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At least 793 records · Page 44Linked to original sources
PubMed1984

Strychnine blocks transient but not sustained inhibition in mudpuppy retinal ganglion cells.

Transient and sustained inhibitory synaptic inputs to on-centre, off-centre, and on-off ganglion cells in the mudpuppy retina were studied using intracellular recording in the superfused eye-cup preparation. When chemical transmission was blocked with 4 mM-Co2+, application of either glycine or gamma-aminobutyric acid (GABA) caused a hyperpolarization and conductance increase in all ganglion cells. For both amino acids, the responses were dose dependent in the range 0.05-10 mM, with a half-maximal response at about 0.7 mM. Glycine and GABA sensitivities were very similar in all three types of ganglion cells. The response to applied glycine was selectively antagonized by 10(-5) M-strychnine and the response to applied GABA was selectively antagonized by 10(-5) M-picrotoxin. In all ganglion cells, 10(-5) M-strychnine eliminated the transient inhibitory events which occur at the onset and termination of a light stimulus. The block of transient inhibition was associated with a relative depolarization of membrane potential and decrease in conductance at these times. Strychnine had no effect on membrane potential or conductance in darkness or during sustained inhibitory responses to light. Picrotoxin (10(-5) M) did not block transient inhibitory events in any ganglion cells, but did affect other components of their responses. The results suggest that in all three classes of ganglion cells transient inhibition, but not sustained inhibition, may be mediated by glycine or a closely related substance.

Animals↗
PubMed1985

Synaptic transmission at N-methyl-D-aspartate receptors in the proximal retina of the mudpuppy.

The effects of excitatory amino acid analogues and antagonists on retinal ganglion cells were studied using intracellular recording in the superfused mudpuppy eyecup preparation. Aspartate, glutamate, quisqualate (QA), kainate (KA) and N-methylaspartate (NMA) caused depolarization and decreased input resistance in all classes of ganglion cells. The order of sensitivity was QA greater than or equal to KA greater than NMA greater than aspartate greater than or equal to glutamate. All of these agonists were effective when transmitter release was blocked with 4 mM-Co2+ or Mn2+, indicating that they acted at receptor sites on the ganglion cells. At a concentration of 250 microM, 2-amino-5-phosphonovalerate (APV) blocked the responses of all ganglion cells to NMA, but not to QA or KA, indicating that NMA acts at different receptor sites from QA or KA. Responses to bath-applied aspartate and glutamate were reduced slightly or not at all in the presence of APV, indicating that they were acting mainly at non-NMDA (N-methyl-D-aspartate) receptors. In all ganglion cells 250 microM-APV strongly suppressed the sustained responses driven by the 'on'-pathway but not those driven by the 'off'-pathway. In most on-off ganglion cells the transient excitatory responses at 'light on' and 'light off' were not reduced by 500 microM-APV. APV-resistant transient excitatory responses were also present in some on-centre ganglion cells. APV did not block the transient inhibitory responses in any class of ganglion cells. At concentrations which blocked the sustained responses of ganglion cells, APV did not affect the sustained responses of bipolar cells, indicating that it acted at sites which were post-synaptic to bipolar cells. The simplest interpretation of these results is that the transmitter released by depolarizing bipolar cells acts at NMDA receptors on sustained depolarizing amacrine and ganglion cells. It may act at non-NMDA receptors at synapses which produce transient excitatory responses, but this could not be proved. The transmitter released by hyperpolarizing bipolar cells does not appear to act at NMDA receptors on any post-synaptic cells.

2-Amino-5-phosphonovalerate↗
PubMed1987

Passive and active membrane properties of mudpuppy taste receptor cells.

1. Intracellular recordings were obtained from taste receptor cells and surface epithelial cells of isolated mudpuppy lingual epithelium. 2. Surface epithelial cells had a mean resting potential of -40.2 +/- 8.9 mV, a mean input resistance of 40.3 +/- 11.3 M omega, and a linear current-voltage (I-V) relationship. Taste receptor cells had a mean resting potential of -61.7 +/- 15 mV, a mean input resistance of 380.3 +/- 177.2 M omega, and the I-V relationship showed pronounced outward rectification; the outward rectification persisted in high-K+ saline, but was abolished by tetraethylammonium bromide (TEA). 3. Surface epithelial cells responded to depolarizing current injection with only passive membrane potential changes. Taste receptor cells responded to brief pulses of depolarizing current injection with regenerative action potentials characterized by an abrupt rising phase, an inflexion on the falling phase, and a prolonged after-potential. 4. The abrupt rising phase of the action potential was blocked by tetrodotoxin (TTX), suggesting that voltage-gated Na+ currents are responsible for the rising phase. 5. Long-duration action potentials were elicited from cells treated with TEA to block outward K+ currents and with TTX to block Na+ currents, and from cells bathed in isotonic CaCl2. These results suggest that the active membrane response contains a significant Ca2+ component. 6. The after-potential was blocked or greatly reduced by the addition of Ca2+ channel blockers to the bathing medium. In contrast, addition of TEA to the bathing medium greatly enhanced the after-potential. These data suggest that a significant portion of the after-potential is Ca2+ mediated. 7. The mean reversal potential for the after-potential (-76.8 +/- 6.0 mV) was significantly different from the mean reversal potential for the undershoot of the action potential (-86 +/- 5.6 mV). Superfusion with TEA reduced the reversal potential of the after-potential to -42.3 +/- 8.2 mV and abolished the undershoot. These results suggest that the after-potential results from at least two conductances, one which is blocked by TEA and the other which is Ca2+ dependent and involves ions other than, or in addition to K+. 8. Our data suggest that taste receptor cells, unlike surface epithelial cells, possess voltage-gated Na+, Ca2+, and K+ channels, as well as Ca2+-mediated channels. The role of the Ca2+ channels may be in part to regulate release of transmitter onto nerve terminals. The role of the other conductances in taste transduction is unknown.

Action Potentials↗
PubMed1987

Push-pull effect of surround illumination on excitatory and inhibitory inputs to mudpuppy retinal ganglion cells.

1. Changes in membrane potential and conductance were measured in on-centre and off-centre ganglion cells during the responses to illumination of different portions of the receptive field. 2. In on-centre ganglion cells the sustained depolarizing response to steady illumination of the receptive field centre was associated with a net increase in conductance. In the presence of centre illumination, stimulation of the surround with an annulus of light caused a hyperpolarization and a net decrease in conductance, and the reversal potential of the light-evoked response was shifted in a negative direction. In the absence of centre illumination the same annular stimulus caused a hyperpolarization and a net increase in conductance. 3. In off-centre ganglion cells the sustained hyperpolarizing response to centre illumination was associated with a net increase in conductance. In the presence of centre illumination, stimulation of the surround with an annulus caused a depolarization and a net decrease in conductance, and the reversal potential of the light-evoked response was shifted in a positive direction. In the absence of centre illumination the same annulus caused a depolarization and a net increase in conductance. 4. The results indicate that illumination of the receptive field surround can affect both the excitatory and inhibitory sustained inputs to a given ganglion cell in a 'push-pull' manner, by decreasing the synaptic input that was increased by centre illumination and increasing the synaptic input of opposite sign. The relative effect of a given surround illumination on these two inputs, and hence the sign and magnitude of the net conductance change, varied with the amount of centre illumination.

Action Potentials↗
PubMed1991

The relationship between light, dopamine release and horizontal cell coupling in the mudpuppy retina.

1. The effect of different experimental conditions on electrical coupling between horizontal cells in the mudpuppy retina was studied by comparing the changes in responses to illumination of the central and peripheral portions of the receptive field, using centred spot and annulus stimuli. An increase in the amplitude of the response to a centred spot stimulus and a decrease in the amplitude of the response to a concentric annulus indicated a decrease in coupling, and vice versa. 2. Dopamine (10-250 microM) caused a decrease in coupling between horizontal cells. The uncoupling effect of dopamine was much greater in dark-adapted than in light-adapted retinas. The effect of the D1-receptor agonist SKF38393 was similar to that of dopamine. The effect of the D2-receptor agonist LY171555 on coupling was opposite to that of dopamine; this was attributed to a reduction in endogenous dopamine release. 3. The D1 antagonist SCH23390 (15 microM) caused an increase in coupling between horizontal cells. This effect was much greater in light-adapted than in dark-adapted retinas. 4. The glutamate analogue 2-amino-4-phosphonobutyrate (APB), which hyperpolarizes on-centre bipolar cells and blocks their responses to light, caused an increase in coupling between horizontal cells. This effect of APB was greater in light-adapted retinas than in dark-adapted retinas. The effect of APB on coupling could be reversed by the addition of dopamine, but the effect of dopamine on coupling could not be reversed by the addition of APB. These results suggest that APB increases horizontal cell coupling by causing a decrease in dopamine release. 5. In dark-adapted retinas, 2.5 min exposure to an adapting light caused a decrease in coupling between horizontal cells; the uncoupling effect of the adapting light was blocked in the presence of either SCH23390 or APB. 6. The results suggest that coupling between horizontal cells in the mudpuppy retina is decreased by dopamine acting at D1 receptors, that the release of dopamine affecting horizontal cells is greater under light-adapted conditions, and that the pathway by which exposure to light increases this dopamine release is mainly via on-centre bipolar cells.

Adaptation, Ocular↗
PubMed1989

Spatial buffering of light-evoked potassium increases by retinal Müller (glial) cells.

Activity-dependent variations in extracellular potassium concentration in the central nervous system may be regulated, in part, by potassium spatial buffering currents in glial cells. The role of spatial buffering in the retina was assessed by measuring light-evoked potassium changes in amphibian eyecups. The amplitude of potassium increases in the vitreous humor was reduced to approximately 10 percent by 50 micromolar barium, while potassium increases in the inner plexiform layer were largely unchanged. The decrease in the vitreal potassium response was accurately simulated with a numerical model of potassium current flow through Müller cells, the principal glial cells of the retina. Barium also substantially increased the input resistance of Müller cells and blocked the Müller cell-generated M-wave, indicating that barium blocks the potassium channels of Müller cells. Thus, after a light-evoked potassium increase within the retina, there is a substantial transfer of potassium from the retina to the vitreous humor by potassium current flow through Müller cells.

Ambystoma↗
PubMed1983

An excitatory amino acid antagonist blocks cone input to sign-conserving second-order retinal neurons.

cis-2,3-Piperidinedicarboxylic acid (PDA), an excitatory amino acid antagonist, reversibly blocked cone input to OFF bipolars and horizontal cells, whereas ON bipolars were relatively unaffected. Kainic acid effects were also blocked, indicating a postsynaptic mechanism of action. The use of PDA helps to characterize one of two classes of excitatory amino acid synaptic receptors that mediate cone influence in the outer retina.

Amino Acids↗
PubMed1990

Sequence homologies among intestinal and renal Na+/glucose cotransporters.

Sodium-dependent glucose transport occurs in the intestine and kidney of most animal species. The cDNA encoding the Na+/glucose cotransporter from rabbit jejunum was used to examine the distribution of homologous mRNA in other rabbit tissues and in the intestines of other species. Northern blots of mRNA extracted from various tissues were probed with radiolabeled cDNA of the cloned rabbit transporter. The probe hybridized with mRNA of approximately 2.2 kb from rabbit jejunum, renal cortex, and renal medulla, indicating that related mRNA of the same size is found in these tissues. With the use of the same cDNA probe, a 1.6-kb partial-length clone encoding 484 amino acids was isolated from a rabbit renal cortex cDNA library. There was greater than 99% identity between the cDNA sequences, and 100% identity between the amino acid sequences, of the renal clone and the rabbit intestinal Na+/glucose cotransporter. The 2.2-kb transcript was seen in mRNA from duodenum, jejunum, and ileum, with a distribution that matched the Na+/glucose transport capacity in these tissues. A faint signal at 2.2 kb was also seen in colon mRNA. There was no detectable hybridization to blots of stomach and heart mRNA. The rabbit probe also hybridized to intestinal mRNA from a number of species from trout to humans. We conclude that a Na+/glucose cotransporter of rabbit renal cortex is very similar to that of the intestine and that the intestinal transporter has been conserved during evolution.

Amino Acid Sequence↗
PubMed1981

Effect of sodium taurocholate on secretion by amphibian gastric mucosa in vitro.

Effects of sodium taurocholate on the electrical and secretory activity of amphibian gastric mucosa have been studied in vitro. Exposure of the luminal surface of fundic mucosa to high concentrations (5 X 10(-2) M) at low pH (2.0 and 3.0) produced a marked fall in potential difference and electrical resistance. At lower concentrations (10(-3) to 10(-4) M) and higher pH (7.4), taurocholate did not alter the electrical properties but significantly increased net acidification from 1.39 +/- 0.27 to 2.01 +/- 0.18 mueq . cm-2 . h-1 (means +/- SE; P less than 0.01). Pretreatment of fundic mucosa with cimetidine resulted in net alkaline secretion (0.27 +/- 0.07 mueq . cm-2 . h-1), and addition of taurocholate (10(-4) M) to the luminal surface at pH 7.4 converted net alkalinization to net acidification (0.94 +/- 0.28 mueq . cm-2 . h-1). This response was not inhibited by atropine (10(-5) M) or somatostatin (10(-6) M) but exhibited marked tachyphylaxis. Taurocholate (10(-4) M) inhibited alkaline secretion in thiocyanate-treated fundic mucosa (0.63 +/- 0.04 to 0.14 +/- 0.09 mueq . cm-2 . h-1; P less than 0.001) and in spontaneously alkaline-secreting antral mucosa (0.36 +/- 0.12 to 0.09 +/- 0.06 mueq . cm-2 . h-1; P less than 0.05), but acidification did not occur. Apparent stimulation of acid secretion and simultaneous inhibition of alkaline secretion of sodium taurocholate may play a role in the pathogenesis of mucosal damage by bile.

Action Potentials↗
PubMed1981

Homocellular regulatory mechanisms in sodium-transporting epithelia: avoidance of extinction by "flush-through".

In recent years electrophysiologic studies on several sodium-transporting epithelia have uncovered two "homocellular" (intrinsic) regulatory mechanisms that appear to protect the absorptive cells from marked changes in sodium and potassium content in response to rapid and wide-ranging physiologic variations in the rate of transcellular sodium transport. These are: 1) an inverse relation between intracellular sodium activity and the sodium conductance of the apical (mucosal) membrane, and 2) a parallel relation between the rate of sodium extrusion from the cell across the basolateral membrane ("pump activity") and the conductance of that barrier to potassium. The purpose of this review is to document these homocellular regulatory mechanisms, discuss their physiologic significance, and speculate on possible underlying mechanism(s).

Amiloride↗
PubMed1984

Does calcium couple the apical and basolateral membrane permeabilities in epithelia?

Tight epithelial cells actively transport sodium against steep electrochemical gradients. To maintain a constant internal ionic content and volume, they must continuously adjust the passive cation permeabilities of their membranes as the rate of transport varies. There is evidence suggesting that changes in cell calcium may accomplish this task. An increase in cell calcium reduces the luminal sodium permeability and increases basolateral potassium permeability. There is basolateral sodium-calcium exchange through which changes in the rate of sodium transport, reflected in the cell sodium activity, are translated into changes in cell calcium. To demonstrate that cell calcium couples the permeability of the cell membrane requires obtaining measurements of cell calcium activity under physiologically relevant conditions, and, to date, there are no measurements during spontaneous changes in the rate of transport. However, there are measurements following ouabain inhibition of the pump indicating that the increase is sufficient to account for the reduction in luminal sodium permeability observed in intact tissues.

Animals↗