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Biomedical subjects

J F Cassell

Publications and source records attributed to J F Cassell.

8 recordsLinked to original sources
PubMed1992

Two movement aftereffects: evidence for luminance- and color-movement pathways.

Two movement aftereffects (MAEs) that bear closely on the issue of visual processing of color and movement have been isolated. Following adaptation with a vertical luminance stimulus a strong MAE occurred with the same stationary test stimulus oriented horizontally and also in a perfectly uniform field. Neither effect occurred following adaptation with a color equiluminance stimulus. These aftereffects have not been reported before. It is concluded that there are at least three pathways for movement, a color, a color-plus-luminance, and a luminance pathway.

Adaptation, Ocular↗
PubMed1988

The effect of temperature on neuromuscular transmission in the main caudal artery of the rat.

1. Excitatory junction potentials (EJPs) recorded in isolated segments of the proximal main ventral artery of the rat tail were reduced in amplitude and prolonged in time course as temperature was lowered from 35 to 15 degrees C. 2. The slow depolarization that followed the EJPs after supramaximal or repetitive perivascular stimulation was markedly slowed in time course, but little affected in amplitude, as temperature was lowered. 3. The time constant (tau EJP) of the exponential decay phase of the EJP recorded from cells deep in the media was similar to the membrane time constant, so that the increase in tau EJP at low temperatures is consistent with a decrease in membrane conductance. 4. The value of tau EJP was also prolonged if the EJP was evoked at the time of the peak of the slow depolarization; this effect was blocked by idazoxan (10(-7) M) but not by prazosin (10(-6) M). 5. During repeated short bursts of high-frequency stimulation, action potential initiation was facilitated by both the prolongation of EJPs and summation of slow depolarizations; these effects were greater at 25 than at 35 degrees C. 6. The interactions between EJPs and alpha-adrenoreceptor-mediated membrane conductance changes are considered with respect to the electrical events occurring during sympathetic neuromuscular transmission at the natural temperatures of the rat tail.

Action Potentials↗
PubMed1987

Muscarinic agonists block five different potassium conductances in guinea-pig sympathetic neurones.

Muscarinic excitation of sympathetic ganglion cells has usually been thought to result from inhibition of an outward K+ current, the M current, although in other neurones several conductances have been shown to be blocked by muscarinic agonists. We report that, as well as resting K+ conductance, all of four different K+ conductances, two voltage-dependent (M currents and A currents) and two calcium-dependent (responsible for slow and very slow afterhyperpolarizations), present in different sub-types of guinea-pig sympathetic neurones, are inhibited by the muscarinic agonists, bethanechol and muscarine. All of these effects increase neurone excitability and can lead to repetitive discharge.

Action Potentials↗
PubMed1987

Two calcium-activated potassium conductances in a subpopulation of coeliac neurones of guinea-pig and rabbit.

1. Some of the sympathetic neurones in coeliac ganglia isolated from young guinea-pigs and rabbits were found to generate action potentials followed by after-hyperpolarizations with durations of 3-8 s, much longer than those (congruent to 300-500 ms) observed in the majority of other mammalian sympathetic neurones. 2. This type of ganglion cell discharged only once at the onset of a depolarizing step unless a very high intensity current was applied. Passive and voltage-dependent membrane conductances studied in detail in guinea-pig ganglia differed from those in the two other classes of sympathetic ganglion cell described previously (Cassell, Clark & McLachlan, 1986). 3. By using a single microelectrode to voltage clamp the soma, it was possible to demonstrate that both fast and slow components of the tail current following initiation of an uncontrolled 'action current' in neurones with long after-hyperpolarizations (l.a.h.) were carried by K+ ions, as was the fast tail current (time constant, tau congruent to 130 ms) present in other coeliac neurones. 4. The amplitude of both components of the tail current in l.a.h. neurones was markedly reduced by the replacement of Ca2+ by Mn2+, Co2+ or Ba2+ ions. These manoeuvres had similar effects on the fast tail current in other coeliac neurones. 5. Both time course and amplitude of the fast tail current were increased when Ca2+ concentration was raised, or when several 'action currents' were initiated, whereas only the amplitude of the slow tail current was affected. 6. The time course of the slow tail current could be described by the sum of two exponentials with tau on = 285 ms and tau off = 1.3 s at 35 degrees C occurring after a delay of 60 ms. This current had a Q10 of about 4 between 35 and 25 degrees C. In contrast, the Q10 of the fast component was about 2. 7. Morphine (10(-6) M) and vasoactive intestinal polypeptide (10(-6) M) had no effect on the outward tail current in l.a.h. neurones, but 5-hydroxytryptamine (10(-6) M) was found to abolish the slow component without affecting the fast component. 8. The slow tail current was activated in the subthreshold range of membrane potentials, and its properties could account for the firing characteristics of this subpopulation of sympathetic neurones. 9. The two calcium-activated potassium conductances that are responsible for the prolonged after-hyperpolarization resemble those in a subpopulation of nodose ganglion cells with unmyelinated axons (Fowler, Greene & Weinreich, 1985).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Characteristics of phasic and tonic sympathetic ganglion cells of the guinea-pig.

Intracellular recording techniques have been used to determine the electrophysiological properties of sympathetic neurones in ganglia of the caudal lumbar sympathetic chain (l.s.c.) and in the distal lobes of inferior mesenteric ganglia (i.m.g.) isolated from guinea-pigs. Passage of suprathreshold depolarizing current initiated transient bursts of action potentials in 97% of l.s.c. neurones, but only 13% of i.m.g. cells ('phasic' neurones). Most i.m.g. neurones fired continuously during prolonged depolarizing pulses ('tonic' neurones). Passive membrane properties varied; mean cell input resistance was similar between groups, but phasic neurones had smaller major input time constants on average than had tonic cells. Current-voltage relations determined under both current clamp and voltage clamp were linear around resting membrane potential (approximately 60 mV), where membrane conductance was lowest. Instantaneous and time-dependent rectification varied in the different neurone types. The current underlying the after-hyperpolarization following the action potential was significantly larger on average in tonic i.m.g. cells than in phasic neurones, although its time course (tau = 100 ms) was similar. Phasic neurones fired tonically when depolarized after adding the muscarinic agonist, bethanechol (10(-5) M to 10(-4) M), to the bathing solution. Bethanechol blocked a proportion of the maintained outward current (presumably the M-current, IM, Adams, Brown & Constanti, 1982) in phasic neurones; this current was small or absent in tonic neurones. Transient outward currents resembling the A-current (IA, Connor & Stevens, 1971 a) were evoked in tonic but not in phasic neurones by depolarization from resting membrane potential. IA could only be demonstrated in phasic neurones after a period of conditioning hyperpolarization. After a step depolarization to approximately --50 mV, IA reached peak amplitude at about 7 ms and then decayed with a time constant of about 25 ms in both neurone types. Activation characteristics of IA were similar for phasic and tonic neurones, but inactivation curves, although having the same shape, were shifted to more depolarized voltages in tonic neurones. That is, IA was largely inactivated at resting membrane potential in phasic, but not tonic neurones. It is concluded that the discharge patterns of the two populations of sympathetic neurones result from differences in the voltage-dependent potassium channels present in their membranes. The anatomical occurrence of the different cell types suggests that phasic neurones are vasoconstrictor and tonic neurones are involved with visceral motility.

4-Aminopyridine↗
PubMed1986

The effect of a transient outward current (IA) on synaptic potentials in sympathetic ganglion cells of the guinea-pig.

The responses to stimulation of preganglionic fibres have been studied in sympathetic neurones in ganglia of the caudal lumbar sympathetic chain (l.s.c.) and in the distal lobes of inferior mesenteric ganglia (i.m.g.) isolated from guinea-pigs. Most l.s.c. neurones were classified as 'phasic' and i.m.g. neurones as 'tonic' (see Cassell, Clark & McLachlan, 1986). The types of preganglionic inputs received by l.s.c. and i.m.g. neurones differed: l.s.c. cells almost invariably received at least one suprathreshold ('strong') input, in addition to several subthreshold ones; i.m.g. neurones more commonly received only subthreshold inputs via the lumbar splanchnic nerves. Prolonged discharges were evoked in some i.m.g. cells by stimulation of lumbar splanchnic nerves at strengths just supramaximal for the conventional fast synaptic responses. These appeared to arise from repetitive discharges evoked in other neurones intrinsic to the i.m.g. The time constants of decay of subthreshold synaptic currents recorded under voltage clamp in l.s.c. neurones (4.9 +/- 0.2 ms) were significantly shorter on average than those recorded in tonic i.m.g. cells (7.1 +/- 0.3 ms), although the values of time constant for the two populations overlapped. In phasic neurones, excitatory synaptic potentials (e.s.p.s) evoked at resting membrane potential by stimulation of preganglionic axons decayed with the same exponential time course as an electrotonic potential. In tonic neurones, the time course of decay of the e.s.p. was briefer, but always followed an exponential with the same time constant as the cell input time constant over the final part of the response. If tonic neurones were hyperpolarized by the passage of current through the recording micro-electrode, the time course of decay of the e.s.p. was prolonged and became the same as that of the electrotonic potential. The shape of e.s.p.s in phasic and tonic neurons could be mimicked in a computer model of the neurones incorporating the different activation/inactivation characteristics of the A current (IA) (Cassell et al. 1986) for each neurone type. It is concluded that, in addition to the contribution of IA to the rhythmic firing properties of tonic sympathetic neurones, this current also markedly inhibits the effects of excitatory synaptic conductance changes in this type of ganglion cell.

Action Potentials↗
PubMed1985

Relation between electromyogram and force in fatigue.

The relationship between the surface electromyogram (SEMG) and force was examined during maximal voluntary contraction (MVC). Isometric MVC of elbow flexors were studied in 18 subjects who performed 27 trials, each consisting of six MVCs lasting 45 s at intervals of 30 s. There was a decrease in the median frequency (Fm) of the SEMG and of the compound action potentials (CAP) during MVC. The CAPs demonstrated that the fall in Fm was associated with a proportional increase in signal power, whereas CAP amplitude did not decrease, indicating intact neuromuscular transmission. The SEMG root-mean-square amplitude remained fairly constant, progressively deviating from force with time of contraction (r = 0.40). When SEMG amplitude was corrected for the Fm change, it tracked force more closely (r = 0.68), indicating a fall in motoneuron drive during MVC. The corrected SEMG was used to calculate the change in the generalized firing rate of motoneurons. The firing rate decreased 60% in the first and sixth contractions, tracked force closely, and corresponded to the firing rate fall seen in late adaptation of motoneurons (r = 0.90, P less than 0.001).

Action Potentials↗