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Biomedical subjects

D O Smith

Publications and source records attributed to D O Smith.

72 records · Page 4Linked to original sources
PubMed1980

Levels of high-energy phosphates in crayfish nerve during prolonged repetitive impulse activity.

1. Levels of ATP and arginine phosphate (ArgP) in the mixed nerve bundle of the crayfish walking leg were assayed in fresh tissue and after prolonged repetitive stimulation. 2. In fresh tissue, ATP and ArgP levels were estimated to be about 34 n-mole/mg protein and 157 n-mole/mg protein, respectively, corresponding to concentrations of 3 . 0 and 13 . 9 mM. 3. Following 5 min of repetitive stimulation at 30 impulses/sec, the ATP concentration in the nerve increased by 0 . 52 mM; after 10 and 20 min of stimulation, the concentrations returned to values similar to those of fresh tissue. 4. The ArgP concentrations were similar to those of fresh tissue after 5 min of stimulation at 30 impulses/sec but dropped to about 85% of those values after 10 and 20 min of stimulation. 5. Increased K+ in the physiological saline reduced [ATP] following stimulation; decreased Na+ in the saline increased the content of ATP in unstimulated nerves. 6. It is concluded that repetitive action potential activity may be associated with relatively constant and perhaps increased production of ATP.

Action Potentials↗
PubMed1978

Ultrastructural specificity of synaptic sites in nerve terminals mediating both presynaptic and postsynaptic inhibition.

The ultrastructural basis of presynaptic inhibition of the excitatory efferent axon innervating the opener muscle of the crayfish walking leg was studied using the electron microscope. The inhibitory efferent axon terminals form axoaxonal synapses onto excitor terminals in very close proximity to sites of excitatory transmitter release. There is no evidence that these synapses are located at regions of low safety factor of action potential conduction in the excitor. In the area of axoaxonal synaptic connections, the inhibitory axon also forms inhibitory neuromuscular junctions on the opener muscle. Synaptic vesicles are clustered in active zones bordered postsynaptically by extensive invaginations, or junctional folds, in the sarcolemma. These results are consistent with the hypothesis that the primary effect of presynaptic inhibition is to shunt depolarization-secretion coupling at specific sites of transmitter release in the target cell, rather than to block impulse propagation into a more generalized population of nerve terminals distal to the axoaxonal synapse. Further physiological implications of this structural arrangement are considered.

Animals↗
PubMed1977

Ultrastructural basis of impulse propagation failure in a nonbranching axon.

The morphological basis of intermittent conduction failure in the excitor axon innervating the crayfish opener and stretcher muscles was investigated using the electron microscope. The connective tissue component of the sheath surrounding the axon was found consistently to be thinner in the region at which blocking occurs than in control regions located one cm either proximally or distally, at which blocking does not occur. Otherwise in these regions differences in the width of the periaxonal spaces, the length or width of the mesaxons, the density of mitochondria, the width of the adaxonal glial cell layer, or the structure of lamination of the sheath are not observed. Because of the thinner connective tissue component of the sheath in the joint region, neighboring axons are distributed more densely around the excitor, and the volume of the extracellular space is reduced. The possibility that the reduced extracellular space might allow excessive accumulation of potassium during repetitive discharge, causing conduction block, is discussed. Alternative mechanisms consistent with this morphology are also considered.

Animals↗
PubMed1976

Synaptic depression related to presynaptic axon conduction block.

1. The depression of synaptic transmission, which occurs during prolonged repetitive activation, was examined in the opener muscle of the crayfish walking leg. 2. Excitatory post-synaptic potentials (e.p.s.p.s) initially facilitated but then declined to low amplitudes after about 4000 stimulus pulses had been delivered; this depression is presynaptic in origin; 3. Axon conduction blocks occured at points of bifurcation along the entire length of the presynaptic nerve. This resulted in failure of the nerve impulse to invade some branches of the terminal arborization. 4. Nerve terminal invasion failure caused either intermittent or complete inactiviation of some synaptic release sites; this was associated with depression of the post-synaptic response. 5. The statistics of transmitter release during prolonged repetitive stimulation were examined by focal extracellular recording methods. Transmitter release could be described by binomial statistics, and depression involved a drop in m, n and p. 6. The rate of spontaneous quantal release did not decrease, however, arguing against transmitter depletion. 7. It is concluded that repetitive stimulation eventually leads to depolarization of the axon membrane. This causes impulse propagation failure which reduces the number of synaptic release sites that are activated and mimics a drop in the effective stimulation rate; both effects cause synaptic depression.

Action Potentials↗
PubMed1976

Non-uniform probabilities of quantal release at the crayfish neuromuscular junction.

1. Transmitter release at the neuromuscular junction of the crayfish walking leg has been found to deviate from binomial predictions immediately after the onset of repetitive stimulation of the presynaptic nerve at frequencies of at least 15 Hz. 2. After several minutes of continuous stimulation, and at lower rates of stimulation, however, the number of quanta released could be described quite well by binomial or Poisson statistics. 3. Deviations from the theoretical expectations were characterized by (a) fewer release failures than predicted, (b) occasions in which the number of quanta released was more than the estimated number of quanta available for release, and (c) a tendency for the data to be underdispersed. 4. Each of these three characteristics are consistent with the hypothesis that different releasable quanta may have different probabilities of responding to a nerve impulse. 5. Using two different methods, different values of the non-uniform probabilities were estimated from the data. At each synaptic site at least one of the estimated probabilities was very high. 6. The need for caution in interpreting statistical description of quantal release is emphasized.

Animals↗
PubMed1976

Axon conduction block in a region of dense connective tissue in crayfish.

1. The excitor nerve which innervates the opener muscle of the crayfish walking leg was stimulated repetitively for prolonged periods of time. 2. After an initial facilitation and subsequent depression of the postsynaptic potentials, occasional stimulus pulses failed to evoke a postsynaptic response; eventually, every second stimulus pulse failed to produce a postsynaptic potential change. This is termed the 1:1 block state. 3. The block resulted from failure of the appropriate nerve action potentials to propagate through an identifiable region of the axon. This region was in the joint between the propodite and the carpopodite and was characterized by dense surrounding connective tissue. 4. Associated with block development is a decrease in axon conduction velocity and an increase in the amplitude of the postsynaptic potentials; this latter phenomenon is termed anomalous facilitation and results from a decrease in the extent of synaptic depression. 5. The cause of the conduction block resides in the associated nonneural tissue and not in some geometrical property of the axon. 6. It is concluded that extracellular accumulation of K+, because of limited diffusion possibilities and possibly reduced Schwann cell tissue, depolarizes the axon, leading to propagation failure.

Animals↗
PubMedDate not supplied

Non-uniform changes in nerve-terminal calcium homeostasis during aging.

Currently unpublished studies indicate reduced rates of calcium clearance from the transmitter release sites in presynaptic terminals of some, but not all, motor nerves in aged rats. Further evidence indicates that deficits in calcium regulation may not necessarily underlie observed age-related changes in evoked transmitter release.

Aging↗