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G D Bittner

Publications and source records attributed to G D Bittner.

88 records · Page 5Linked to original sources
PubMed1978

Facilitation of transmitter release at squid synapses.

Facilitation is shown to decay as a compound exponential with two time constants (T1, T2) at both giant and non-giant synapses in squid stellate ganglia bathed in solutions having low extracellular calcium concentrations ([Ca++]o). Maximum values of facilitation (F1) were significantly larger, and T1 was significantly smaller in giant than non-giant synapses. Decreases in [Ca++]o or increases in [Mn++]o had variable effects on T1 and F1, whereas decreases in temperature increased T1 but had insignificant effects on F1. The growth of facilitation during short trains of equal interval stimuli was adequately predicted by the linear summation model developed by Mallart and Martin (1967. J. Physiol. (Lond.). 193:676--694) for frog neuromuscular junctions. This result suggests that the underlying mechanisms of facilitation are similar in squid and other synapses which release many transmitter quanta.

Action Potentials↗
PubMed1978

Presynaptic potentials and facilitation of transmitter release in the squid giant synapse.

Presynaptic potentials were studied during facilitation of transmitter release in the squid giant synapse. Changes in action potentials were found to cause some, but not all, of the facilitation during twin-pulse stimulation. During trains of action potentials, there were no progressive changes in presynaptic action potentials which could account for the growth of facilitation. Facilitation could still be detected in terminals which had undergone conditioning depolarization or hyperpolarization. Facilitation could be produced by small action potentials in low [Ca++]o and by small depolarizations in the presence of tetrodotoxin. Although the production of facilitation varied somewhat with presynaptic depolarization, nevertheless, approximately equal amounts of facilitation could be produced by depolarizations which caused the release of very different amounts of transmitter.

Action Potentials↗
PubMed1976

Differential survival of isolated portions of crayfish axons.

Electron microscopic studies show that transplanted segments of sensory axons of varying lengths degenerate within 7-14 days whereas transplanted segments of crustacean motor axons survive morphologically intact for 20-30 days. The middle portion of an isolated motor axon segment degenerates less rapidly than portions of the same axon located nearer the periphery or nearer the ventral nerve cord. One week after transplantation, glial cells appear to phagocytize sensory axons whereas glial cells around motor axons appear to hypertrophy and to have more rough endoplasmic reticulum. After three weeks, motor axons also appear to be phagocytized by glial cells. These data suggest that the glia surrounding isolated motor axons can change from a supportive to a destructive function, whereas glial cells surrounding severed sensory axons primarily have a destructive function. These and other data also indicate that crustacean motor axons receive significant trophic inputs from their own perikaryon, from post-synaptic contacts, and from adjacent glial cells. The possibility that adjacent healthy cells may supply metabolically deficient cells with needed substances could be a significant adaptive advantage for the evolution of multicellular organisms.

Animals↗
PubMed1975

Degeneration of sensory and motor axons in transplanted segments of a crustacean peripheral nerve.

Segments of sensory and motor axons 0.3-0.5 mm in length were taken from crayfish peripheral limb nerves and transplanted into the abdominal cavity of the same animal. Transplanted sensory axons showed relatively few ultra-structural changes after one week, many had undergone complete lysis within two weeks, and almost all degenerated within three weeks. Transplanted motor axons appeared normal after one week, except for some hypertrophy of their surrounding glial sheaths. After two weeks, glial sheaths were grossly hypertrophied around motor axons; axonal mitochondria had increased in number and many had migrated from the periphery to the centre of the axon. The axonal membranes of all motor axons were still intact after three weeks, although most were no longer continuous after four weeks. By five weeks, all axonal material had completely disintegrated. These data suggest that axonal synthetic processes in crayfish sensory (and presumably motor) axons can maintain the axons relatively intact for 7-14 days and that transfer of substances form hypertrophied glial cells to motor axons may account for the longer survival times of transplanted motor axons.

Animals↗
PubMed1970

Quantitative aspects of transmitter release.

The opener-stretcher motor neuron in crayfish makes 50 endings upon each of 1200 muscle fibers. We have calculated the quantal content of junctional potentials produced by individual terminals and by the whole cell at various physiological frequencies. The results show that when the motor neuron is active at 20 impulses/second, it releases 50 quanta/impulse per muscle fiber, or a total of 4.5 x 10(9) quanta/hr. These figures are similar to those for vertebrate muscles per fiber, but larger for the entire neuron because the opener motor unit is so large. On the basis that the quanta correspond to synaptic vesicles each containing 10(3)-10(4) molecules of transmitter, the release rate must be around 10(-11) mole/hr. This value is within an order of magnitude of the release figures obtained for mammalian neurons by collecting transmitter in perfusates, but it is far lower than the value reported for a crustacean inhibitory neuron. If the membrane materials surrounding each vesicle were lost in the release process, the replacement synthesis would involve 24 mm(2) of membrane/hr. We conclude that the metabolic load in terms of transmitter synthesis is probably sustainable, but that the release mechanism must operate in such a way that vesicle membrane materials are neither lost nor incorporated into the terminal membrane.

Animals↗
PubMed1970

A reconsideration of the Poisson hypothesis for transmitter release at the crayfish neuromuscular junction.

1. Transmitter release from excitor nerve terminals in the crayfish opener muscle was studied with both intra- and extracellular electrodes.2. The amplitude distribution of quanta recorded extracellularly from a single release site did not fit the compound Poisson hypothesis in two thirds of the data sets.3. Some data appeared to be non-Poisson because specific quantal multiples were released; the non-Poisson nature of release for other sets could be due to variable invasion of the axonal spike into the terminal region.4. In some muscle fibres, the number of quanta released at one ending to any given impulse in a stimulus train was correlated with the number of quanta released at other endings on the same fibre. This suggests that such endings may be supplied by nerve twigs arising from a common branch point with a very low safety factor for transmission.5. No consistent relationship was found between the amplitudes of the intra- and extracellular spontaneous potentials recorded from the same muscle fibre.

Action Potentials↗
PubMed1968

Differentiation of nerve terminals in the crayfish opener muscle and its functional significance.

Junctional potentials (jp's) recorded from superficial distal fibers of the crayfish opener muscle are up to 50 times larger than jp' in superficial central fibers when the single motor axon that innervates the muscle is stimulated at a frequency of 1/sec or less. At 80/sec, in contrast, central jp's are up to four times larger than those observed in distal fibers. The tension produced by single muscle fibers of either type is directly proportional to the integral of the time-voltage curve minus an excitation-contraction coupling threshold of 3 mv. Distal fibers therefore produce almost all the total muscle tension at low frequencies of stimulation and central fibers add an increasingly greater contribution as their nerve endings begin to facilitate in response to increased rate of motor discharge. Differentiation of muscle membrane characteristics (input resistance, space constant, time constant) cannot account for these differences in facilitation ratios. The mechanism of neuronal differentiation is not based upon the size or effectiveness of transmitter quanta, since equal sized jp's have equal variances;: mjp sizes and variances are also equal. No differences were found between fiber types in rates of transmitter mobilization, density of innervation, or the relationship between transmitter release and terminal depolarization. Single terminals on distal fibers were found to release transmitter with a greater probability than central terminals. More effective invasion of distal terminals by the nerve impulse at low frequencies can account for the difference.

Axons↗
PubMed1967

Regeneration in crustacean motoneurons: evidence for axonal fusion.

Crayfish motor axons remain excitable for over 100 days after severance from their central cell bodies, and continue to store and release normal amounts of transmitter substance. Evidence indicates that regeneration occurs by fusion of the central process with its surviving peripheral segment.

Animals↗