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P Mobbs

Publications and source records attributed to P Mobbs.

26 records · Page 2Linked to original sources
PubMed1992

Transmitter-operated channels in rabbit retinal astrocytes studied in situ by whole-cell patch clamping.

Glutamate and GABA open ion channels in the membranes of astrocytes found on the vitreal surface of the rabbit retinal visual streak. The glutamate-operated channels are opened by kainate, quisqualate, and AMPA, but not by NMDA, aspartate, or the metabotropic agonist 1-aminocyclopentane-1 S,3R-dicarboxylic acid. The effects of glutamate and its analogs can be blocked by 20 microM 6-cyano-7-nitroquinoxaline-2,3-dione. The conductance increase evoked by 10 microM glutamate, a concentration of this transmitter near to that found in the vitreous humor that bathes these cells, was equivalent to 22% of the cell's resting conductance. The conductance increase evoked by 1 microM GABA, a concentration near that found in the vitreous, was equivalent to 131% of the cell's resting conductance. The effects of GABA can be blocked by bicuculline. These data show that GABA, and non-NMDA-type glutamate receptors play an important part in determining the resting potential of visual streak astrocytes in situ and that these channels may be of general importance for the functions of astrocytes in vivo.

Animals↗
PubMed1988

A quantitative analysis of glial cell coupling in the retina of the axolotl (Ambystoma mexicanum).

The strength of gap junctional coupling of radial glial cells (Müller cells) in the isolated axolotl retina was assessed by monitoring the spread of dye between cells, and by injecting current into one cell and recording the voltage response in surrounding cells. Dye injected into one Müller cell spread to surrounding Müller cells, and could be detected up to 130 micron away, i.e. over 4 times the mean Müller cell spacing of 30 micron. Injecting 1 nA of current into a Müller cell evoked responses of 7 mV in that cell, 1 mV in next neighbour cells, and 0.2 mV in cells at 60 micron distance. Analysis of these data indicates an electrical space constant for the Müller cell network of 15 micron, and predicts that isolated cells should have a resistance of 11.4 M omega. Müller cells isolated by papain dissociation of the retina were found, by whole-cell patch-clamping, to have a mean resistance of 12.4 M omega. These results on lateral coupling are combined with data showing that over 90% of the Müller cell potassium conductance is in the vitreal endfoot of these cells to provide a fairly complete electrical description of the radial glial cell network in the retina. Gap junctional coupling of Müller cells increases by 60% the 'spatial buffering' that these glial cells can carry out to reduce localized rises in extracellular potassium concentration. The location of the majority of the Müller cell potassium conductance in the cell endfoot ensures that laterally buffered K+ is deposited in the vitreous, rather than depolarizing surrounding retinal neurones.

Ambystoma↗
PubMed1988

Membrane currents in retinal bipolar cells of the axolotl.

By whole-cell patch-clamping bipolar cells isolated from enzymatically dissociated retinae, we have studied the nonsynaptic ionic currents that may play a role in shaping the bipolar cell light response and in determining the level of voltage noise in these cells. Between -30 and -70 mV, the membrane current of isolated bipolar cells is time independent, and the input resistance is 1-2 G omega. Depolarization past -30 mV activates an outward current (in less than 100 ms), which then inactivates slowly (approximately 1 s). Inactivation of this current is removed by hyperpolarization over the range -20 to -80 mV. This current is carried largely by K ions. It is not activated by internal Ca2+. The membrane current of isolated bipolar cells is noisy, and the variance of this noise has a minimum between -40 and -60 mV. At its minimum, the standard deviation of the voltage noise produced by nonsynaptic membrane currents is at least 100 microV. The membrane currents of depolarizing bipolar cells in slices of retina were investigated by whole-cell patch-clamping. Their membrane properties were similar to those of isolated bipolar cells, but with a larger membrane capacitance and a smaller input resistance. Their membrane current noise also showed a minimum near -40 to -60 mV. The time-dependent potassium current in axolotl bipolar cells is not significantly activated in the physiological potential range and can therefore play little role in shaping the bipolar cells' voltage response to light. Differences in the waveform of the light response of bipolar cells and photoreceptors must be ascribed to shaping by the synapses between these cells. The noise minimum in the bipolar membrane current is near the dark potential of these cells, and this may be advantageous for the detection of weak signals by the bipolar cells.

Adenosine Triphosphate↗
PubMed1987

Neurotransmitter-induced currents in retinal bipolar cells of the axolotl, Ambystoma mexicanum.

1. Whole-cell patch clamping was used to study the membrane properties of isolated bipolar cells and the currents evoked in them by putative retinal neurotransmitters. 2. Isolated bipolar cells show an approximately ohmic response to voltage steps over most of the physiological response range, with an average input resistance of 1.3 G omega and resting potential of -35 mV. These values are underestimates because of the shunting effect of the seal between the patch electrode and the cell membrane. Depolarization beyond -30 mV produces rapid activation (10-100 ms) of an outward current (carried largely by potassium ions), which then inactivates slowly (0.5-2 s). 3. Of five candidates for the photoreceptor transmitter, four (aspartate, N-acetylhistidine, cadaverine, putrescine) had no effect on bipolar cells. The fifth substance, L-glutamate, opened ionic channels with a mean reversal potential of -12 mV in some cells (presumed hyperpolarizing bipolar cells), and closed channels with a mean reversal potential of -13 mV in other cells (presumed depolarizing bipolar cells). 4. The conductance increase induced by glutamate in presumed hyperpolarizing bipolar cells was associated with an increase in membrane current noise. Noise analysis suggested a single-channel conductance for the glutamate-gated channel of 5.4 pS. The power spectrum of the noise increase required the sum of two Lorentzian curves to fit it, suggesting that the channel can exist in three states. 5. The conductance decrease induced by glutamate in presumed depolarizing bipolar cells was associated with a decrease in membrane current noise that could be described as the sum of two Lorentzian spectra, and which suggested a single-channel conductance of 11 pS. The noise decrease implies that the channels closed by glutamate are not all open in the absence of the transmitter. 6. GABA (gamma-aminobutyric acid) and glycine, transmitters believed to mediate lateral inhibition in the retina, open chloride channels in isolated bipolar cells, and increase the membrane current noise. Noise analysis suggested that the channels gated by GABA and glycine have conductances of 4.4 and 7.5 pS respectively. The noise spectra required the sum of two Lorentzian curves to fit them. 7. By whole-cell patch clamping cells in retinal slices, the synaptic transmitter released by photoreceptors was shown to close channels with an extrapolated reversal potential around -3 mV in depolarizing bipolar cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1985

Lead and mercury toxicity and the rod light response.

Lead and mercury have been reported to alter selectively the rod component of the electroretinogram, and to inhibit the phosphodiesterase in rod outer segments which may be responsible for generating the rods' light response. The authors have investigated the effect of lead and mercury on the voltage response to light of rods, and compared these effects with those of the phosphodiesterase inhibitor papaverine. Lead and mercury, like papaverine, slow the light response. In addition, papaverine increases the light response amplitude while lead decreases it. Mercury initially increases and then decreases the amplitude. The late decrease in amplitude produced by mercury is associated with rod degeneration: an effect which may mimic degenerative diseases in which the rod phosphodiesterase is insufficiently active. These results demonstrate that the changes of electroretinogram induced by lead and mercury can be accounted for by the changes in receptor potential these heavy metals produce. The changes in receptor potential seen are consistent with mercury inhibiting the rod phosphodiesterase, and with lead having an action in addition to phosphodiesterase inhibition.

Ambystoma↗
PubMedDate not supplied

Endfeet of retinal glial cells have higher densities of ion channels that mediate K+ buffering.

A major function of glial cells in the central nervous system is to buffer the extracellular potassium concentration, [K+]o. A local rise in [K+]o causes potassium ions to enter glial cells, which have membranes that are highly permeable to K+; potassium then leaves the glial cells at other locations where [K+]o has not risen. We report here the first study of the individual ion channels mediating potassium buffering by glial cells. The patch-clamp technique was employed to record single channel currents in Müller cells, the radial glia of the vertebrate retina. Those cells have 94% of their potassium conductance in an endfoot apposed to the vitreous humour, causing K+ released from active retinal neurones to be buffered preferentially to the vitreous. Recordings from patches of endfoot and cell body membrane show that a single type of inward-rectifying K+ channel mediates potassium buffering at both cell locations. The non-uniform density of K+ conductance is due to a non-uniform distribution of one type of K+ channel, rather than to the cell expressing high conductance channels at the endfoot and low conductance channels elsewhere on the cell.

Ambystoma↗