scholarly journals Passive membrane properties and electrotonic signal processing in retinal rod bipolar cells

2009 ◽  
Vol 587 (4) ◽  
pp. 829-849 ◽  
Author(s):  
Leif Oltedal ◽  
Margaret Lin Veruki ◽  
Espen Hartveit
Keyword(s):  
Signal Processing ◽  
Bipolar Cells ◽  
Membrane Properties ◽  
Retinal Rod ◽  
Passive Membrane Properties ◽  
Rod Bipolar Cells ◽  
Passive Membrane

scholarly journals Two Functional Classes of Rod Bipolar Cells in the Healthy and Degenerated Optogenetically Treated Murine Retina

2022 ◽  
Vol 15 ◽  
Author(s):  
Giulia Schilardi ◽  
Sonja Kleinlogel
Keyword(s):  
Membrane Potential ◽  
Bipolar Cell ◽  
Bipolar Cells ◽  
Membrane Properties ◽  
Current Voltage ◽  
Passive Membrane Properties ◽  
Rod Bipolar Cells ◽  
Passive Membrane

Bipolar cells have become successful targets for optogenetic gene therapies that restore vision after photoreceptor degeneration. However, degeneration was shown to cause changes in neuronal connectivity and protein expression, which may impact the quality of synthetically restored signaling. Further, the expression of an optogenetic protein may alter passive membrane properties of bipolar cells affecting signal propagation. We here investigated the passive membrane properties of rod bipolar cells in three different systems, the healthy retina, the degenerated retina, and the degenerated retina expressing the optogenetic actuator Opto-mGluR6. We found that, based on the shape of their current-voltage relations, rod bipolar cells in healthy and degenerated retinas form two clear functional groups (type 1 and type 2 cells). Depolarizing the membrane potential changed recorded current-voltage curves from type 1 to type 2, confirming a single cell identity with two functional states. Expression of Opto-mGluR6 did not alter the passive properties of the rod bipolar cell. With progressing degeneration, dominant outward rectifying currents recorded in type 2 rod bipolar cells decreased significantly. We demonstrate that this is caused by a downregulation of BK channel expression in the degenerated retina. Since this BK conductance will normally recover the membrane potential after RBCs are excited by open TRPM1 channels, a loss in BK will decrease high-pass filtering at the rod bipolar cell level. A better understanding of the changes of bipolar cell physiology during retinal degeneration may pave the way to optimize future treatment strategies of blindness.

Long-Term Alteration of S-Type Potassium Current and Passive Membrane Properties in Aplysia Sensory Neurons Following Axotomy

2002 ◽  
Vol 87 (5) ◽  
pp. 2408-2420 ◽  
Author(s):  
Mark A. Ungless ◽  
Xavier Gasull ◽  
Edgar T. Walters
Keyword(s):  
Leakage Current ◽  
Sensory Neurons ◽  
Outward Current ◽  
The Body ◽  
Membrane Properties ◽  
Resting Membrane Potential ◽  
Current Component ◽  
Passive Membrane Properties ◽  
Passive Membrane

In many neurons, axotomy triggers long-lasting alterations in excitability as well as regenerative growth. We have investigated mechanisms contributing to the expression of axotomy-induced, long-term hyperexcitability (LTH) of mechanosensory neurons in Aplysia californica. Electrophysiological tests were applied to pleural sensory neurons 5–10 days after unilateral crush of pedal nerves. Two-electrode current-clamp experiments revealed that compared with uninjured sensory neurons on the contralateral side of the body, axotomized sensory neurons consistently displayed alterations of passive membrane properties: notably, increases in input resistance ( R in), membrane time constant (τ), and apparent input capacitance. In some cells, axotomy also depolarized the resting membrane potential (RMP). Axotomized sensory neurons showed a lower incidence of voltage relaxation (“sag”) during prolonged hyperpolarizing pulses and greater depolarizations during long (2 s) but not brief (20 ms) pulses. In addition to a reduction in spike accommodation, axotomized sensory neurons displayed a dramatic decrease in current (rheobase) required to reach spike threshold during long depolarizations. The increase in τ was associated with prolongation of responses to brief current pulses and with a large increase in the latency to spike at rheobase. Two-electrode voltage-clamp revealed an axotomy-induced decrease in a current with two components: a leakage current component and a slowly activating, noninactivating outward current component. Neither component was blocked by agents known to block other K+ currents in these neurons. In contrast to the instantaneous leakage current seen with hyperpolarizing and depolarizing steps, the late component of the axotomy-sensitive outward current showed a relatively steep voltage dependence with pulses to V m > −40 mV. These features match those of the S-type (“serotonin-sensitive”) K+ current, I K,S. The close resemblance of I K,S to a background current mediated by TREK-1 (KCNK2) channels in mammals, raises interesting questions about alterations of this family of channels during axotomy-induced LTH in both Aplysia and mammals. The increase in apparent C in may be a consequence of the extensive sprouting that has been observed in axotomized sensory neurons near their somata, and the decrease in I K,S probably helps to compensate for the decrease in excitability that would otherwise occur as new growth causes both cell volume and C in to increase. In peripheral regions of the sensory neuron, a decrease in I K,S might enhance the safety factor for conduction across regenerating segments that are highly susceptible to conduction block.

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