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Biomedical subjects

R Iansek

Publications and source records attributed to R Iansek.

77 records · Page 5Linked to original sources

The effects of reserpine on motor activity and pallidal discharge in monkeys: implications for the genesis of akinesia.

1. A reversible disturbance of basal ganglia function was produced in monkeys by the intramuscular administration of reserpine.2. Pallidal discharge was then compared with that recorded in the same animals during movement performance and following passive manipulation of the limbs.3. Akinesia, loss of postural support of the trunk, head and neck and absent postural reflexes were the predominant motor abnormalities produced by reserpine administration.4. Occasionally, postural tremor and catatonia were apparent. Rigidity and resting tremor were absent.5. Recordings made in the pallidum during the presence of akinesia revealed a marked reduction in natural neuronal discharge.6. Some pallidal neurones that remained active were driven in an uncharacteristic manner by peripherally generated afferent inputs from wide territories and by a variety of peripheral stimuli.7. The findings suggest the hypothesis that the akinesia in these animals was due to the diminished pallidal activity, and that pallidal discharge is normally a prerequisite for the performance of spontaneous motor activity. Pallidal neuronal firing may provide a background excitability to motor regions involved in the maintenance and elaboration of natural motor activity.

Action Potentials↗

An analysis of the cable properties of spinal motoneurones using a brief intracellular current pulse.

1. A brief intracellular current pulse, with duration less than 500 musec, has been applied to lumbosacral motoneurones in anaesthetized cats. The resulting voltage transients have been analysed by the procedure suggested in Jack & Redman (1971b) to obtain the cable parameters for each motoneurone.2. Forty-three motoneurone responses were analysed. In all cases the voltage response indicated that the dendrites could be represented as uniform, finite length cables, with either a sealed distal end, or at least a high resistance distal termination. The electrical length of the equivalent uniform dendritic cable ranged from 1.0 to 2.1 space constants, with a mean value of 1.5.3. The initial decay of the membrane potential following the removal of the current pulse was more rapid than was predicted by the Rall model for the motoneurone, in approximately two thirds of the responses. Consequently a value of dendritic to soma conductance ratio could not be obtained for these motoneurones.4. The explanation given for the departure from the theoretical response to a brief current pulse is that the specific resistivity of the soma membrane is lower than the specific resistivity of the dendritic membrane. This explanation is complicated by the possibility of the electrode tip not lodging in the isopotential soma region. The contribution that each of these effects has on the early decay phase of the current pulse response has been assessed.5. It is concluded that the specific resistivity of the soma membrane could be as low as one third of the dendritic membrane resistivity. Tonic inhibitory activity restricted to the soma is suggested as an explanation.

Animals↗

The amplitude, time course and charge of unitary excitatory post-synaptic potentials evoked in spinal motoneurone dendrites.

1. Group Ia e.p.s.p.s were recorded from lumbosacral motoneurones in anaesthetized cats after almost complete section of the appropriate dorsal roots. The cable parameters of these same motoneurones were obtained from the voltage response to a brief intracellular current pulse, as described in Iansek & Redman (1973).2. A total of thirty-three e.p.s.p.s, recorded in thirty different motoneurones, were analysed. E.p.s.p.s which were recorded in motoneurones which were not studied using an intracellular current pulse, or in which the resting membrane potential fell below 50 mV, were not considered. Also, e.p.s.p.s whose time course indicated more than one synaptic site of origin were not analysed. The selected e.p.s.p.s were plotted on a semilogarithmic amplitude scale, and their 10-90% rise time, half-width and peak amplitudes were measured.3. Using the previously determined values of the cable parameters L, rho(infinity) and tau(m), the rise time and half-width of each e.p.s.p. were used to determine the synaptic location (X), and the synaptic current time course (alpha). Twenty-seven e.p.s.p.s had time courses which allowed a value of X and alpha to be determined within the constraints of the measured cable parameters. The remaining six e.p.s.p.s either required an extension of the dendritic cable to be localized, or their time course was not compatible with a brief synaptic current.4. The synaptic locations lie in the range 0 (soma) to 1.25 space constants. When expressed as a fraction of the length of the dendritic cable, all but four of the twenty-seven e.p.s.p.s were located on the proximal half of the dendrites.5. The time to peak of synaptic current for each e.p.s.p. ranged from 30 to 390 musec, although a majority (70%) lay in the range 50 to 200 musec. There was no significant correlation between time to peak of synaptic current and synaptic location.6. The peak amplitude of e.p.s.p.s at the soma showed no significant correlation with synaptic location.7. The peak amplitude, and the cable parameters for each e.p.s.p. were used to compute the time course and amplitude of each e.p.s.p. at its point of generation on various fractions of the total dendritic cable, using the results derived in Redman (1973). These calculations showed the greatly increased rate of decay of e.p.s.p.s at their point of generation. Assuming that the synaptic input was restricted to one tenth of the total dendritic tree, the range of peak amplitudes at the synaptic site was from less than 100 muV (soma) to 20 mV.8. The net inward positive charge crossing the synaptic junction was calculated from the voltage-time integral of the e.p.s.p., as was the net outward positive charge crossing the soma membrane. These calculations showed that dendritic synapses caused up to ten times more net charge to be displaced across the synaptic junction than did synapses on or near to the soma, for similar durations of synaptic current. Similarly, dendritic synapses were generally more effective than somatic synapses in displacing charge across the soma membrane. It was concluded that the average quantal content in the conductance change at dendritic synapses is significantly greater than for somatic synapses.9. Some implications of the results for general integrative mechanisms in dendrites are discussed.

Animals↗

Clinical identification of TIAs due to carotid stenosis.

A retrospective case note survey of 139 cases of carotid territory TIAs was carried out. Angiographic evidence of carotid stenosis was more frequently encountered when the patient's attacks consisted of symptoms suggestive of ischemia of small cortical territories with involvement restricted to the arm or leg or to dysphasia. Attacks of hemiparesis affecting face, arm and leg, or arm and leg were less often associated with carotid stenosis. If patients described any attacks of a restricted nature the chance of finding carotid stenosis was 47%, if not 16%. It is argued that these findings are a reflection of the varied pathogenesis of TIAs, and the relevance of this heterogeneity to the interpretation of clinical trials is briefly mentioned.

Arterial Occlusive Diseases↗

Motor instability in parkinsonian speech intensity.

OBJECTIVE: This study examined progressive speech intensity decay using two speech tasks: sustained vowel phonation (Experiment 1) and sentence reading (Experiment 2). BACKGROUND: Parkinsonian speech intensity has often been clinically observed to fade out or trail off. This gradual diminution of intensity is not unlike the well-documented progressive reduction of force underlying (upper limb) micrographic parkinsonian handwriting and (lower limb) marche à petit pas. Motor instability in speech intensity has yet to be investigated in a controlled experimental setting, however. METHOD: Thirteen Parkinson disease (PD) patients and their matched controls participated in Experiment 1: data from 6 PD patients and controls who naturally (i.e., without prior instruction) read the target sentence within a breath span were included in the analysis for Experiment 2. Participants were instructed to inhale maximally before vocalizing, and the extent of intensity declination over the breath span was measured. RESULTS: Parkinson disease patients demonstrated a consistently greater level of progressive intensity decay compared with matched controls for both speech tasks. This successful documentation and analysis of fading speech was interpreted as evidence for motor instability within the speech motor system in PD. CONCLUSIONS: It was concluded that the control of force in complex motor sequences involving speech and limb movement is affected by a common deficit in the frontostriatal circuit.

Aged↗