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J Crist

Publications and source records attributed to J Crist.

9 recordsLinked to original sources
PubMed1989

Effect of cold temperature on membrane potential responses in opossum esophageal circular muscle.

The effects of cold temperature on resting membrane potential (RMP) and membrane potential responses to depolarizing electrical current and intramural nerve stimulation were examined in opossum esophageal circular smooth muscle. Intracellular recordings were made in smooth muscle strips obtained from 7 to 8 cm (proximal site) and 1 to 2 cm (distal site) above the lower esophageal sphincter. RMP was not affected by changes in temperature between 34 and 22 degrees C. Cooling caused progressive inhibition of the amplitude and a slight increase in the duration of the spike potential produced by depolarizing current. Cooling did not modify the threshold for spike potential generation but decreased the spike amplitude from 34.0 +/- 0.5 mV at 34 degrees C to 14.1 +/- 2.2 mV at 22 degrees C (P less than 0.01). Electrical field stimulation with single electrical pulses (1.0 ms) produced tetrodotoxin-sensitive biphasic membrane responses consisting of initial hyperpolarization, or an inhibitory junction potential followed by depolarization that increased in amplitude as temperature was decreased from 34 to 26 degrees C and then decreased in amplitude as temperature was further decreased. At both proximal and distal sites cooling from 34 to 22 degrees C caused more than a twofold increase in the duration of hyperpolarization and time to peak depolarization. However, the increase in the absolute time of the duration of hyperpolarization and the time to peak depolarization was significantly greater at the distal than proximal esophageal site. Cooling to 16 degrees C decreased RMP and nearly abolished the biphasic membrane potential response.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗
PubMed1988

Electrophysiological characterization of functionally distinct 5-hydroxytryptamine receptors on guinea-pig submucous plexus.

Intracellular recordings were made from neurons of the guinea-pig submucous plexus and the actions of 5-hydroxytryptamine on the postsynaptic membrane and on evoked synaptic potentials were examined. 5-Hydroxytryptamine produced two types of direct postsynaptic responses: (1) A depolarization associated with a fall in input resistance was observed in all cells. Voltage-clamp and ion substitutions showed that this depolarization resulted primarily from an inward sodium current. This response could be as brief as 30 ms; it showed desensitization and was selectively abolished by 0.2-2 microM ICS 205-930. (2) A depolarization (or inward current) associated with a decreased conductance was observed in about 50% of neurons, usually after the first response was blocked by ICS 205-930. This response was due to a decreased potassium conductance; the minimum time course of this response was 8-10 s. It did not show desensitization and was not sensitive to blockade by currently available antagonists of 5-hydroxytryptamine, nicotinic and/or muscarinic receptors. Higher concentrations of 5-hydroxytryptamine were required to produce the sodium conductance increase than the potassium conductance decrease; 2-methyl-5-hydroxytryptamine was equally effective in producing these responses. 5-Hydroxytryptamine also caused a barrage of "spontaneous" nicotinic excitatory post-synaptic potentials which were sensitive to tetrodotoxin. This response desensitized, was blocked by ICS 205-930 and is presumed to reflect excitation of other cholinergic cell bodies in the plexus by the sodium conductance increase mechanism described. The evoked nicotinic excitatory postsynaptic potential and the adrenergic inhibitory postsynaptic potential were decreased by 5-hydroxytryptamine; a portion of this inhibition showed desensitization and was blocked by ICS 205-930 as well as by the muscarinic receptor antagonists, atropine and pirenzepine. The ICS 205-930-insensitive portion of this inhibition could not be attributed to activation of 5-hydroxytryptamine-1 or 5-hydroxytryptamine-2 receptors. Thus, the following conclusions are drawn: 5-hydroxytryptamine excites submucous plexus neurons by activating two distinct 5-hydroxytryptamine receptors. Activation of the 5-hydroxytryptamine-3 receptor (sensitive to ICS 205-930) produces a depolarization mediated by an increased sodium conductance. The same effect occurring in other cholinergic cell bodies initiates action potentials which are responsible for the 5-hydroxytryptamine-induced release of acetylcholine.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

Intracellular studies of electrical membrane properties of opossum esophageal circular smooth muscle.

It has been suggested that regional differences in membrane properties of circular esophageal smooth muscle play an important role in the mechanism of esophageal peristalsis. The purpose of this study was to examine both the passive and active membrane properties of circular smooth muscle at proximal and distal esophageal sites so as to delineate the role of myogenic properties in the intramural mechanism of peristalsis. Intracellular recordings were made in circular muscle strips taken from proximal (8 cm above the gastroesophageal junction) and distal (2 cm above the gastroesophageal junction) sites in 10 opossums using the partition method of Abe and Tomita. At both esophageal sites, determinations were made of resting membrane potentials, time constants, space constants, thresholds for action potentials, action potential amplitudes, rates of rise of action potentials, and action potential durations at half-amplitude. The values for these parameters at the proximal and distal sites, respectively, were as follows: mean resting membrane potential, 49.7 +/- 0.24 and 49.5 +/- 0.3 mV; length constant, 4.0 +/- 0.4 and 3.8 +/- 0.4 mm; time constant, 513 +/- 49 and 456 +/- 53 ms; threshold for action potentials, 9.3 +/- 0.4 and 8.8 +/- 0.3 mV; amplitude of action potentials, 36.0 +/- 5.2 and 35.3 +/- 1.7 mV; rate of rise of action potentials, 2.3 +/- 0.3 and 2.6 +/- 0.4 mV/ms; duration of action potentials at half-amplitude, 5.0 +/- 1.2 and 4.1 +/- 0.4 ms; and the conduction velocity for evoked potentials, 3.9 +/- 0.3 and 3.8 +/- 0.4 cm/s. Our studies show that there are no differences between proximal and distal esophageal sites in any of these determinations. These studies also show that regional differences in the electrical membrane properties of circular smooth muscle do not account for esophageal peristalsis.

Action Potentials↗
PubMed1987

Evidence that 8-hydroxy-2-(n-dipropylamino)tetralin (8-OH-DPAT) is a selective alpha 2-adrenoceptor antagonist on guinea-pig submucous neurones.

1 Intracellular recordings were made from neurones of the submucous plexus and from submucosal arteriolar smooth muscle of guinea-pig ileum for the purpose of examining the the actions of 8-hydroxy-2-(n-dipropylamino)tetralin (8-OH-DPAT). 2 8-OH-DPAT (10 nM-20 microM) had no direct presynaptic or postsynaptic actions on submucous plexus neurones. 3 Membrane hyperpolarizations induced in neurones by noradrenaline or UK 14304 were competitively antagonized by 8-OH-DPAT. For dose-ratios up to 40, Schild plots were linear with slopes not significantly different from unity; pA2 values for the 8-OH-DPAT antagonism of postsynaptic alpha 2-adrenoceptors were 6.9-7.2. 4 The inhibitory synaptic potential, which is due to activation of alpha 2-adrenoceptors located on submucous plexus neurones, was selectively inhibited by 8-OH-DPAT; the IC50 value for inhibition of the inhibitory synaptic potential was 250 nM. 5 Neuronal hyperpolarizations mediated through activation of delta-opioid receptors or somatostatin receptors were unaffected by 8-OH-DPAT (0.1-1 microM). 6 The ability of noradrenaline and UK 14304 to inhibit the release of acetylcholine at synapses in the submucous plexus, and to inhibit the release of the transmitter which mediates the excitatory junction potential in the submucosal arteriolar smooth muscle, was also blocked by 8-OH-DPAT. 7 These results suggest that some of the actions of 8-OH-DPAT previously ascribed to agonism at 5-hydroxytryptamine (5-HT) receptors may actually result from blockade of the actions of endogenously released noradrenaline acting on alpha 2-adrenoceptors.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1986

Role of substance P nerves in longitudinal smooth muscle contractions of the esophagus.

Longitudinal muscle strips from different sites along the opossum esophagus were stimulated transmurally so as to produce neurally mediated contractions. Low-frequency transmural stimulation produced contractions after termination of the stimulus ("off" contractions), whereas high-frequency stimuli produced contractions beginning during the stimulus and extending beyond termination of the stimulus (extended-duration contractions). The intrastimulus portion of the extended-duration contraction was partially antagonized by atropine or substance P desensitization, whereas the poststimulus portion of the contraction was selectively and fully antagonized by desensitization with substance P. A combination of atropine and substance P desensitization abolished the extended-duration contraction. The amplitude of contraction was greater in the proximal than in the distal strips, irrespective of the mode of stimulation. The poststimulus portion of the extended-duration contraction was significantly longer in muscle strips taken from more distal than proximal portions of the esophagus. This gradient in duration of contractions was abolished by substance P desensitization but was not affected by atropine. Exogenously applied substance P (10 microM) produced equally sustained long-duration contractions at all sites along the esophagus. These observations suggest that a) both acetylcholine- and substance P-containing nerves are responsible for the extended-duration contraction of longitudinal muscle, and b) transmural stimulation causes an aborally directed increase in the duration of contractions; this gradient of increasing duration of contraction appears to be due to a more prolonged neural release of substance P at more distal sites.

Animals↗
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