External Potassium Concentration Research Articles

Localization of ARG-vasopressin-like material in central neurones and mechanism of action of ARG-vasotocin on identified neurones of the snail Helix aspersa

Immunocytochemical and electrophysiological studies were made on neurones in the suboesophageal ganglia of Helix aspersa. A group of neurones in the anterior dorsal surface of each parietal ganglion showed positive immunoreactivity to an antibody to arginine vasopressin (AVP), as did the neuropile and the nerves associated with the parietal and visceral ganglia. The only peripheral tissue to exhibit positive immunoreactivity to AVP was the optic tentacle, where positive immunoreactive fibres were present in the optic nerve and cell bodies below the retinal cell layer. Two central neurones, Fl and E13 were excited by arginine vasotocin (AVT), threshold 1–10 nM, and the ionic mechanism associated with this response was investigated. This excitation involved both sodium and calcium ions with an overall increase in resistance. In low sodium Ringer, the AVT response was greatly reduced, while in calcium-free 3 mM cobalt Ringer, the response was potentiated. Changing the external concentrations of potassium and chloride ions had no apparent effect on the response. The amplitude of the excitation induced by AVT was enhanced when the cells were hyperpolarized. Most of the other neurones tested failed to respond to AVT though the excitatory response of certain cells to acetylcholine was enhanced by 0.1 μM AVT. Excitation by 5-hydroxytryptamine was unaffected in the cells tested. This study provides further evidence for a role for an AVT-like peptide in the nervous system of Helix.

Electrophysiological effects of labetalol on canine atrial, cardiac Purkinje fibres and ventricular muscle.

1. Using conventional microelectrode techniques for the intracellular recordings of the membrane potential, the effects of labetalol were studied on cardiac Purkinje, atrial and ventricular muscle fibres of the dog. 2. Labetalol (1-10 microM) reduced, in a concentration-dependent manner, the action potential amplitude (APA) and the maximum rate of rise of the action potential (Vmax) in Purkinje fibres. 3. The action potential duration (APD) was decreased in Purkinje fibres but significantly increased in ventricular fibres after small concentrations of labetalol (1-3 microM). The atrial fibres were not very sensitive to labetalol. 4. Depolarization of the cardiac Purkinje fibres by increasing the external potassium concentration (8-12 mM), potentiated the labetalol effects on APA and Vmax but blocked its effects on the APD. 5. The effects of labetalol on Vmax of Purkinje fibres were dependent on the frequency of stimulation. 6. The ratio of the effective refractory period to the APD was increased both in normally polarized and depolarized Purkinje fibres after treatment with labetalol (10 microM). 7. Labetalol (10 microM) shifted the membrane responsiveness curve of Purkinje fibres by about 10 mV in the hyperpolarizing direction. 8. The slow response obtained in K-depolarized, Ba-treated Purkinje fibres was not significantly affected by labetalol (10-100 microM). 9. It is suggested that labetalol can exert Class I and Class III antiarrhythmic actions in cardiac muscle of the dog in vitro.

The properties and function of inward rectification in rod photoreceptors of the tiger salamander.

1. Rod photoreceptors were isolated from the retinae of tiger salamanders and voltage clamped using the whole-cell patch-clamp technique. 2. Hyperpolarizing the cell to potentials more negative than -50 mV evoked an inward current termed Ih. 3. Ih did not turn on immediately following a hyperpolarizing step but showed a marked delay. The activation time course of Ih could be described by the sum of two exponential components of opposite polarity. 4. The steady-state chord-conductance was half activated at -67 mV. 5. The reversal potential of Ih was close to -30 mV in normal standard salt solution. Increasing the external potassium concentration tenfold shifted the reversal potential by +17 mV. 6. The conductance-voltage relation and the kinetic parameters were not affected by changes in the external potassium concentration. 7. When fully activated, the zero-current conductance underlying Ih depended on the square root of the concentration of external potassium. 8. The permeability ratio PNa/PK depended on the external potassium concentration. It was 0.2 at an external potassium concentration of 2.0 mM and 0.3 at an external potassium concentration of 10.0 mM. The interaction of potassium with Ih suggests that Ih is a multi-ion pore. 9. It is concluded that Ih differs from the inward rectifier that is found in egg cells, frog muscle and heart muscle. 10. The kinetics and voltage sensitivity of Ih suggest that it does not play a role in the dark resting state or in the response to dim flashes of light. Its properties indicate that it may have a major role in the response to bright flashes.

Somatostatin increases an inwardly rectifying potassium conductance in guinea‐pig submucous plexus neurones.

1. Intracellular recordings were made from neurones in the submucous plexus of the guinea-pig caecum and ileum. 2. Somatostatin hyperpolarized more than 90% of the neurones. The lowest effective concentration was 300 pM and the maximum hyperpolarization (about 30-35 mV) was caused by 30 nM. Under voltage clamp at -60 mV, somatostatin caused outward currents which reached a maximum of 350-700 pA. 3. The hyperpolarization or outward current reversed polarity at a membrane potential (about -90 mV in control solutions) which changed according to the logarithm of the external potassium concentration. 4. The somatostatin current showed inward rectification; when the inward rectification of the resting membrane was prevented by extracellular caesium or rubidium, the inward rectification of the somatostatin current also disappeared. 5. A potassium conductance with the same properties was increased by alpha 2-adrenoceptor agonists and by delta-opioid receptor agonists; however, the effects of somatostatin were unaffected by antagonists at alpha 2- or delta-receptors. The somatostatin analogue, cyclo-aminoheptanoyl-Phe-D-Trp-Lys-(benzyl)Thr, also did not antagonize the actions of somatostatin. 6. The hyperpolarization (or outward current) was unaffected by forskolin, cholera toxin, sodium fluoride, phorbol esters or intracellular application of adenosine 5'-O-(3-thiotriphosphate) (ATP-gamma-S). However, when the recording electrode contained guanosine 5'-O-(3-thiotriphosphate) (GTP-gamma-S) the hyperpolarizations reversed only partially when somatostatin application was discontinued, and repeated applications caused the membrane potential to approach and remain close to the potassium equilibrium potential. 7. It is concluded that somatostatin increases the conductance of a set of inwardly rectifying potassium channels in submucous plexus neurones. The coupling between somatostatin receptor and ion channel involves a guanosine 5'-triphosphate-binding protein, but is not likely to result from changes in intracellular levels of cyclic adenosine 3',5'-monophosphate.

The Electrical Constants of the Fibres from Two Leg Muscles of the Locust Schistocerca Gregaria*

ABSTRACT The passive electrical properties of the fibres from the M. extensor tibiae and the M. retractor unguis in the hindleg of the locust Schistocerca gregaria were investigated using short cable theory. The dependence on various physicochemical parameters was determined. The sarcoplasmic resistivity (R,) was the same in the extensor and in the retractor muscle. R, was ≈175 Ωcm at 20°C. The specific membrane resistance (Rm) was considerably lower in the retractor muscle (≈5100 Ωcm2) than in the extensor muscle (≈13 000 Ωcm2; [K+]o = 10mmoll−1; temperature = 20°C). Rm increased by more than 100% if the external potassium concentration was lowered from 10 to 5 mmol l−1 and it decreased by approximately 75 % if the calcium concentration was lowered from 2 to 0·2 mmol l−1. The specific membrane capacity (Cm) increased with fibre diameter. The different mean values for Cm in the extensor (8·5μFcm−2) and retractor muscle (6·3 μF cm−2) can be accounted for by the different mean fibre diameters. The temperature coefficients (Q10) of the electrical constants were 0·74 for Ri, 0·48 for Rm, 1·01 for Cm and 1·21 for the resting membrane potential (temperature, 16– 27 °C). There was close agreement between the membrane time constant (rm) derived from the decay of the excitatory junction potential (EJP) and that derived from injection of current pulses. Thus Rm and the length constant (λ) can be derived from the EJP and the fibre diameter if the sarcoplasmic resistivity and the specific membrane capacity are known. The temporospatial dependence of miniature EJPs in a fibre can be predicted satisfactorily from the electrical constants as is demonstrated by an example given in the Appendix.

Effects of hypoxia, hyperkalemia, and metabolic acidosis on canine subendocardial action potential conduction.

We have studied the individual and combined effects of elevated external potassium concentration (8 mM [K+], metabolic acidosis (pH = 6.8), and hypoxia at different stimulation 400 milliseconds) on Purkinje (P) and ventricular (V) conduction velocities and on Purkinje-ventricular junctional conduction delay (PVJ delay) in in vitro preparations from canine ventricles. Elevated [K+] had opposite effects on P and V velocities, increasing V velocity by 8% while reducing P velocity by 7%. Acidosis reduced P velocity by 9% while reducing V velocity by only 4%. Hypoxia and rapid stimulation rates had no significant effect on either P or V velocities. All test solutions (except hypoxia alone) significantly increased the PVJ delay. The magnitude of the increase in PVJ delay was much greater than the effects on either P or V velocity. In addition, hypoxia and rapid stimulation augmented the increase in PVJ delay in the presence of elevated [K+] and/or acidosis. The special features of conduction at the PV junctional sites may produce altered pathways of excitation of the ventricles during myocardial ischemia.

Retraction and degeneration of sympathetic neurites in response to locally elevated potassium

Sympathetic neurons from superior cervical ganglia of newborn rats were plated into center compartments of 3-compartment culture dishes, allowing exposure of distal neurites to media of different composition than provided to cell bodies and proximal neurites. Cultures were maintained initially with an external potassium concentration ([K +] o) of either 5 mM in all compartments or 50 mM in all compartments. After neurites had elongated into distal compartments, the culture medium was changed such that: the cell bodies and proximal neurites were exposed to 5 mM [K +] o; the distal neurites in one side compartment of each culture were also exposed to 5 mM [K +] o; but the distal neurites in the opposite side compartment were exposed to 50 mM [K +] o. During the next 7–10 days, the distal neurites locally exposed to 50 mM [K +] o degenerated. Many neurites developed a stretched appearance before degenerating, and detailed observations suggest that the neurites retracted to the point where mechanical tension exceeded their strength and then abruptly disintegrated. Neurites in opposite side compartments exposed to 5 mM [K +] o were normal in appearance and did not degenerate. These results suggest that a proximo-distal increase in [K +] o causes an extreme retraction of neurites distal to the increase. These results raise the possibility that K + released by active nerve endings might cause the retraction of inactive nerve endings, thus providing a possible mechanism for the influence of activity on competition for synaptic sites, a pervasive phenomenon in the developing nervous system.

Microelectrode measurement of cell membrane potential in isolated hepatocytes attached to collagen

Isolated spherical rat hepatocytes attached to collagen-coated cover slips generate a mean membrane potential ( E m) of −78±9 mV as measured with high-resistance microelectrodes. The recordings were biphasic and were stable for upto 20 minutes. The correlation between external potassium concentration and E m was not linear. Several potassium-channel blockers did not effect the membrane potential. Addition of ouabain added to the incubation solution slowly depolarized the cells. The results indicate a high potassium permeability of the isolated spherical hepatocytes attached to collagen.

Modulatory synaptic actions of an identified histaminergic neuron on the serotonergic metacerebral cell of Aplysia

Possible sources of excitatory synaptic input to the serotonergic metacerebral cell (MCC) were determined by stimulating various neurons in the cerebral ganglion. Firing of the previously identified histaminergic neuron C2 was found to produce synaptic input to the MCC. The synaptic input consists of fast excitatory-inhibitory synaptic potentials on a background of a slow EPSP. The slow EPSP appears to be monosynaptic and chemically mediated since it persists in a solution of high divalent cations; broadening of the presynaptic spike enhances the EPSP; the size of the EPSP is a function of the Mg2+ and Ca2+ concentrations of the bathing solution; and the EPSP can be mimicked by application of histamine to the MCC. The slow EPSP, in addition to firing the MCC, can increase the excitability of the cell, even under conditions in which C2 is fired at a rate too slow to produce a measurable EPSP when the MCC is at rest potential. This property appears to be due to the fact that the slow EPSP results from an apparent decrease of membrane conductance so that the size of the EPSP increases markedly as the cell is depolarized, and the EPSP appears to be highly voltage-dependent so that it is small or absent close to the rest potential of the MCC. When the MCC is voltage-clamped, application of histamine to the bath results in an inward current that disappears when the MCC is hyperpolarized. The potential at which the histamine-induced current reverses or disappears is dependent on the concentration of external potassium, suggesting that, at least in part, the slow EPSP is due to a decrease of potassium conductance. The data on C2 are consistent with its being an element of the neuronal system that mediates a state of food arousal in Aplysia.

Frequency-dependent effects of phenytoin on the maximum upstroke velocity of action potentials in guinea-pig papillary muscles

Phenytoin, at 50 to 200 micrograms reduced the maximum upstroke velocity of action potentials (Vmax) with increases in frequency from 0.25 to 5 Hz and in the external potassium concentration [( K+]0) from 2.7 to 8.1 mM. The drug-induced shortening of action potential duration was evident at 0.25 to 2 Hz but little at 3 to 5 Hz. Time courses of recovery of Vmax was studied by applying premature responses between the conditioning responses at 1 Hz both in control and in drug-treated preparations. Concerning the time courses of the difference between the Vmax values before and after drug treatments at the same diastolic interval, with increases in drug concentrations the intercepts at APD90 were increased but the time constants were not changed or slightly decreased in 8.1 to 5.4 mM [K+]0, whereas they were increased in 2.7 mM [K+]0. To understand the kinetic behavior of this drug on sodium channels, rate constants for the interaction of phenytoin with three states of channels in terms of Hondeghem-Katzung model were estimated from the above experiments of Vmax. The model most consistent with the present experiments was that with an affinity for inactivated channels 20 times greater than that for resting channels and with a minor affinity for open channels. Phenytoin produced a delay in the time course of recovery of overshoot and action potential duration at 0 mV (APD0), suggesting an additional inhibition of the slow channel by this drug.

A Potassium-Selective Channel in Isolated Lymnaea Stagnalis Heart Muscle Cells

ABSTRACT Lymnaea stagnalis heart ventricle muscle cells, isolated by enzymatic dispersion, are suitable for patch clamp recording. A channel has been identified which is primarily selective for potassium, although it also appears to conduct sodium. This channel is not blocked by 4-aminopyridine or tetraethylammonium but is sensitive to quinidine. The relationship between the membrane potential, the external potassium concentration and the channel currents, when compared with results obtained from whole cell recording, suggests that this channel could mediate a large part of the cell’s resting conductance. The probability of this channel being open is increased by stretching the patched cell membrane. This has led to speculations about further possible functional roles for this channel.

Potassium ion accumulation slows the closing rate of potassium channels in squid axons

Potassium ion accumulation in the periaxonal space between squid axonal membrane and the Schwann cell surrounding the axon slows the rate of potassium channel closing to a degree that is consistent with the effect on channel closing of an equivalent change in the bulk external potassium concentration. The alteration of channel gating is independent of membrane potential, V, for V less than or equal to -60 mV, which suggests that the effect is mediated at a site on the outer surface of the membrane, rather than a site within the channel.

Measurement of steady currents around the frog lens

Steady electrical currents were measured and mapped around the frog lens using a vibrating probe. Ion substitutions and ouabain were used to help identify the ionic basis of the observed currents. In physiological frog Ringer solution, current densities at the equator averaged 26 μA cm −2 and were directed outward. At both optical poles, inward currents were measured, with those at the posterior pole about 30% greater than those at the anterior pole. Currents at all loci decreased when external potassium concentration was increased at the expense of sodium, and when Na and K concentrations approached those of lens cytosol, all currents approached zero. Current direction reversed in a solution containing 105 m m K and 2·5 m m Na. In an Na-free medium, where sodium was replaced with choline, currents were reduced significantly at the poles and equator, but they changed direction only at the anterior pole. This effect was fully reversible on return to solution containing sodium. Ouabain (0·1 m m) caused a significant decrease in currents only at the equator, and this effect had two components. A rapid 10% decline in current was complete in 2 min, followed by a steady, slower decrease which stabilized 8–12 min later at a new level approximately 30% lower than the initial current.

Effects of external potassium concentrations on the cell sodium and potassium contents of isolated rat kidney tubules

The effects of 20 mumol/l amiloride, 10 mumol/l furosemide and 1 mmol/l ouabain on cell Na and K concentrations were investigated by flame microphotometry in isolated rat medullary collecting tubules and medullary thick ascending limbs (MCT and MAL) as a function of the external potassium concentration [Ke]. The results are expressed as Na and K concentrations per liter cell volume ([Nac] and [Kc], mmol/l) and relative sodium content, [Nac]/([Nac] + [Kc]). From the experimental curves, [Ke]1/2 is defined as the [Ke] value corresponding to half maximal exchange of K against Na in cells. When [Ke] was 5 mmol/l, the relative Na content was less than 15% in control and amiloride-treated MCT as well as in control and furosemide-treated MAL, and about 24% in ouabain-treated MCT and MAL. In MCT, relative cell Na content increased up to 90% or more when [Ke] was reduced from 2.5 to 0.25 mmol/l. [Ke]1/2 was 0.55, 0.45 and 1.25 mmol/l for control, amiloride-treated and ouabain-treated MCT respectively. In MAL, similar increases in relative Na content were observed when [Ke] was reduced from 0.5 to 0.05 mmol/l. [Ke]1/2 was 0.25, 0.10 and 1.75 mmol/l for control, furosemide-treated and ouabain-treated MAL respectively. When [Ke] was reduced from 5 to 1 mmol/l, [Nac] dropped from 16.4 to 8.4 mmol/l (P less than 0.01) in control MAL. When [Ke] was 5 mmol/l, [Nac] was lower in furosemide-treated MAL (7.8 mmol/l) than control MAL (P less than 0.01). At 1 mmol/l [Ke], [Nac] was similar in both groups. These results are discussed in terms of the balance between the active and passive components of Na and K fluxes across apical and basolateral cell membranes. They indicate that a K-dependent passive Na entry process exists in the membranes of MAL cells but not of MCT cells. This process was proportionally more inhibited than the active Na pump when [Ke] was reduced from 5 to 1 mmol/l. In addition, it was found sensitive to furosemide.(ABSTRACT TRUNCATED AT 250 WORDS)

Receptor-responses in fresh human ciliary muscle.

The physiological and pharmacological properties of ciliary muscle isolated from fresh human eyes were investigated. The muscle exhibited no spontaneous activity. Concentration-dependent contractions in response to carbachol were competitively antagonized by atropine (pA2 = 8.95). The muscle, precontracted by carbachol (2.7 X 10(-4)M), responded to the application of isoprenaline by concentration-dependent relaxation blocked by propranolol (3.5 X 10(-9)M to 3.5 X 10(-8)M; pA2 = 9.15). Angiotensin-evoked contractions were antagonized by 8-Ala-angiotensin II (4.5 X 10(-8)M) in a competitive manner, but were not inhibited by phentolamine or propranolol. Contractions generated by electrical stimulation of the muscle (30 ms, 20 Hz, 60 pulses) were antagonized by atropine (10(-7) M) and tetrodotoxin (6.3 X 10(-7) M). Phentolamine and propranolol did not influence these responses. An increase of the external potassium concentration ([K+]o) from 5.4 to 158.8 mM produced a mechanical response, antagonized by atropine, but not influenced by tetrodotoxin, phentolamine or propranolol. The human ciliary muscle appears to carry muscarinic and angiotensin receptors and beta 2-adrenoceptors. The estimate of Katropine for muscarinic receptors mediating carbachol-induced contractions agrees with estimates of Katropine reported for human and rabbit iris.

Electrophysiological studies on isolated human eccrine sweat glands.

Human eccrine sweat glands were isolated by shearing and the potential differences across the basolateral membranes determined using bevelled micro-electrodes filled with 4 M potassium acetate. Stable resting potentials of up to -81 mV were recorded. Alterations in external potassium concentration from 1.2 to 100 mM caused the membrane potential to change over a 70 mV range in cells of high resting potential, indicating that the basolateral membrane is largely potassium permeable. Input impedance was determined by constant current injection and found to be in the range 4-80 M omega. On giving a bolus injection of acetylcholine to produce a final concentration of 10(-6)-10(-7) M, four types of response were observed: depolarization, in a proportion of cells with resting potentials of -66 to -80 mV (n = 19), hyperpolarization, in a group of cells with resting potentials of -47 to -70 mV (n = 22), no change, in some cells of -40 to -81 mV resting potential (n = 22) and micro-electrode dislodgement (n = 8). In cells depolarizing to acetylcholine, the depolarization was short-lived and in thirteen cases was followed by a 'rebound' hyperpolarization. Input impedance decreased during depolarization in one-third (n = 5) of the cells in which satisfactory measurement could be made and increased during the final phase of depolarization or during rebound hyperpolarization. In cells hyperpolarizing to acetylcholine, the hyperpolarization was usually accompanied by an increase in input impedance. In ten of the twenty-two cells which showed no change to a first dose of acetylcholine, the agonist was administered at least two more times. In two cells (resting potentials -62 mV, -64 mV) a hyperpolarization was observed whereas in three others (resting potentials -66 mV, -70 mV, -81 mV) depolarization occurred. The effects of acetylcholine, whether depolarizing or hyperpolarizing, were reversibly inhibited by atropine and irreversibly reduced by ouabain. Experiments performed on glands maintained for up to 30 h in supplemented RPMI 1640 tissue culture medium yielded essentially similar results to those performed on freshly isolated glands.

Potassium channels in Eremosphaera viridis

To characterize the assumed potassium channels in the plasma membrane of the green alga Eremosphaera viridis (Köhler et al. 1985), current-voltage (I/V)-curves under resting conditions and during an action-potential-like response (CAP) were constructed using voltage- and current-clamp techniques. Under resting conditions the I/V-curves of Eremosphaera showed a distinct upward bending when approaching zero mV, a nearly straight line in the medium part and a downward bending during strong hyperpolarization. Measurements in light and darkness frequently displayed a parallel shift of the I/V-curve in the middle part, indicating a current source which is slowed down by light-off. Using the voltage-clamp technique, N-shaped I/V-curves were sometimes observed. The potassium concentration outside influenced the downward-bending part of the I/V-curve whereas the tetraethylammonium cation, known to block potassium channels, reduced the upward-bending part in particular. A change in external pH, either to pH 7 or pH 3.1 from a standard pH 5.5, caused an increase in conductivity. Chemically induced action potentials were released in Eremosphaera under voltage-clamp conditions by light-off and there was both a current flow and an increase in conductivity during the CAP. Clamping the membrane potential at a value more negative than Nernst potential of potassium revealed an inward current, whereas clamping at a more-positive value revealed an outward current. The experiments demonstrate that there is no threshold potential in releasing a CAP. The I/V-curves performed under current clamp at the peak of CAP verify a previously found increased conductivity with hyper- or depolarization depending on the external potassium concentration. These experiments provide further evidence that in Eremosphaera potassium channels are involved in the CAP caused by a light-off signal. Additional experiments indicate that after light-off a transient acidification of the cytoplasm takes place in correlation with the CAP and the opening of potassium channels. A preliminary "battery model" is discussed to understand the role of potassium channels during a CAP in pH-regulation of the cytoplasm.

Ion Transport inSuaeda maritima: Its Relation to Growth and Implications for the Pathway of Radial Transport of Ions across the Root

The ion relations of the halophytc Suaeda maritima are described. When plants grew in 340 mol m−3 sodium chloride (—1⋅76 MPa) leaf solute potentials decreased, and were sustained around —2⋅5 MPa Inorganic ion concentration (mostly of sodium chloride) accounted for this. Comparable shoot ion concentrations of potassium, nitrate and sulphate occurred when plants grew on different salinity types characterized by these ions. Net sodium transport and shoot sodium concentration increased dramatically with increases in external sodium chloride concentration up to 85 mol m−3; thereafter, further increases in external sodium chloride concentration had relatively little effect upon either shoot sodium concentration or upon net transport of sodium to the shoot. The net transport of sodium plus potassium only doubled when the external concentration of sodium plus potassium increased from 24 to 687 mol m−3 Shoot ion concentrations were remarkably constant with time, external concentration and salinity type. The membrane flux rates and symplasmic ion concentrations needed to sustain the observed net transport of sodium (of some 10 mmol g−1 dry wt. of roots d−1) are calculated from anatomical and stereological data for the root system of this species. The minimum net sodium chloride flux to load the symplasm would be 260 nmol m−2s−1 if the whole cortical and epidermal plasmalemmal surface area were used uniformly, but the flux rate required would be 3000 nmol m−2s−1 if uptake took place only at the root surface. A flux rate of at least 1000 nmol m−2s−1 is needed between symplasm and xylem. The symplasmic concentration of NaCl would be at least 80 mol m−3. It is argued (1), that both symplasmic and xylem loading are likely to be passive processes mediated by ion channels rather than active carriers, (2), that net ion transport at 340 mol m−3 sodium chloride is close to the maximum which is physiologically sustainable and (3), that growth of this halophyte is limited by NaCl supply from the root.

Potassium channels in Eremosphaera viridis

The dependence of the membrane potential of Eremosphaera viridis on different external concentrations of potassium, sodium, calcium, and protons was compared with the diffusion potential measured in the dark and in the presence of NaN3. In contrast to some other algae, the membrane potential in the light as well as in the dark seemed to be predominantly determined by the calculated diffusion potential and less by an electrogenic pump which, however, seemed to be involved at potassium concentrations >1 mol·m(-3) and at higher pHos (>pH 6). Furthermore, some characteristics of an action-potential-like response (CAP) triggered by light-off, and independent of the membrane-potential threshold value, were determined. The CAP had a delay period of 5.4 s and needed 4.5 s for polarization to a plateau. On average, the plateau held for 8.8 s and the CAP lasted 37.7 s. The peak amplitudes of CAP (P AP) exactly followed the Nernst potential of potassium. Other cations like sodium, calcium and protons did not appreciably affect the peak amplitudes of CAP. From these and other results it can be assumed that the CAP is caused by a temporary opening of potassium channels in the plasma membrane of Eremosphaera (Köhler et al., 1983, Planta 159, 165-171). The release of a CAP by light-off has been partly explained by the participation of a transient increase of proton concentration in the cytoplasm. It was possible to trigger a CAP by external pH changes and by the addition of sodium acetate, thus supporting the hypothesis that a pH decrease in the cytoplasm may be one element of the signal transfer from the photosynthetic system to the potassium channels in the plasmalemma. Calcium also seemed to have an influence on triggering the CAP.

Morphological and pharmacological analysis of putative serotonergic bipolar and amacrine cells in the retina of a turtle, Pseudemys scripta elegans.

Using immunocytochemical methods, we have been able to demonstrate serotonin-like immunoreactivity (SLI) in amacrine and bipolar cells of the turtle retina. Inhibition of monoamine oxidase with pargyline drastically increases the amount of 5-hydroxytryptamine within both cell types. The indoleamine 6-hydroxytryptamine is taken up by both cell types and both types are destroyed within 10 days following intraocular injection of 5,7-dihydroxytryptamine. Increasing the external potassium concentration induces release of serotonin in both cell types. Our data support the idea that these neurons use serotonin during neuronal processing. Morphologically, amacrine and bipolar cells with SLI can be subdivided into two and three subclasses, respectively, based on their ramification pattern within the inner plexiform layer. A comparison of the morphological data with those of intracellularly stained amacrine and bipolar cells suggests that all bipolar cells with SLI are center-hyperpolarizing cells and all amacrine cells center-depolarizing cells.