Sensory Mechanisms in Paramecium

1972 ◽  
Vol 56 (3) ◽  
pp. 683-694
Author(s):  
R. ECKERT ◽  
Y. NAITOH ◽  
K. FRIEDMAN

1. Specimens of Paramecium caudatum were stimulated mechanically with a piezoelectrically driven microstylus. Membrane potentials were monitored and intracellular polarizing currents were passed with glass microelectrodes. 2. Mechanical stimulation of the anterior 15% of the cell's length produced depolarizing transients in membrane potential. This ‘anterior response’ was amplitude-graded up to a maximum with stimuli of increasing intensities, and was accompanied by a drop in membrane resistance. 3. The anterior response consists of two components, a receptor potential in direct response to stimulus transduction, and a secondarily evoked regenerative component. Both are graded. With hyperpolarization of the cell membrane the regenerative component was suppressed and the receptor potential alone was seen. With hyperpolarization the size of the receptor potential was increased. 4. The regenerative component is identical with the ‘calcium response’ which is elicited by direct stimulation with injected depolarizing current. This conclusion is supported by similar sensitivity of the overshoot to extracellular concentrations of calcium, similar refractory periods, similar inactivation by depolarization and suppression by hyperpolarization, and similar prolongation of the time course by TEA. 5. It is concluded that local inflow of receptor current through the stimulated membrane of the anterior end depolarizes the cell membrane by electrotonic spread, activating the electrically excited calcium conductance of the membrane, and thereby eliciting the regenerative calcium response.

1990 ◽  
Vol 63 (2) ◽  
pp. 303-318 ◽  
Author(s):  
C. C. Bell

1. Physiologically and morphologically identified primary afferent fibers from mormyromast electroreceptor organs were recorded intracellularly. The fiber recordings were made from the nerve root of the posterior lateral line nerve, where the fibers enter the brain, and from the electrosensory lateral line lobe (ELL), near the central terminals of the fibers. 2. The intracellular recordings reveal a variety of potentials, synaptic and nonsynaptic, in addition to the large orthodromic action potentials from the periphery. The goal of the present study was to describe and interpret these various potentials in mormyromast afferent fibers as a first step in understanding the processing of electrosensory information in ELL. 3. Three types of synaptic potentials were recorded inside mormyromast afferent fibers: 1) electric organ corollary discharge (EOCD) excitatory postsynaptic potentials (EPSPs), driven by the motor command that elicits the electric organ discharge (EOD); 2) EPSPs evoked by electrosensory stimulation of electroreceptors in the skin near the electroreceptor from which the recorded fiber originates or by direct stimulation of an electrosensory nerve; and 3) inhibitory postsynaptic potentials (IPSPs) evoked by electrosensory stimulation of more distant electroreceptors. These synaptic potentials can be attributed to synaptic input to postsynaptic cells in ELL that is observed inside the afferent fibers because of electrical synapses between the fibers and the postsynaptic cells. 4. The peripherally evoked EPSPs could frequently be shown to be unitary. The unitary EPSPs were identical to the orthodromic spikes in originating from a single electroreceptor, in threshold, and in latency shift with increasing stimulus intensity. These similarities suggest that the unitary EPSPs are electrotonic EPSPs caused by impulses in other mormyromast afferent fibers that terminate on some of the same postsynaptic cells as the recorded fiber. The peripherally evoked IPSPs had a longer latency than the EPSPs or orthodromic spikes, requiring the presence of an inhibitory interneuron. 5. The peripherally evoked EPSPs, both unitary and nonunitary, show absolute refractory periods of 3-8 ms, followed by relative refractory periods of approximately 8 ms, when tested with two identical stimuli to a nerve. These refractory periods are interpreted as because of refractoriness in the fine preterminal branches of the axonal arbor. 6. A depolarizing afterpotential is commonly associated with the orthodromic spike and probably results from the successful propagation of the spike into the entire terminal arbor. The depolarizing afterpotential has a refractory period that is similar to that of the peripherally evoked EPSPs and that is also interpreted as refractoriness in the fine preterminal branches.(ABSTRACT TRUNCATED AT 400 WORDS)


1996 ◽  
Vol 270 (4) ◽  
pp. G619-G633 ◽  
Author(s):  
M. Hocker ◽  
Z. Zhang ◽  
D. A. Fenstermacher ◽  
S. Tagerud ◽  
M. Chulak ◽  
...  

The enzyme L-histidine decarboxylase (HDC; EC 4.1.1.22), which converts L-histidine to histamine, plays a key role in the regulation of acid secretion. In the rat and human stomach, the peptide hormone gastrin appears to be one of the main regulators of HDC expression. In rats, marked elevation of gastric HDC mRNA abundance was observed within 12 h after induction of hypergastrinemia by a single injection of the proton-pump blocker omeprazole. In situ hybridization revealed that HDC expression occurred in the basal third of gastric glands where enterochromaffin-like cells are localized. To study the regulation of HDC gene transcription, 1,291 nucleotides of the 5'-flanking region of the rat HDC gene and the noncoding portion of exon 1 were cloned and sequenced. Gastrin and cholecystokinin (CCK) octapeptide equipotently stimulated the transcriptional activity of the rat HDC promoter three- to fourfold, and deletion analysis revealed the presence of a gastrin response element within 201 nucleotides upstream of the translational start site. Time-course studies revealed maximal activation of the HDC promoter after 12-36 h. Direct stimulation of protein kinase C (PKC) with the phorbol ester phorbol 12-myristate 13-acetate (PMA) substantially elevated rat HDC promoter activity, whereas induction of Ca2+ -dependent signaling pathways with thapsigargin was without effect. Downregulation or blockade of PKC abolished the effects of gastrin and PMA on the HDC promoter. These data indicate that stimulation of the CCK-B/gastrin receptor activates the rat HDC promoter in a time- and dose-dependent fashion and that this effect is primarily mediated via a PKC-dependent signaling pathway. Use of HDC as a model gene will allow further investigation of the intracellular pathways that are involved in gastrin-dependent gene regulation.


1974 ◽  
Vol 64 (1) ◽  
pp. 26-48 ◽  
Author(s):  
L. H. Pinto ◽  
W. L. Pak

The time-course of the light-induced changes in membrane voltage and resistance were measured for single photoreceptors in the retina of Gekko gekko. In the surgically isolated retina, small stimuli directed toward the impaled receptor produced a membrane hyperpolarization the time-course of which was identical to that of the increase in membrane resistance. In the eyecup preparation nearly identical time-courses were evoked only after perfusion of the vitreous surface with solution having high (Mg++). Disparate time-courses were obtained in (a) the isolated retina when large or displaced stimuli were used, and (b) the eyecup preparation when it was treated normally (see Pinto and Pak. 1974. J. Gen. Physiol. 64:49) and when it was exposed to aspartate ions or hypoxia. These results are consistent with the hypothesis that the receptor potential (elicited in the impaled receptor as a result of quanta only it captures) is generated by a single ionic process that decreases membrane conductance. These measurements provide a means to distinguish the receptor potential from interactions. From direct measurements of membrane time constant and total resistance in darkness, total membrane capacitance was calculated. The mean capacitance was 7.1 x 10-5 µF. This high value is consistent with anatomical observations of membrane infoldings at the base of gecko photoreceptors.


1994 ◽  
Vol 72 (6) ◽  
pp. 3026-3028 ◽  
Author(s):  
M. Juusola ◽  
E. A. Seyfarth ◽  
A. S. French

1. Intracellular microelectrodes recorded the receptor potential and receptor current in the neurons of spider slit sense organs during mechanical stimulation of the slits. 2. Mechanical stimulation produced two patterns of action potential discharge, corresponding to the two groups of neurons described previously by electrical stimulation. 3. Tetrodotoxin eliminated the action potentials and revealed a receptor potential with both static and adapting components. Voltage clamp gave an inward receptor current with a similar time course. 4. Replacement of sodium ions in the bath reversibly eliminated the receptor current, indicating that it is carried by sodium ions. However, this effect was comparatively slow, suggesting that the tips of the sensory dendrites lie in a chemically restricted environment.


1988 ◽  
Vol 66 (11) ◽  
pp. 1386-1397 ◽  
Author(s):  
L. P. Jager ◽  
M. W. G. Van Der Schaar

Effects of stimulation of intramural nerves in the circular smooth muscle layer of the porcine colon (Sus scrofa domestica) were studied using the sucrose-gap technique. Electrical field stimulation of the preparation, superfused with Krebs solution at 21 °C, induced a transient hyperpolarization of the smooth muscle cell membrane. This hyperpolarization was an inhibitory junction potential (IJP). The responses obtained from circular muscle originating from either the centripetal or centrifugal gyri of the ascending colon did not differ significantly. The UP was characterized as being mediated by intramural, nonadrenergic, noncholinergic (NANC) nerves. The amplitude and latency of the IJP changed linearly with temperature (15–25 °C: +1 mV and −0.1 s per degree Celsius, respectively) reflecting a temperature-dependent synchronization of transmitter release. The membrane resistance decreased during the IJP. The IJP amplitude decreased or increased during conditioning hyperpolarizations or depolarizations, respectively, and reversed at membrane potentials about 30 mV more negative than the resting membrane potential. Potassium conductance blocking agents, barium (1 mM), tetraethylammonium chloride (TEA, 20 mM), 4-aminopyridine (4-AP, 5 mM), apamin (1 μM), and aminacrine (10−4 M) added to the superfusion medium increased the membrane resistance. Only barium, TEA, and apamin depolarized the smooth muscle cell membrane. The IJP amplitude decreased in the presence of aminacrine and apamin to 75 and 35%, respectively, suggesting that apamin-sensitive Ca2+-activated K+ channels are involved in this response. ATP, adenosine, and related adenine nucleotides in concentrations up to 10−3 M did not mimic the IJP. Superfusion with ATP for 15 min revealed a gradually increasing attenuation by up to 20% of the IJP. This might suggest that the release of neurotransmitter from intramural NANC nerves is modulated presynaptically via purinoceptors. Exogenously applied vasoactive intestinal polypeptide (VIP) in concentrations of 10−9 to10−4 M did not affect the preparation. Also at elevated temperatures (up to 35 °C), VIP (10−7 to 10−4 M) did not cause measurable effects. It is concluded that the inhibitory mediator of the intramural NANC nerves present in the circular muscle layers of the porcine colon is neither a purine nor VIP.


1974 ◽  
Vol 64 (1) ◽  
pp. 49-69 ◽  
Author(s):  
L. H. Pinto ◽  
W. L. Pak

The time-course of light-induced changes in membrane voltage and resistance were measured in single photoreceptors in eyecup preparations of Gekko gekko. A small circular stimulus directed toward the impaled receptor produced membrane hyperpolarization. Application of a steady annular light to the receptor periphery resulted in diminution of the receptor's response to the stimulus. The effects of illumination of the surrounding receptors were isolated by directing a small, steady desensitizing light to the impaled receptor and then applying a peripheral stimulus. Brief stimuli produced a transient decrease in resistance with rapid onset and offset, a time-course similar to that of the response diminution. For some cells a depolarization that coincided with the resistance decrease was seen. During illumination with prolonged stimuli the resistance decrease was followed by a slow increase. After offset resistance rose transiently above the original value and then returned slowly to its original value. The slow resistance changes were not accompanied by changes in membrane voltage. The response diminution, resistance decrease, and depolarization were not observed in retinas treated with aspartate or hypoxia. It is therefore concluded that these effects are mediated by horizontal cells. The diminution is achieved by shunting the receptor potential and may play a role in field adaptation.


1979 ◽  
Vol 73 (6) ◽  
pp. 703-723 ◽  
Author(s):  
W T Clusin ◽  
M V Bennett

When physiological conditions are simulated, skate electroreceptors produce small maintained oscillatory currents. Larger damped oscillations of similar time-course are observed in voltage clamp. Subtraction of leakage in voltage clamp data shows that the oscillations involve no net outward current across the lumenal surface of the epithelium. The oscillations are much faster than the late outward current generated by the lumenal membranes of the receptor cells. Treatment of the basal surface of the epithelium with tetraethyl ammonium (TEA), high K, Co, or EGTA reversibly blocks the oscillations in voltage clamp, but has little or no effect on the epithelial action potential in current clamp or on the current-voltage relation. The TEA sensitivity of the oscillations indicates that they involve a potassium conductance in the basal membranes of the receptor cells. Treatment of the basal membranes with TEA and high calcium, with strontium, or with barium causes these membranes to produce large regenerative responses. Direct stimulation of the basal membranes then elicits a lumen-positive action potential whereas stimulation of the lumenal membranes elicits a diphasic action potential. Excitability of the basal membranes is abolished by extracellular Co, Mn, or La. Modulation of the lumenal membrane calcium conductance by the basal membrane conductances probably gives rise to the oscillatory receptor currents evoked by small voltage stimuli. The slower calcium-activated late conductance in the lumenal membranes may be involved in sensory accommodation.


1992 ◽  
Vol 68 (05) ◽  
pp. 545-549 ◽  
Author(s):  
W L Chandler ◽  
S C Loo ◽  
D Mornin

SummaryThe purpose of this study was to determine whether different regions of the rabbit vascular system show variations in the rate of plasminogen activator (PA) secretion. To start, we evaluated the time course, dose response and adrenergic specificity of PA release. Infusion of 1 µg/kg of epinephrine stimulated a 116 ± 60% (SD) increase in PA activity that peaked 30 to 60 s after epinephrine administration. Infusion of 1 µg/kg of norepinephrine, isoproterenol and phenylephrine had no effect on PA activity. Pretreatment with phentolamine, an alpha adrenergic antagonist, blocked the release of PA by epinephrine while pretreatment with the beta blocker propranolol had no effect. This suggests that PA release in the rabbit was mediated by some form of alpha receptor.Significant arterio-venous differences in basal PA activity were found across the pulmonary and splanchnic vascular beds but not the lower extremity/pelvic bed. After stimulation with epinephrine, PA activity increased 46% across the splanchnic bed while no change was seen across the lower extremity/pelvic bed. We conclude that several vascular beds contribute to circulating PA activity in the rabbit, and that these beds secrete PA at different rates under both basal and stimulated conditions.


1990 ◽  
Vol 17 (3) ◽  
pp. 224-227
Author(s):  
Henning F. Bjerregaard

The aim of the present study was to investigate the site and mode of trifluoperazine (TFP) action on cell membrane transport by the use of isolated frog skin. This cellular system gives access to the apical (outer) and basolateral (inner) membranes of the polarised epithelial cells. Both apical and basolateral TFP addition induced a dose-dependent stimulation of Na transport, and depolarised the cellular potential. The data indicate that TFP acts by increasing the Na permeability of the apical membrane. However, the mechanisms localised in the apical and basolateral membranes are quite different. Basolateral TFP addition increased Na transport due to a stimulation of PGE2 synthesis, whereas apical TFP addition abolished Na inhibition of the apical Na channels, and thereby enhanced the Na transport. An acute toxic effect on the electrophysiological parameters was noted after addition of high apical TFP concentrations (50–100μM). This toxic effect was dependent on the presence of Na in the apical solution.


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