Search PubMed⌕ Search

Biomedical subjects

J J Jack

Publications and source records attributed to J J Jack.

At least 37 records · Page 2Linked to original sources
PubMed1989

Monosynaptic EPSPs in cat lumbosacral motoneurones from group Ia afferents and fibres descending in the spinal cord.

1. Excitatory postsynaptic potentials (EPSPs) were elicited in lumbosacral motoneurones of pentobarbitone-anaesthetized cats by stimulating the ventral quadrants (VQ) of the thoracic spinal cord. These EPSPs were compared with monosynaptic EPSPs from small numbers of group Ia afferents, obtained by stimulating hindlimb muscle nerves with most of the dorsal roots severed. 2. EPSPs with average peak amplitude less than 1 mV were selected for fluctuation analysis. Three out of fourteen (21%) VQ EPSPs with peak voltage less than 150 mu V fluctuated in amplitude from trial to trial no more than could be accounted for by the background intracellular noise. Similarly, nine out of thirty-nine (23%) Ia EPSPs smaller than 150 mu V fluctuated to a comparable extent as the noise. These results are consistent with the view that there is little variation in the postsynaptic signal produced by an individual transmitter release event. 3. Of the EPSPs which did fluctuate more than the background noise, maximum likelihood estimates were obtained for the fluctuation patterns of ten VQ and fourteen Ia EPSPs. This was achieved by assuming that synaptic signals sum linearly with noise, but without constraining the results to conform to a statistical description of transmitter release. The fluctuation of both VQ and Ia EPSPs was made up of discrete amplitudes separated by roughly equal increments, in accordance with the quantal hypothesis of synaptic transmission. 4. Fluctuation patterns were obtained simultaneously for VQ and Ia EPSPs in seven motoneurones. The amplitudes of the quanta, defined as the mean increments between discrete amplitudes, were correlated (r = 0.90), suggesting common postsynaptic mechanisms. 5. For most EPSPs the time course of the voltage transient could be used to estimate the electrical distance from the soma at which the synaptic current was injected. There was a comparable distribution for VQ and Ia EPSPs. For those in which a quantal analysis was performed (nine VQ and eleven Ia), quantal size measured at the soma appeared to be independent of the deduced site of origin. 6. The results indicate no qualitative or quantitative differences in the behaviour of VQ and Ia EPSPs.

Animals↗
PubMed1989

Reduction by baclofen of monosynaptic EPSPs in lumbosacral motoneurones of the anaesthetized cat.

1. Monosynaptic excitatory postsynaptic potentials (EPSPs) were elicited in lumbosacral motoneurones of pentobarbitone anaesthetized cats by stimulating group Ia muscle afferents with most of the dorsal roots severed. In some experiments Ia EPSPs were recorded together with monosynaptic EPSPs elicited by stimulating the ipsilateral ventral quadrants (VQ) of the thoracic spinal cord. Injection of (+/-) baclofen (1 mg kg-1 I.V.) caused a reduction in the peak amplitudes of both Ia and VQ EPSPs, which started immediately upon injection and progressed gradually. No recovery in EPSP amplitude was seen during the recording period, which lasted up to 60 min. 2. The Ia EPSP peak amplitude was reduced by 18-61% (mean +/- S.D., 38 +/- 14%; n = 30), while VQ EPSPs were reduced by 7-42% (23 +/- 13%; n = 5). Baclofen had a significantly larger effect on Ia EPSPs than VQ EPSPs (P less than 0.001; t test). 3. Baclofen did not cause any consistent change in the membrane potential, nor in the membrane time constant, as estimated from the exponential decay of the tail of the EPSP. There was no tendency for the reduction in peak EPSP amplitude to be related to the estimated electrical distance on the dendritic tree at which the synaptic current was injected. 4. For two I a and two VQ EPSPs, the trial-to-trial fluctuation in the peak amplitude was resolved into quantal parameters before and after baclofen was administered. The reduction in peak amplitude was in all cases accounted for by a reduction in the probability of release of neurotransmitter, with no change in quantal size. Other EPSPs either showed negligible trial-to-trial amplitude fluctuation, or could not be resolved into quantal parameters without ambiguity. 5. By comparing the variance components of the EPSP peak amplitude distribution, the hypothesis was tested that the entire action of baclofen was to reduce quantal amplitude. This was rejected for sixteen out of thirty Ia and three out of five VQ EPSPs (P less than 0.05). 6. These results support a presynaptic site of action of baclofen on the terminals of Ia afferents, by decreasing the probability of release of neurotransmitter. They also indicate a similar, although weaker, action on VQ terminals. No evidence was found for an action on the postsynaptic membrane properties or synaptic conductance.

Animals↗
PubMed1989

Autogenetic inhibition from contraction receptors in the decerebrate cat.

1. Autogenetic inhibition from contraction receptors was measured by eliciting contractions of the soleus muscle in the decerebrate cat. Inhibitory feedback was detected when the tension increment f, produced by stimulating motor fibres in the presence of a background reflex contraction, was smaller than the tension d elicited by the same stimulus in the absence of reflex action. Tendon vibration was applied throughout to clamp primary spindle afferents at a constant firing rate, thereby preventing spindle unloading from disfacilitating the reflex contraction. 2. The reduction in tension d--f varied roughly linearly with the size of the tension stimulus f. Feedback gain was proportional to d--f/f, i.e. the ratio of inhibited tension to stimulus tension. It was computed by averaging over several measurements obtained with stimuli of different sizes, and ranged between 0 and 0.88 in ten animals. The average gain, 0.39, implies that voluntary muscle force is reduced by approximately 27% through the direct inhibition of alpha-motoneurones from homonymous contraction receptors. 3. Inhibitory feedback gain did not appear to co-vary with the background reflex contraction. When measured without vibration, however, a positive covariance did emerge, suggesting that this is due to unloading of muscle spindles, either by extrafusal muscle shortening or by inhibition of fusimotor neurones. 4. Inhibited tension varied linearly with the estimated increment in Ib afferent firing. On the assumption that group Ib afferents carried the entire inhibitory signal, inhibitory feedback gain measured with vibration was used to predict the size of the gain if vibration had not been applied. Feedback gain calculated in this way was reduced by still did not vary with reflex tension. 5. In one animal with signs of brain stem trauma, feedback gain was increased to around six. It is argued that inhibitory feedback in the intact animal can rise to comparable values, as a result both of convergence of signals from different muscles and of supraspinal facilitation.

Animals↗
PubMed1989

The effects of lesions on autogenetic inhibition in the decerebrate cat.

1. The effects of spinal and brain lesions on autogenetic inhibition from contraction receptors were studied in the decerebrate cat. Inhibitory feedback gain was estimated by measuring the effect of tension perturbations on reflex contractions of the soleus muscle. Tendon vibration was used to clamp the firing rate of primary spindle afferents, to prevent spindle unloading from disfacilitating the reflex contraction. In addition, secondary spindle afferents could be selectively excited by stimulating fusimotor fibres during muscle vibration. 2. Following an acute contralateral or bilateral dorsal transection of the spinal cord at L3, the vibration reflex tension fell by between 50 and 74% in three decerebrate animals. This was accompanied by a variable increase in inhibitory feedback, ranging between 180 and 360%. 3. In two animals, selective stimulation of fusimotor fibres supplying soleus muscle was without effect in the presence of muscle vibration both before and after the spinal lesion. In the third animal, a small and variable reduction in tension could be obtained only after the lesion, implying that an inhibitory pathway from homonymous secondary spindle afferents to alpha-motoneurones was released. 4. In a separate series of experiments, contralateral cerebral lesions were made 2-12 months prior to the acute inhibitory feedback measurement. Inhibitory feedback gain was increased, on average twofold in decerebrate animals with chronic cerebral lesions, when compared to control decerebrate animals. 5. Selective stimulation of fusimotor fibres to excite spindle secondary afferents was uniformly without effect in decerebrate animals with chronic cerebral lesions. In one animal spinal transection had only a minor effect on extensor tone and on inhibitory feedback gain, in contrast to the control decerebrate cats. 6. The implications of these findings are discussed in relation to the use of animals with spinal and supraspinal lesions as models of spasticity.

Animals↗
PubMed1988

An electrophysiological action of acetylcholinesterase independent of its catalytic site.

Acetylcholinesterase (AChE) is released from the cell bodies and/or dendrites of dopaminergic neurones in the substantia nigra. Extracellular AChE can modify both the electrical activity of dopaminergic nigral neurones and the associated motor behaviour of the animal. These effects seem to be unrelated to hydrolysis of acetylcholine, but the underlying cellular mechanisms of these actions of AChE are unknown. The possible non-cholinergic action of AChE on the membrane properties of dopaminergic neurones was thus investigated by intracellular recording from midbrain slices in vitro. Application of AChE resulted in a marked hyperpolarization of the membrane accompanied by a decrease in input resistance, sometimes preceded by a period of spontaneous firing. Butyrylcholinesterase (BuChE) was without effect. AChE pre-treated with an irreversible inhibitor (Soman) of its enzymic activity caused similar changes to those seen following administration of untreated AChE. It is concluded that AChE can modify the membrane properties of nigrostriatal neurones in a way that is independent of its ability to hydrolyse acetylcholine. This novel biological property of AChE provides a possible mechanism by which this neurosecretory protein could modulate the functioning of the neurones from which it is secreted and suggests that other 'non-cholinergic' actions of AChE might exist.

Acetylcholinesterase↗
PubMed1981

The components of synaptic potentials evoked in cat spinal motoneurones by impulses in single group Ia afferents.

1. Excitatory post-synaptic potentials (e.p.s.p.s) were evoked in cat spinal motoneurones by impulses in single group Ia afferent fibres. The probability density of the fluctuations in peak amplitude of each e.p.s.p. was calculated from the recorded peak amplitude and the probability density of the recording noise. 2. Most e.p.s.p.s fluctuated between different components (i.e. individual e.p.s.p.s of a particular discrete amplitude) with peak amplitudes which were integer multiples of the increment between successive components. The average peak amplitude of this incremental e.p.s.p. was about 90 microV for e.p.s.p.s generated at or near the soma. 3. In general, the probability density of the peak amplitude could not be described using Poisson or binomial distributions. 4. For many e.p.s.p.s the complete time course of each component could be calculated. There was no variability in the amplitude of these components nor in their latency of onset. For some e.p.s.p.s there were differences in the latency and time course of the components. 5. The increments between successive components of e.p.s.p. generated proximally were no larger (at the soma) than the corresponding increments for e.p.s.p.s generated at more distal dendritic sites. 6. These results and those from subsequent papers (Jack, Redman & Wong, 1981; Hirst, Redman & Wong, 1981) reinforce earlier suggestions that each bouton behaves in an all-or-nothing manner with respect to post-synaptic effect, and the probability of failure varies at different boutons arising from the same afferent.

Animals↗
PubMed1981

Modifications to synaptic transmission at group Ia synapses on cat spinal motoneurones by 4-aminopyridine.

1. The average amplitude of e.p.s.p.s evoked in cat spinal motoneurones by impulses in single group Ia afferents usually increased following the intravenous injection of 4-aminopyridine (4-AP). Most of this increase occurred over the first 30 min following injection of 4-AP. 2. The increase in the average amplitude following 4-AP occurred by a reduction in the probability of occurrence of component e.p.s.p.s with smaller peak amplitudes, and an increase in the probability of occurrence of component e.p.s.p.s with larger peak amplitudes. There was no evidence that the discrete amplitudes of components after 4-AP were a result of graded increases of the discrete amplitudes before 4-AP. 3. The interpretation suggested for these results is that each component e.p.s.p. is generated by transmission at a different combination of boutons. At each of these boutons sufficient transmitter is released to saturate all available receptors. The effect of 4-AP is to decrease the probability of failure to release transmitter at each bouton, including some boutons which, before 4-AP, did not release transmitter.

4-Aminopyridine↗
PubMed1975

Physiology of peripheral nerve fibres in relation to their size.

There is evidence that peripheral nerve fibres, both myelinated and unmyelinated, have different membrane properties correlated with their size. Smaller fibres have a lower conduction velocity, and longer action potential time course, than would be expected if their membrane properties were identical with those of larger size. There are several possible explanantions of this result; it is suggested that at least part of the difference is due to a systematic variation in the size of the conductances (per unit area of membrane) responsible for generating the action potential.

Action Potentials↗
PubMed1971

The propagation of transient potentials in some linear cable structures.

1. Analytical solutions have been given for the time course of voltage transients occurring in one-dimensional cable structures, with linear uniform membrane properties.2. These solutions show how the time course of the voltage transients generated at different distances are affected by variations in the time course of current injection (at one point on the cable) and by alterations in the length of the cable, with either sealed or open end terminations. These effects are illustrated with computed results.3. Simple measurements from the time course of a membrane potential displacement, occurring in a one-dimensional cable structure following a brief current injection across the membrane, are used to evaluate the parameters which describe the cable model. These parameters are the membrane time constant, the electrotonic length of the cable, the cable end termination, and in the case of a post-synaptic potential, the distance between the electrode and the active synapse.

Action Potentials↗
PubMed1971

An electrical description of the motoneurone, and its application to the analysis of synaptic potentials.

1. The Rall model of the motoneurone, which consists of a lumped resistance and capacitance, representing the soma, in parallel with a distributed resistance-capacitance network of finite length, representing the equivalent dendritic cable, has been used to investigate the effects of varying electrical and geometrical parameters on the time course of transients generated at the model soma.2. An analytical solution has been obtained for the voltage at the model soma, following a brief current injection at any point on the dendritic cable, in terms of the dendritic to soma conductance ratio, the electrotonic length of the cable, the membrane time constant, and the electrotonic distance between the point of current injection and the soma. This solution has been used to study the response at the soma to currents with a smooth time course, and to brief rectangular current pulses. Computations of these voltage transients are given to illustrate the effect of the above parameters on voltage time course.3. A method for determining the membrane time constant, the dendritic to soma conductance ratio, and the electrotonic length of the dendritic cable, is described. The method involves measurements from the decay time course of the transient at the soma following a brief current pulse being applied at the soma.4. A method is described whereby the time course of a synaptic potential, assumed to be generated by synaptic knobs located exclusively at the soma, may be used to determine the motoneurone parameters, and a parameter describing the time course of current injection.5. A method for estimating the distance between soma and origin of a non-somatic synaptic potential, once the parameters of the motoneurone are known, is described.

Computers↗
PubMed1971

The time course of minimal excitory post-synaptic potentials evoked in spinal motoneurones by group Ia afferent fibres.

1. Group Ia EPSPs were recorded from lumbosacral motoneurones in anaesthetized cats after almost complete section of the relevant dorsal roots. The EPSPs were usually of small amplitude (median value of 230 muV) and an averaging device was used to improve the definition of their time course.2. From a total of over 500 averaged EPSPs a smaller number (342) were subjected to analysis. The other EPSPs were rejected either because they showed signs of multiple origin in the rising phase of their time course (see Methods) or because the resting membrane potential of the cell was less than 50 mV. All the selected EPSPs had their rise time (from the 10 to the 90% level) and half-width measured, and a semilogarithmic plot of their decay time course was made.3. 252 of the EPSPs showed an exponential decline in their later time course and the slope of this line was used to give an estimate of the membrane time constant. The range of the time constant for different motoneurones was 2.3-12.9 msec, with a mean value of 5.8 msec.4. In ten cells an EPSP was recorded which was judged to be generated exclusively by synaptic knobs located on the soma. On this assumption measurements of the normalized rise time, half-width and break point time were used to estimate alpha, rho(infinity) and L by the method suggested in Jack & Redman (1971b). The estimated value of alpha ranged from 18 to 65. A positive correlation was found between alpha and tau(m), indicating that for these EPSPs the duration of current injection was independent of the membrane time constant. The peak time of the wave form of current injection was between 0.1 and 0.25 msec. The estimates of rho(infinity) were not thought to be very accurate. A lower limit of 4 was assumed and the highest measured value was 12, but in three cells the time course of the EPSP could not be fitted even with a very high value of rho(infinity). Some possible explanations for this discrepancy are mentioned in the Discussion. The electrotonic length of the dendrites (L) was usually greater than 1.0 lambda and ranged between 0.75 and 1.5 lambda. Evidence for an open-circuit termination of the dendrites was found in some cells.5. The normalized values of the rise time and half-width were used to make an electrotonic distance allocation to the 246 EPSPs which were judged to be non-somatic. The method of allocation was not precise because individual values of rho(infinity) and L were not available for these motoneurones. Instead, a maximum possible range was assumed: for rho(infinity), 4-25; for L, 0.75-1.5. The range of alpha was also assumed, from 12 to 100. With these values the motoneurone model (Jack & Redman, 1971b) was used to set limits within which the normalized rise time and half-width of all EPSPs, generated by current at a single point, should lie. Twenty of the 246 EPSPs lay outside these boundary lines and hence they did not receive a distance allocation. The remaining 226 were assigned values between 0.2 and 1.6 lambda (in 0.2 lambda steps); the majority of the allocations (183) were to the proximal electrotonic part of the dendrites (0.2, 0.4 or 0.6 lambda). The relationship of these distance allocations to the histological results of Conradi (1969) is discussed.6. It is concluded that there is no good evidence against the view that the main time course of minimal Ia EPSPs can be explained by their generation by a brief pulse of synaptic current and subsequent passive spread.

Animals↗