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Biomedical subjects

B Walmsley

Publications and source records attributed to B Walmsley.

53 records · Page 3Linked to original sources
PubMed1984

Synaptic input from identified muscle afferents to neurones of the dorsal spinocerebellar tract in the cat.

Single identified group I a and I b muscle afferent fibres were injected with horseradish peroxidase in the lumbar dorsal columns of anaesthetized cats. The morphological details of the axon collaterals and terminal boutons of these muscle afferents within Clarke's column were subsequently reconstructed. The rostro-caudal extent of synaptic terminals from a single afferent fibre within Clarke's column was found to be restricted to less than 1 mm. In the same experiments, dorsal spinocerebellar tract (d.s.c.t.) neurones were retrogradely labelled by injection of horseradish peroxidase into the cerebellum. Synaptic contacts between labelled group Ia and Ib afferent fibres and the soma and proximal dendrites of d.s.c.t. neurones were found. The synaptic contacts from both Ia and Ib fibres varied greatly in size, from 1 X 1 micron up to 'giant' synapses of 20 X 3 micron. Excitatory post-synaptic potentials (e.p.s.p.s) were evoked in d.s.c.t. neurones by impulses in single group I muscle afferent fibres. The fluctuations in peak amplitude of each e.p.s.p. were determined from e.p.s.p. and noise recordings, using a numerical deconvolution procedure. In general, these single-fibre e.p.s.p.s fluctuated between discrete amplitudes separated by an incremental amplitude which was approximately constant. This incremental amplitude did not depend on the average peak amplitude of the particular e.p.s.p. examined. Our anatomical observations of 'giant' boutons arising from Ia and Ib afferent fibres contacting d.s.c.t. neurones raises the possibility of multiple transmitter release sites within an individual synaptic bouton. It is proposed that synaptic transmission between group I muscle afferents and d.s.c.t. neurones occurs with discrete all-or-nothing e.p.s.p.s associated with transmitter release sites.

Action Potentials↗
PubMed1983

The effect of transection and cold block of the spinal cord on synaptic transmission between Ia afferents and motoneurones.

Composite excitatory postsynaptic potentials were elicited in lumbar motoneurones by Ia afferents from muscles of the triceps surae group. These excitatory postsynaptic potentials were examined in the same cell before, during and after interruption of descending spinal pathways. After transection or cold block of the spinal cord at T12-T13, the amplitude of composite excitatory postsynaptic potentials showed no significant change for a period of up to seven hours after transection. However, there was a reduction in amplitude of the monosynaptic reflex in the extensor motoneurones which may be due to an observed hyperpolarization and reduction in membrane time constant in these neurones. The reduction in amplitude of the monosynaptic reflex observed in spinal shock can be attributed to the effects of these changes, rather than to a decrease in the size of the monosynaptic excitatory postsynaptic potential.

Afferent Pathways↗
PubMed1983

The time course of synaptic potentials evoked in cat spinal motoneurones at identified group Ia synapses.

Excitatory post-synaptic potentials (e.p.s.p.s) were evoked in motoneurones by impulses in single group Ia axons. After recording the e.p.s.p., the motoneurone and the group Ia axon were injected with horseradish peroxidase. The morphological details of the connexion formed by each group Ia axon with a motoneurone were subsequently reconstructed. Four Ia axon-motoneurone pairs were obtained. The electrotonic distance from the soma to each synaptic bouton in the connexion was calculated. The electrotonic lengths of those dendrites on which synaptic connexions were found were also calculated. The shape indices of each recorded e.p.s.p. and the standard cable model of the motoneurone were used to calculate the electrotonic distance from the soma to the point on the equivalent dendritic cable at which the e.p.s.p. originated. This distance was compared with the distance obtained from the reconstruction of the synaptic connexion at which the e.p.s.p. was generated. For two of the four connexions, the locations calculated by both methods agreed to within 0.1 lambda. Similar agreement could only be obtained for the other two connexions if synaptic transmission did not occur at some of the boutons in the termination. Evidence that some boutons were not involved in transmission is presented in the following paper (Redman & Walmsley, 1983).

Animals↗
PubMed1983

Amplitude fluctuations in synaptic potentials evoked in cat spinal motoneurones at identified group Ia synapses.

Excitatory post-synaptic potentials (e.p.s.p.s) were evoked in spinal motoneurones (of anaesthetized cats) by impulses in single group Ia axons. The morphological details of the Ia axon-motoneurone connexion involved in generating each e.p.s.p. were subsequently reconstructed, as described by Redman & Walmsley (1983). The fluctuation pattern of the peak amplitude of each e.p.s.p. was determined using a deconvolution method, taking into account the recording noise. Four e.p.s.p.s were analysed. One did not fluctuate in amplitude; the others fluctuated between discrete amplitudes which were separated by quantal increments. The number of increments which must be added to produce the largest peak amplitude of each e.p.s.p. was always less than, or equal to, the number of synaptic boutons in the connexion at which the e.p.s.p. was generated. The results are consistent with the hypothesis that transmission occurs in an all-or-none manner at each synaptic bouton. Different boutons in the termination of a Ia axon with a motoneurone have different probabilities of releasing transmitter, and this probability is sometimes zero at low stimulation rates. The results support the idea that the discrete amplitudes of an evoked e.p.s.p. result from intermittent transmission, in an all-or-none manner, at some or all of the boutons in the termination.

Animals↗
PubMed1982

Cost of force development as a function of stimulus rate in rat soleus muscle.

The energy cost (determined myothermically) and mean stress (force per cross-sectional area) development of soleus muscles from adult rats were determined. Muscles were stimulated at various frequencies from 0.25 to 100 Hz over a 4-s interval, and the resulting stress-time integral was averaged over this period to yield a total heat vs. mean stress relation. This relation was characterized by three zones, i.e., 1) a linear zone corresponding to unfused twitches, 2) an intermediate zone corresponding to partial fusion during the relaxation phase only, and 3) a second linear zone corresponding to partially and fully fused tetani. The energy cost of mean stress development in the twitch zone was about four times higher than that of the fusion zone. The results are discussed in terms of the firing frequencies at which motor unit recruitment occurs in mammalian slow-twitch muscles.

Animals↗
PubMed1981

An intracellular study of Renshaw cells.

Intracellular recordings were made from Renshaw cells in the cat. Recurrent excitatory postsynaptic potentials (EPSPs) were elicited by antidromic stimulation of the ventral roots. These EPSPs had a simple monophasic time course without a spike-like peak reported by previous authors. No hyperpolarization could be detected following averaged EPSPs. However, after bursts of impulses an afterhyperpolarization could be detected which probably contributes to a pause in firing after the initial response. Depolarizing current pulses elicited a burst of impulses similar in pattern to the initial response to stimulation of the ventral roots.

Animals↗
PubMed1980

'Long-loop' reflexes can be obtained in spinal monkeys.

Extensor muscles of the fore- and hindlimb were stretched in the lightly anaesthetized monkey (Macaca fascicularis) and cat. The resulting electromyogram contained a short latency peak consistent with a monosynaptic, segmental pathway; this peak was identified as the M1 peak of Tatton et al. [21]. A longer latency peak, identified as M2 and said to involve a pathway including supraspinal centres, was also present. After spinal section at a high cervical level, the electromyogram was reduced in amplitude, but both short (M1) and longer latency (M2) peaks were present. It is concluded that neither the cerebral cortex nor the cerebellum are necessary parts of the neural circuitry generating longer latency components of the electromyographic response to muscle stretch.

Animals↗
PubMed1976

Statistical fluctuations in charge transfer at Ia synapses on spinal motoneurones.

1. Net inward charge is calculated for unitary Ia e.p.s.p.s. evoked in spinal motoneurones. Fluctuations in this charge are used to describe the fluctuations in transmission at the Ia synapse. 2. The statistical details of variation in transmission at Ia synapses are largely obscured by noise, arising from spontaneous activity and recording apparatus. 3. A computational procedure is described, which utilized the measured statistical properties of the recording noise, and the measured charge histogram of the evoked e.p.s.p. (with noise) to calculate the variations in charge due to the e.p.s.p. alone. 4. The fluctuation in charge transmission at Ia synapses are, in general, non-quantal. Nor are they described by binomial or Poisson statistics. 5. It is suggested that the basic mode of transmission at a single terminal is all-or-none. The fluctuations result from the combined effect of failures at several terminals arising from a single afferent fibre. This hypothesis is supported by further analysis of these results in a subsequent paper (Edwards, Redman & Walmysley, 1976a).

Animals↗
PubMed1976

Non-quantal fluctuations and transmission failures in charge transfer at Ia synapses on spinal motoneurones.

1. The origins of fluctuations in charge transfer during the generation of Ia e.p.s.p.s have been investigated. The discrete components which make up the fluctuating e.p.s.p. have been separated. 2. Some e.p.s.p.s fluctuate between two different amplitudes and time courses. These fluctuations have been analysed to show that charge transmission always occurs at one synaptic location, but not always at a second synaptic location. 3. The failures in transmission were study by stimulating the afferent fibre at different frequencies. Although different probabilities of failure were obtained at different frequencies, there was no systematic change in probability with increasing frequency. 4. Single afferents were tetanized and histograms of charge transfer computed during post-tetanic potentiation (p.t.p.). Only half of the units studied showed any p.t.p. In those that did, evidence was found for a decrease in the probability of failure during potentiation. 5. The results could not be used to distinguish between failure of the impulse to always propagate into the terminals, and failure of the terminals to release transmitter following adequate depolarization. 6. The fluctuations in transmission at a single synapse can be described by a binomial process with n = 1 and p less than or equal to 1. Junctional mechanisms consistent with this description are discussed. Alternative mechanisms which associate failures with failure of impulse transmission at afferent fibre branch points are also suggested.

Action Potentials↗
PubMed1976

The effect of polarizing currents on unitary Ia excitatory post-synaptic potentials evoked in spinal motoneurones.

1. Depolarizing and hyperpolarizing currents were applied to motoneurones in which unitary Ia e.p.s.p.s were evoked. The results concentrate on those e.p.s.p.s which had time courses which were compatible with somatically located synapses. 2. No reversal of these e.p.s.p.s was observed. Depolarizing currents up to 150 nA simply reduced the peak amplitude. 3. Hyperpolarizing currents caused little, if any, increase in the peak amplitude of the e.p.s.p. The time course of decay became briefer as the membrane was hyperpolarized. 4. Changes in decay time course of the e.p.s.p. which accompanied depolarization and hyperpolarization could be attributed to changes in membrane conductances, rather than to changes in synaptic current time course. 5. The failure of the e.p.s.p. to increase with hyperpolarization was shown to be due to the failure of the synaptic current to increase, rather than to the shunting of anomalous rectification. 6. Chemical and electrical transmission are evaluated against these results and those of the preceding papers.

Action Potentials↗