In evolved aggregates of accidentally invented elements, retained when statistically good enough to identify limitations of antecedent systems, survival value might favor operators incorporating aspects of, while not identical with, feedback, feedforward, state varible, and "homeostatic" control. Generally, simple organizational increments should predominate. After invention, an internal controller with readily modifiable rules could facilitate evolution of compound inventions, but criteria controlling rule changes would be only indirectly (probably imperfectly) survival referent. Consequent to combination of independent invention with indirect criteria and statistical acceptance, evolved control logic could be: both redundant and incomplete; good enough with malefic aspects; built of loosely linked or autonomous sublogics; and a source of good enough solutions from incomplete information. The partially explicit rules are defined more by rejections than by ratifications. Study of the result based on formal logic, engineering conventions, and familiar coordinate systems could conceive illegitimate illusions of understanding.

Biological Evolution↗
PubMed1980

Calcium independence of slow currents underlying spike frequency adaptation.

This study assessed the role of calcium in the activation of the slow potassium current responsible for spike frequency adaptation in molluscan neurons. Inward calcium currents were eliminated by using Co2+, Cd2+, or OCa2+ EGTA in the bathing solution. In each case adaptation was found to persist, as did the slow current believed to be responsible for adaptation. Injection of EGTA into neurons was also found not to block adaptation. This potassium current provides an example of a slow voltage-dependent potassium process which is independent of calcium influx.

Action Potentials↗
PubMed1980

Probability of peripheral interaction between motor units and implications for motor control.

Potential and importance of mechanical interactions between motor units are examined. Studies were conducted on simple physical models of systems of motor units assembled from separate muscles and driven with electrical stimulus. Two separate muscles were connected to move a common load to represent mechanically coupled motor units while avoiding other interactions present between natural units. Force, velocity, length, power, and work outputs of one unit were measured with and without stimulus to the other unit. Excitation of one unit modified all response measures in the other. The basis for these interactions appears equally applicable to real motor units. Consequently, unqualified use of such terms, which imply independence, as quantal, summation, and average unit response is not acceptable without qualification when referring to activity of motor units. It is argued that the effects of force-velicty and length-tension relationships will cause appreciable mechanical interaction between motor units. Therefore, central nervous system strategies for organization of motor control cannot depend on unchanging response of individual units, and the principle of superposition should not be assumed in analyses of motor activities. The nature of the interactions suggests that the total effect of a unit response may include a "negative force" phase, and also energy exchanges can be expected between motor units in some configurations.

Action Potentials↗
PubMed1979

Current-voltage relationships of repetitively firing neurons.

The current-voltage curves of repetitively firing neurons show non-linearities in the subthreshold region. Microsurgically isolated molluscan neuron somata were studied under voltage clamp using ramp voltage command signals. During the depolarizing 1/2 cycle a region of negative slope conductance was observed. Ion substitution experiments suggest that this results from non-inactivating or slowly inactivating Na+ and Ca2+ currents. The hyperpolarizing 1/2 cycle reveals a hysteresis effect which results at least in part from a Ca2+ activated 5+ current. Similar characteristics have been described in bursting neurons. Their occurrence in the non-bursting neurons studied here shows that they are not unique to this class of neurons and suggests that their primary contribution is to create electrical instability necessary for repetitive firing.

Animals↗
PubMed1978

A mechanism for minimizing temperature effects on repetitive firing frequency.

The magnitudes and time courses of conductance changes in molluscan neurons show marked temperature dependence. Interestingly, though, the relationship between repetitive firing frequency and stimulus current is not greatly affected by moderated temperature changes (6-8 degrees C). The transient potassium current, IA, is largely reponsible for the interspike voltage trajectory, hence, repetitive interval, in molluscan neurons. It is shown in this study that temperature dependencies of the rate constants and magnitude of the IA system are balanced in such a way that the observed temperature insensitivity of the repetitive response is predicted.

Action Potentials↗
PubMed1976

The effects of lithium and sodium on the potassium conductance of snail neurones.

1. The iontophoretic injection of lithium into snail neurones reversibly increased the resting relative potassium permeability (PK). 2. Long exposures to snail Ringer containing 25 mM-Li and correspondingly reduced Na also caused an increase in PK. This did not occur with Ringer in which the same reduction of Na was made by replacing it with Tris. 3. Replacement of part of the Ringer Na by either Li or Tris led to proportional decreases in internal Na. 4. Injecting large quantities of Na into ouabain-treated cells caused effects similar to those of Li injection. Without ouabain, Na injection stimulated the electrogenic Na pump. 5. A number of tests failed to produce any clear evidence that intracellular Ca was involved in the response to Li.

Animals↗
PubMed1976

A mechanism for spike frequency adaptation.

1. Spike frequency adaptation was studied in large neurones of the marine molluscs Archidoris montereyensis and Anisodoris nobilis. These cells respond to a current step with a rapid rise in spike frequency followed by a gradual decline to a new steady level.2. An exponentially declining current, I(s), was measured when the cell was voltage clamped following an adapting spike train. The initial amplitude of this current depended on the preceding number of spikes and on the voltage to which the cell was clamped. A reversal potential (V(s)) for this current was obtained by clamping to various potentials following a spike train. The time constant (tau(s)) of decay of the current was dependent upon the clamping potential.3. Clamping the membrane potential to a constant test level from various initial levels initiates an exponentially decaying current of similar time constant. The voltage dependence of the steady-state conductance (g(s)a(s)(V, infinity)) associated with this current was determined using this technique.4. Equations for neural repetitive firing (Connor & Stevens, 1971c) were modified by the addition of a term describing these slow membrane currents: [Formula: see text]. The solution to the modified equation was in good agreement with the spike frequency adaptation observed in these cells.

Journal Article↗