Search PubMed⌕ Search

Biomedical subjects

R M Jell

Publications and source records attributed to R M Jell.

34 records · Page 2Linked to original sources
PubMed1976

Action of prostaglandin synthetase inhibitors on rostral hypothalamic neurones: thermoregulation and biogenic amines.

Sensitivity of neurones in the rostral hypothalamus of methoxyflurane anesthetized cats to the prostaglandin synthetase inhibitors (PGSIs), salicylate and fenoprofen, has been examined using the technique of microiontophoresis. Results were compared with sensitivity to prostaglandin (PG) E1 and no noradrenaline (NA) and 5-hydroxytryptamine (5HT). Simultaneous applications of PGSIs and NA or 5HT were made to investigate the role of PG in monoamine induced changes in neuronal excitability. PGSIs did not excite these cells, but depression were common, particularly with fenoprofen. PGE1 did not reverse the depressions. NA and 5HT responses were generally unaffected by simultaneous PGSI application and responsiveness to PGSIs was found to be unrelated to amine sensitivity. The results support the conclusion that PGSIs have a depressant action on neurones in this region, which may not be related to inhibition of prostagladin synthesis, and that the actions of microiontophoretically applied NA and 5HT are not dependent upon PG.

Action Potentials↗
PubMed1974

Responses of rostral hypothalamic neurones to peripheral temperature and to amines.

1. Five-barrelled micropipettes have been used to record extracellularly the activity of neurones in the rostro-medial hypothalamus of methoxyflurane-anaesthetized cats, and to apply acetylcholine (ACh), noradrenaline (NA) and 5-hydroxytryptamine (5-HT) by micro-iontophoresis to the vicinity of each neurone encountered. Peripheral thermal stimulation was achieved by blowing warm (42 degrees C) and cold (4 degrees C) air in the face of the animal, and thermoresponsiveness was compared with amine responsiveness.2. One hundred and twenty-two neurones were obtained from ten cats. Eleven (9%) were warm-responsive and sixteen (13%) were cold-responsive. The rest did not respond to facial warming or cooling.3. No consistent relationship was observed between amine responses and responsiveness to facial temperature. Warm-responsive neurones were mainly depressed or unaffected by amines. Cool-responsive neurones were excited, depressed or unaffected by amines with the exception that no 5-HT excitations were seen. Thermoresponsive neurones were more likely to be amine depressed than non-thermoresponsive neurones.4. Six thermoresponsive neurones responded to peripheral temperature and to amines in a way which fitted the amine model of Myers (1971). Fifteen thermoresponsive neurones fitted the model of Bligh, Cottle & Maskrey (1971), according to the same criteria.5. The results lend little support to the amine model, as predicted from amine micro-injection and release studies in primates, but support more strongly the model of Bligh et al. (1971) which is based on intraventricular injections of amines in sheep, goats and rabbits. On the basis of the latter model, functional identification was possible in 63% of the thermoresponsive rostral hypothalamic neurones tested.

Acetylcholine↗
PubMedDate not supplied

Human optokinetic afternystagmus. Slow-phase characteristics and analysis of the decay of slow-phase velocity.

Events following the extinction of lights after 1-minute exposures of naive, normal subjects to an optokinetic stimulus at 40 deg/sec have been closely examined and quantified. Mean eye displacement in each slow phase decreased from 10.12 +/- 1.61 deg during optokinetic nystagmus (OKN) to 3.36 +/- 2.32 deg during optokinetic afternystagmus (OKAN). Slow-phase duration increased from 0.26 +/- 0.03 sec during OKN to 0.45 +/- 0.195 sec during OKAN. Eye displacement per slow phase remained fairly constant during OKAN, suggesting a spatial reference for the resetting of gaze. OKAN decay is a two-component process which can be closely approximated by a sum of two exponentials, one with a short time constant of 1.15 sec and the other with a long time constant of 48.8 sec. OKAN decay commenced at a time after lights out which depended upon the presence and timing of an intervening fast phase. When a fast phase intervened, OKAN decay commenced about 230 msec after it, and about 460 msec after lights out. When lights out occurred during the fast phase, OKAN decay commenced about 340 msec later.

Adult↗
PubMedDate not supplied

Human optokinetic afternystagmus. Effects of repeated stimulation.

Normal human subjects were exposed to repeated optokinetic afternystagmus (OKAN) testing in either one direction or alternating directions of stripe movement. Sessions were conducted at intervals of either one week or several weeks. Repeated exposure to OKAN stimulation in one direction produced significant response decrements in cumulative displacement, short time constant, long time constant, and the coefficient of the long time constant component (C). The data suggest that the decrease in C and cumulative displacement occurred most noticeably between trials 3 and 4 of the first session. Retesting after 1 week, and up to 8 weeks later revealed no recovery. Repeated exposure to alternating leftward and rightward stimuli resulted in response decrement in both cumulative displacement and C. Responses to leftward stimuli were indistinguishable from responses to rightward stimuli.

Adult↗
PubMedDate not supplied

Human optokinetic afternystagmus. Charging characteristics and stimulus exposure time dependence in the two-component model.

The dependence of human optokinetic afternystagmus (OKAN) velocity storage (charging) and optokinetic nystagmus (OKN) characteristics on optokinetic (OK) stimulus exposure time was investigated, using the two-component double exponential model for OKAN decay. Results are compatible with our previously proposed concept of two velocity storage integrators, one responsible for the short time constant decay (pursuit-mediated) and the other for the long time constant decay (OK system-mediated). The dependence of the long time constant integrator of OKAN on stimulus exposure time was clearly demonstrated. The short time constant integrator appeared to be independent of stimulus exposure time within the range studied. We conclude that the charging time-course of each component is distinct from that of the other. The time constants of each component decay were found to be invariant. A left-right asymmetry observed in both OKN and OKAN responses suggests that the integrators are direction sensitive.

Adult↗
PubMedDate not supplied

Human optokinetic afternystagmus. Stimulus velocity dependence of the two-component decay model and involvement of pursuit.

The dependence of human OKAN characteristics on optokinetic (OK) stimulus velocity was examined using the two-component double exponential model for OKAN decay. Drum velocities studied were between 10 degrees and 70 degrees deg/sec over a constant exposure period of 60 sec. Results reveal two distinct types of response: a 'low'-level response at lower drum velocities (10 degrees, 20 degrees, 30 degrees/sec) and a 'high'-level response at higher drum velocities (40 degrees, 60 degrees, 70 degrees /sec). These findings support our previous proposal that OKAN decay is a two-component process, and extend it by demonstrating that these two components have differing stimulus velocity sensitivities, as would be predicted if it were assumed that they represented direct (pursuit) and indirect (non-pursuit) pathways respectively.

Adult↗
PubMedDate not supplied

Human optokinetic afternystagmus. Is the fast component of OKAN decay due to smooth pursuit?

Eye movement after-effects subsequent to pursuit of a single LED target were studied in human subjects to test the hypothesis that constant velocity pursuit activates a velocity storage system in the neuronal pathway. The temporal characteristics of observed after-effects fall within those predicted from the Robinson model of eyeball mechanics, indicating that neuronal integration was not a factor.

Eye Movements↗
PubMedDate not supplied

Suppression of optokinetic velocity storage in humans by static tilt in pitch.

The effects of static tilts about the pitch axis on human horizontal optokinetic after-nystagmus OKAN (HOKAN) were examined. Static tilts in pitch produced tilt-dependent HOKAN suppression. The slow decay (indirect pathway) component (coefficient C and long time constant 1/D) of the two-component model for OKAN was significantly reduced, while the short decay (direct pathway) component (coefficient A and short time constant 1/B) remained invariant as angle of tilt was increased. These results provide further evidence that otolith organ activity can couple to horizontal velocity storage in humans, in accordance with models proposed in the literature.

Adolescent↗
PubMedDate not supplied

Suppression of optokinetic velocity storage in humans by static tilt in roll.

The effects of static tilts about the roll (anterior-posterior) axis on human horizontal optokinetic afternystagmus (HOKAN) were examined. Static tilts in roll, with subjects lying on their left side, produced significant tilt-dependent HOKAN suppression. Only the slow (indirect pathway) component time constant (1/D) of the double exponential model for human HOKAN decreased with angle of roll tilt. The effect was direction specific in that suppression occurred only following a leftward-going stimulus. These findings provide further support for the postulate that otolith-organ-mediated activity can couple to the horizontal velocity storage mechanism in humans. A slight trend towards a tilt-dependent reduction of coefficient A (initial slow phase velocity of fast component decay) was revealed, suggesting the possibility that otolith-organ-mediated activity could couple to direct (pursuit-mediated?) pathways as well. No horizontal-to-vertical cross-coupling occurred, indicating that this aspect of the 3-dimensional model for velocity storage proposed by Raphan & Cohen (1988) may not completely apply to humans.

Adolescent↗