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Biomedical subjects

W H Calvin

Publications and source records attributed to W H Calvin.

At least 19 recordsLinked to original sources
PubMed1983

A stone's throw and its launch window: timing precision and its implications for language and hominid brains.

Did bigger brains for more precise throwing lead to language, much as feathers for insulation may have set the stage for bird flight? Throwing rocks even at stationary prey requires great precision in the timing of rock release from an overarm throw, with the "launch window" narrowing eight-fold when the throwing distance is doubled from a beginner's throw. Paralleled timing neurons can overcome the usual neural noise limitations via the law of large numbers, suggesting that enhanced throwing skill could have produced a strong selection pressure for any evolutionary trends that provided additional timing neurons. This enhanced timing circuitry may have developed secondary uses for language reception and production.

Animals↗
PubMed1981

Dendritic analysis of lobster stretch receptor neurons: electrotonic properties with single and distributed inputs.

Using steady-state cable analysis as derived by Rall, electrotonic properties of the dendritic trees of the tonic stretch receptor neurons of the spiny lobster. Panulirus interruptus, have been examined. By directly measuring the somatic input resistance and by visualizing the dendritic trees of this neuron by backfilling the axon with cobalt, the electrotonic properties of the dendritic trees have been derived. The Calculated membrane resistivity is 800-3600 omega-cm2. Voltage and current transfer functions were calculated for (a) single dendritic tips the size observed in the cobalt preparation and (b) for processes 2 micrometer or smaller, as observed in electron microscopy. Current transfer to the soma was high in both cases (greater than 80%). Voltage transfer was 22% for large and 4% for small dendrites. When a more natural simultaneous conductance change at the tips of all major dendrites was modeled, voltage transfer was 84% and current transfer 56%. But the dynamic range of the cell (rheobase to saturation) is well-predicted by varying the simultaneous inputs, not by scaling up a single input, thus illustrating that convenient indices of electrotonic properties may not prove useful in appreciating the integrative properties of a neuron.

Action Potentials↗
PubMed1977

Pathophysiology of trigeminal neuralgia.

Tic douloureux is a painful affliction of man without known similarities to diseases in infrahuman species or to other human afflictions. It seems to be associated with structural abnormalities encroaching upon the trigeminal nerve, gasserian ganglion, or root entry zone. The multiple unique features of tic douloureux can be explained by a theory which is based upon presynaptic inhibition and reflection sites due to focal changes in axon diameter or myelination. We believe that this theory satisfactorily explains the varied phenomena of tic douloureux and is compatible with the limited anatomical and physiological data relevant to tic douloureux. It makes use of known physiological and anatomical concepts. It is capable of verification or refutation by experimental means.

Humans↗
PubMed1977

Retrograde invasion of lobster stretch receptor somata in control of firing rate and extra spike patterning.

1. Extra spikes may be interleaved in the otherwise rhythmic discharge pattern of the lobster stretch receptor neuron, about 2 ms after an expected spike. A constant input to the neuron is maintained by injecting current intrasomatically. The axon recovers its excitability while the retrograde invasion of the soma and dendrites is still in progress, which provide electrotonic currents to reexcite the axon. 2. While extra spikes in the axon often arise from a prolonged somatic (dendritic?) depolarization, they may also arise from a delayed retrograde invasion of the soma. 3. Failure of retrograde invasion may cause a sudden jump in the rate of rhythmic discharge, demonstrating the role of the soma-dendritic afterhyperpolarization in the regulation of rhythmic firing rate. 4. The history of repetitive firing is often important. Because extra spikes often first appear during a decline in firing rate, turning on and then off, an additional current may sometimes activate the extra spike mode, thus doubling the resting firing rate in a metastable manner. Another mestastable state is associated with failure of retrograde invasion. 5. Extra spikes augment the high end of the frequency-current curve in some receptor neurons; in other cases, the extra spikes are seen only at low rhythmic firing rates, dropping out as current reaches intermediate values to create a paradoxical negative-sensitivity region (decline in total spikes per second with increasing current). 6. The results suggest that both the extent and the speed of active retrograde invasion of the soma and dendrites are likely candidates for pathophysiological mechanisms, since they may control whether extra spikes are generated.

Animals↗
PubMed1976

Fast and slow pyramidal tract neurons: an intracellular analysis of their contrasting repetitive firing properties in the cat.

1. Intracellular recordings were made from an estimated 500 neurons in the sensorimotor cortex of barbiturate-anesthetized cats. Of those which were antidromically identified from the medullary pyramids, 70 were selected which also exhibited steady repetitive firing to steps of current injected through the recording electrode; 81% were "fast" (conduction velocity greater than 20 m/s) and 19% were "slow". 2. As shown by earlier workers, the spike duration is a function of conduction velocity; a spike duration of 1.0 ms is the dividing line between fast and slow. 3. Of the 57 fast pyramidal tract neurons (PTNS), 14 exhibited double spikes during otherwise rhythmic firing patterns to a step of injected current. These very short interspike intervals (usually 1.5-2.5 ms) were first seen interspersed in a rhythmic discharge (e.g., 50-ms intervals) but, with further increases in current strength, would come to dominate the firing pattern; e.g., double spikes every 40 ms. Further increases in current would typically shorten only the long intervals; e.g., 40-30 ms, but some fast PTNS developed triple spikes, etc. 4. The extra spike appears to arise from a large hump which follows most spikes in fast PTNS; while this humplike "depolarising after-potential" can also be seen in slow PTNS, it is small. Extra spikes were seen only in fast PTNS with large postspike humps; in perhaps half of the fast PTNS, extra spikes probably contributed to "adaptation." 5. Slow PTNS often had frequency-current curves which were not repeatable; a "hysteresis" phenomenon could often be seen, where the proportionality constant relating current to firing rate decreased following high firing rates. 6. The B spike was distinguishable from the A spike in differentiated antidromic spikes in 77% of the slow PTNS, in only 14% of the fast PTNS which later exhibited double spikes during current-induced repetitive firing, and in 53% of the other fast PTNS. 7. The antidromic spike heights of doublet PTNS were not significantly different from those of other repetitively firing PTNS.

Animals↗
PubMed1975

Generation of spike trains in CNS neurons.

The membrane potential waveforms to be expected from many asynchronous inputs to CNS neurons are described, along with modes for repetitive firing through which the input waveforms are converted into spike trains. Area beneath a postsynaptic potential (PSP), rather than PSP peak height, is shown to be an important parameter susceptible to modification. Occasional crossings of threshold produce occasional spikes, but a sustained depolarizing waveform which attempts to hold the membrane potential above threshold elicits rhythmic firing. Firing rate is graded with the amount by which the synaptic depolarizing currents exceed the minimum current for rhythmic firing (approximately rheobase). A systematic sequence of alterations in the membrane potential trajectory between spikes, quite different from those of receptors and invertebrate neurons, may control the firing rate and give rise to sudden changes in the "gain" of this conversion of depolarizing current into firing rate. The different implications of synaptic location during the occasional spike mode and the rhythmic firing mode are discussed, as is the role of the antidromic invasion of the soma-dendritic region during rhythmic firing. Less frequently an"extra spike mode" is seen where depolarizing afterpotentials following a spike themselves cross threshold to elicit an extra spike, which may similarly elicit another extra spike, etc., in a regenerative cycle. The character of the underlying depolarizing afterpotentials (or "delayed depolarizations") is reviewed, along with theories for their origin from the antidromic invasion of the dendritic tree. The stereotyped burst firing patterns characteristic of the extra spike mode can also be seen in deafferented neurons and neurons studied in chronic syndromes such as epilepsy and central pain. This raises the question as to whether some disease states may augment extra spike firing, thus multiplying many-fold the response to a normal input.

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