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T O Neild

Publications and source records attributed to T O Neild.

At least 55 records · Page 3Linked to original sources
PubMed1982

Noradrenaline receptors on the rat basilar artery.

1. Intracellular recordings were obtained from the arterial smooth muscle cells of rat basilar artery during perivascular nerve stimulation and during the application of adrenoceptor agonists and antagonists. 2. Perivascular nerve stimulation evoked excitatory junction potentials. Increased stimulation resulted in action potentials which were associated with arterial constriction. 3. Bath-applied noradrenaline did not cause constriction but at high concentrations caused membrane depolarization. The depolarization caused by a given dose of noradrenaline was larger in the presence of cocaine. 4. Neither the depolarizations obtained by nerve stimulation nor those obtained by bath-applied noradrenaline were blocked by adrenoceptor blocking agents. 5. Unlike alpha-receptors, the receptors on the rat basilar artery were activated equally well by dopamine, adrenaline, and both optical isomers of noradrenaline. 6. Excitatory junction potentials could be obtained in the presence of high bath concentrations of noradrenaline.

Adrenergic Agonists↗
PubMed1982

Modification of the response to nerve stimulation in small arteries of guinea-pig caused by distension of the artery.

1. Intracellular recordings of membrane potential were made from the smooth muscle of small arteries taken from the guinea-pig ear. The arteries were internally perfused at constant pressures ranging from 0 to 60 mmHg. 2. The resting membrane potential of the smooth muscle was not affected by altering the perfusion pressure. 3. At the higher pressures the smooth muscle membrane showed an enhanced ability to generate rapidly rising action potentials. 4. The amplitude of the excitatory junction potential evoked by a single stimulus to the perivascular nerves was increased when the perfusion pressure was raised. 5. Excitatory junction potentials and action potentials could be recorded in the presence of tetrodotoxin (3 x 10(-6) M) although increased stimulus voltages were required. These responses were abolished by guanethidine (2 x 10(-5) M). 6. The effects of increased perfusion pressure could still be observed in tetrodotoxin.

Action Potentials↗
PubMed1981

Localization of specialized noradrenaline receptors at neuromuscular junctions on arterioles of the guinea-pig.

1. Noradrenaline was applied by ionophoresis to various positions on the surface of an arteriole, and any changes in membrane potential of the arteriolar smooth muscle were recorded. 2. At a proportion of positions noradrenaline produced membrane depolarization. 3. The positions where noradrenaline produced these membrane potential changes were restricted to regions close to the sympathetic nerves which innervated the arterioles.

Animals↗
PubMed1980

Evidence for two populations of excitatory receptors for noradrenaline on arteriolar smooth muscle.

We have recorded the responses of arteriolar smooth muscle cells to iontophoretically applied noradrenaline. Records of both muscle movement and muscle membrane potential were made. We found that two distinct types of response could be detected, depending on the position of the noradrenaline micropipette. One type of response consisted of a localised constriction near the noradrenaline source: this effect could be abolished by the alpha-antagonist phentolamine and was not associated with a change in arteriolar membrane potential. The other type of response was a depolarisation similar to the excitatory junction potentials (e.j.ps) produced by sumpathetic nerve stimulation. These observations suggest that there are two populations of receptors for noradrenaline on arterioles, and could explain the paradoxical failure of alpha-antagonists to block neuromuscular transmission at some sutonomic end organs such as the vas deferens, arteries and arterioles.

Animals↗
PubMed1980

Some properties of spontaneous excitatory junction potentials recorded from arterioles of guinea-pigs.

1. Spontaneous excitatory junction potentials were recorded from electrically short segments of arterioles taken from the intestinal submucosa of guinea-pigs. 2. Histograms of the amplitudes of these spontaneous potentials were unimodal; their amplitudes often corresponded with the amplitudes of the smallest evoked potentials recorded from the same preparation. 3. The time courses of both spontaneous and evoked potentials were very similar and it is suggested that evoked potentials are made up by the simultaneous occurrence of several spontaneous potentials. 4. The mean quantal content of evoked potentials was always far fewer than the number of varicosities present in the preparations. 5. It is suggested that during neuromuscular transmission, transmitter is released at relatively few sites throughout the ground plexus for each nerve impulse.

Animals↗
PubMed1978

Slowly-developing depolarization of neurones in the guinea-pig inferior mesenteric ganglion following repetitive stimulation of the preganglionic nerves.

Intracellular recordings were made from cells of the isolated guinea-pig inferior mesenteric ganglion. Stimulation of both hypogastric nerves at 30 Hz for 2 sec caused a slowly developing depolarization (SD) and fall in cell input resistance which reached a peak 10-30 sec after the end of stimulation. The amplitude of the SD was increased in a graded manner if the stimulus voltage was increased. The SD was unaffected by tubocurarine, atropine or guanethidine, but was blocked by removing external Ca. These results suggested that the SD was caused by the release of some substance from a large number of nerve terminals.

Animals↗
PubMed1978

Life time and elementary conductance of the channels mediating the excitatory effects of acetylcholine in Aplysia neurones.

1. The excitatory effects of acetylcholine (ACh) on an identified group of Aplysia neurones have been studied under voltage clamp in an attempt to measure the average life time. tau, of the channels opened by ACh and the elementary current, iel, flowing through these channels. The value of tau was determined both from spectral noise analysis and from current relaxations after voltage steps. Both methods lead to similar values. iel was calculated from the ratio of the variance of the ACh induced noise to the mean ACh induced current. 2. tau is increased by hyperpolarization, or by lowering the temperature. At 12 degrees C, tau = 27 msec AT -80 MV, tau = 17 msec at mV. tau is about 5 times smaller at 21 degrees C than at 12 degrees C. 3. iel increases linearly with hyperpolarization. At -80 mV, in Tris-buffered sea water, the mean value of iel was 0.8 X 10)-12) A at 12 degrees C. At 21 degrees C, this value was multiplied by 1.8. 4. The estimate of the ACh reversal potential Erev obtained by extrapolation of the relation between iel and the membrane potential V was + 30 mV. The estimate obtained from the analysis of the instantaneous current changes produced by voltage steps was + 15 mV. The difference between the two values appears to be due to the development of a K curent activated by the entry of Ca into the cell during the ACh response. This current introduces an error in opposite directions into the two estimates of Erev, which can therefore be assumed to be intermediate between + 15 and + 30 mV. An assumed value of + 20 mV yields an elementary conductance of 8 X 10(-12) omega-1 at 12 degrees C in Tris-buffered sea water. 5. The total ACh induced current measured in steady-state conditions increases more with hyperpolarization than does iel. The difference can be entirely accounted for by the fact that hyperpolarization increases tau. 6. When carbachol or tetramethylammonium is applied instead of ACh, the value of iel is identical to that found with ACh, but tau is slightly shorter (about 75%). 7. Inward ACh induced currents can still be observed in solutions where all Na has been replaced by Cs, Mg, or Ca. 8. iel increases when Na is replaced by Cs; it decreases when Na is replaced by Mg or Ca. In all Na-free solutions, tau is larger than in Na sea water: the lengthening of tau is largest for Ca sea water, smallest for Cs sea water. An interpretation of these changes of gamma is proposed. This interpretation may also account for the voltage sensitivity of gamma in normal sea water. 9. Partial replacement of NaCl by TrisCl strikingly reduces the ACh induced current. gamma is not modified by Tris substitution, and the reduction of the total current is entirely accounted for by a steep decrease of iel. Tris does not seem to affect the pore opening and closing processes, but to block the ACh controlled channel.

Acetylcholine↗
PubMed1978

The mode of action of antagonists of the excitatory response to acetylcholine in Aplysia neurones.

1. The mode of action of various antagonists of acetylcholine (ACh) excitatory effects on Aplysia neurones was studied under voltage clamp. ACh was applied by iontophoresis whereas antagonists were applied in the bath. Tubocurarine and hexamethonium were the most thoroughly studied compounds. 2. The 'elementary current', calculated as the ratio of the variance of the ACh noise to the mean ACh induced current, was not modified by any of the antagonists tested. 3. The evolution of the ACh induced current after a voltage jump, which is normally described by a single exponential, was modified by all the antagonists tested. A common feature of the modified relaxations was the appearance, over a certain concentration range of the antagonist, of two successive and opposite exponential components. 4. The characteristics of the composite relaxations depend on the antagonist. For a given antagonist they vary with membrane potential, ACh concentration, and antagonist concentration. 5. The noise power spectra of the ACh induced current showed changes consistent with those of the relaxations. 6. In the absence of antagonists, the current induced by a steady application of ACh increases linearly with hyperpolarization. In the presence of antagonists, the I-V curve shows a marked curvature, indicating a proportionally larger reduction of the ACh response at more negative membrane potentials. 7. The voltage sensitivity of the blocking action of hexamethonium and decamethonium is noticeably stronger than that of monovalent antagonists. 8. A model is proposed which accounts for the observed effects. It assumes that the antagonists studied bind perferentially to the 'activated' ACh-receptor complex, and convert it to a non-conducting state. Kinetic constants can be calculated for this reaction; e.g. for curare, at 12 degrees C and -80 mV, the dissociation and association constants were estimated at 0.1 sec-1 and 4 X 10(5) M-1 sec-1. 9. Partial replacement of the extracellular Na by Tris modifies the relaxations observed in the presence of hexamethonium. Hexamethonium appears less effective in the presence of Tris, which supports the hypothesis that the binding site of the antagonists is linked to the ionic channel.

Acetylcholine↗
PubMed1978

An analysis of excitatory junctional potentials recorded from arterioles.

1. Arterioles were impaled with two independent micro-electrodes, one to pass current and the other to record membrane potential. 2. When current was injected into one branch of an arteriole, a membrane potential change could be detected either in the same branch or in an adjoining branch indicating that the arteriolar smooth muscle cells were electrically connected. 3. Fine dissection of the arteriolar tree gave short segments of arteriole which appeared to behave electrically as short cables with sealed ends. 4. Analysis of the electrotonic potentials recorded from isolated segments of arterioles allowed a determination of the arteriole cable properties. 5. Using the data from the cable analyses it was concluded that the junctional current underlying an excitatory junction potential has a duration that is brief when compared with that of the potential.

Animals↗
PubMed1976

Chloride distribution in Aplysia neurones.

1. The intracellular Cl(-) concentration (Cl(i)) and the membrane potential (E(m)) were measured in the medial pleural neurones of Aplysia under various experimental conditions designed to determine the Cl(-) conductance of the neurones and investigate the possibility of an active Cl(-) transport.2. The magnitude of the Cl(-) conductance of the cell depends on the experimental conditions.3. In normal sea water, large changes of E(m) produced by passing current across the cell membrane caused no change of Cl(i), suggesting that the Cl(-) conductance was low. Similarly, moderate changes of E(Cl) produced by decreasing Cl(o) or increasing Cl(i) had little or no effect on E(m).4. A high Cl(-) conductance was observed in high K(o) or very low Cl(o). It was greatly reduced if the external Ca(2+) was replaced by Co(2+), or in the presence of tubocurarine, or if the experiment was performed on an isolated cell soma. The high Cl(-) conductance is therefore attributed to the release of ACh and perhaps other transmitters from synaptic terminals.5. High concentrations of tetraethylammonium ions or procaine induced a depolarization of the cell, but a decrease of Cl(i). The rate of fall of Cl(i) was increased by lowering external K(+) or raising external Ca(2+), and was decreased by replacing external Ca(2+) by Co(2+).6. NH(4) (+) ions applied externally had effects similar to those of K(+) ions. In situations in which intracellular NH(4) (+) might be increased a fall in Cl(i) was observed.7. The changes of Cl(i) caused by TEA, procaine, or internal NH(4) (+) occur against the driving force for passive Cl(-) movements. They are still observed in isolated cell bodies, and cannot be attributed to the activation of synaptic channels.8. Some interpretations of these anomalous Cl(-) movements are discussed which could also account for the difference between E(Cl) and E(m) observed under normal conditions.

Journal Article↗
PubMed1974

Intracellular chloride activity and the effects of acetylcholine in snail neurones.

1. Cl(-)-sensitive micro-electrodes were used to measure intracellular Cl(-) in snail neurones. The electrodes consisted of a sharpened and chlorided silver wire mounted inside a glass micropipette.2. The electrodes appeared to record changes in internal Cl(-) accurately but in H cells the chloride equilibrium potential (E(Cl)) as measured by the Cl(-)-sensitive electrode was always less negative than E(ACh).3. In some H cells ACh caused a measurable increase in internal Cl(-) when the cell was at its resting potential. In voltage-clamped cells there was a close correlation between the change in internal Cl(-) and the extra clamp current caused by a brief application of ACh. This confirmed that ACh increases the cell's membrane permeability only to Cl(-) ions, and that E(ACh) was equal to E(Cl).4. There was good agreement between the measured change in internal Cl(-) and that calculated from the cell size and clamp charge only when it was assumed that a constant voltage offset was added to the potential of the Cl(-)-sensitive electrode while it was inside the nerve cell.5. Cl(-)-sensitive electrodes with AgCl as the sensitive material appear to be unsuitable for intracellular measurement of Cl(-), although they might be suitable for following changes in E(Cl).6. In certain D cells ACh also caused an increase in internal Cl(-) although it decreased the membrane potential. In the presence of hexamethonium, ACh caused a hyperpolarization and a smaller increase in internal chloride.7. It is concluded that the intracellular Cl(-) in both H and D cells is about 8.3 mM, giving an E(Cl) of about -58 mV.

Acetylcholine↗