scholarly journals Changing The Firing Threshold for Normal Optic Nerve Axons by The Application of Infra-Red Laser Light

2021 ◽  
Author(s):  
Lavinia J Austerschmidt ◽  
Nadine I Schottler ◽  
Alyssa M Miller ◽  
Mark D Baker
Keyword(s):  
Membrane Potential ◽  
Optic Nerve ◽  
Light Guide ◽  
Laser Light ◽  
Recording Site ◽  
Axonal Membrane ◽  
Ir Laser ◽  
Infra Red ◽  
Current Threshold ◽  
Effect Of Light

Abstract Normal optic nerve axons exhibit a temperature dependence, previously explained by a membrane potential hyperpolarization on warming. We now report that near infra-red (IR) laser light, delivered via a fibre optic light guide, also affects axonal membrane potential and threshold, at least partly through a photo-thermal effect. Application of light to optic nerve, at the recording site, gave rise to a local membrane potential hyperpolarization over a period of about a minute, and increased the size of the depolarizing after potential (DAP). Application near the site of electrical stimulation reversibly raised current-threshold, and the change in threshold recorded over minutes of irradiation was significantly increased by the application of the Ih blocker, ZD7288 (50 µM), indicating Ih limits the hyperpolarizing effect of light. Light application also had fast effects on nerve behaviour, increasing threshold without appreciable delay (within seconds), probably by a mechanism independent of Na+ channels and kinetically fast K+ channels, and hypothesized to be caused by reversible changes in myelin function.

scholarly journals Evoked membrane potential change in rat optic nerve fiber: Computer simulation

2007 ◽  
Vol 23 (6) ◽  
pp. 348-356 ◽  
Author(s):  
Vincent Cazenave-Loustalet ◽  
Qing-Li Qiao ◽  
Li-Ming Li ◽  
Qiu-Shi Ren
Keyword(s):  
Computer Simulation ◽  
Membrane Potential ◽  
Optic Nerve ◽  
Nerve Fiber ◽  
Potential Change ◽  
Membrane Potential Change ◽  
Optic Nerve Fiber

Three Conformers of 2-Furoic Acid: Structure Changes Induced with Near-IR Laser Light

2015 ◽  
Vol 119 (6) ◽  
pp. 1037-1047 ◽  
Author(s):  
Anna Halasa ◽  
Leszek Lapinski ◽  
Igor Reva ◽  
Hanna Rostkowska ◽  
Rui Fausto ◽  
...  
Keyword(s):  
Laser Light ◽  
Furoic Acid ◽  
Near Ir ◽  
Ir Laser ◽  
Structure Changes ◽  
Acid Structure

Enormous Size Growth of Thiol-passivated Gold Nanoparticles Induced by Near-IR Laser Light

2000 ◽  
Vol 29 (4) ◽  
pp. 310-311 ◽  
Author(s):  
Yasuro Niidome ◽  
Ayako Hori ◽  
Takuro Sato ◽  
Sunao Yamada
Keyword(s):  
Gold Nanoparticles ◽  
Laser Light ◽  
Near Ir ◽  
Ir Laser ◽  
Size Growth

Classes of Light-Evoked Response in the Retina of Strombus

1979 ◽  
Vol 80 (1) ◽  
pp. 287-297
Author(s):  
FREDERICK N. QUANDT ◽  
HOWARD L. GILLARY
Keyword(s):  
Optic Nerve ◽  
Action Potentials ◽  
Input Resistance ◽  
Resting Potential ◽  
Recording Site ◽  
Charging Time ◽  
Rate Of Decay ◽  
Hyperpolarizing Response ◽  
Strombus Luhuanus ◽  
A Site

Two general classes of light-evoked responses were recorded intracellularly from the retina of Strombus luhuanus. In one class, retinal illumination caused depolarization, the amplitude of which was graded with light intensity. In the other, it produced hyperpolarization and concomitant inhibition of repetitive action potentials. There were two types of depolarizing waveform. Each was associated with a different type of intraccllular recording site, characterized on the basis of electrical properties in the dark. In general, the type of response with a more rapid rate of decay was recorded from a site which exhibited a lower resting potential, higher input resistance, and longer ‘membrane charging time.’ The two depolarizing responses and the hyperpolarizing response apparently each arose from a different type of neurone. The depolarizing types, at least one of which is a photoreceptor, apparently give rise to the cornea-negativity of the electroretinogram and ‘on’ activity in the optic nerve fibres. The hyperpolarizing type apparently mediates ‘off’ activity in the optic nerve.

Sustained depolarizing potentials in reticulospinal axons during evoked seizure activity in lamprey spinal cord

1978 ◽  
Vol 41 (2) ◽  
pp. 384-393 ◽  
Author(s):  
G. Matthews ◽  
W. O. Wickelgren
Keyword(s):  
Spinal Cord ◽  
Membrane Potential ◽  
Input Resistance ◽  
Response Amplitude ◽  
Resting Potential ◽  
Mammalian Brain ◽  
Extracellular Potassium ◽  
Synaptic Potential ◽  
Axonal Membrane ◽  
Passive Current

1. Intracellular recordings were made from lamprey reticulospinal axons (Muller axons) during seizures evoked by electrical stimulation of the isolated spinal cord in saline containing either 0 Cl or 1 mM picrotoxin. The seizures had tonic and clonic-phases similar to ictal seizures in mammalian brain. 2. During seizures Muller axons were depolarized by 10-15 mV. These seizure-depolarizations were not due to any direct effect of the evoking stimulus on the Muller axons themselves nor were they initiated by an accumulation or extracellular potassium. 3. A decrease in axonal input resistance occurred during a seizure-depolarization. Also, the amplitude of a seizure-depolarization was decreased by depolarizing the axon 5-15 mV with injected current. Further, hyperpolarizing the axon increased the amplitude of the seizure-depolarization, but the growth flattened out beyond 30-40 mV of hyperpolarization. The decrease in input resistance during the seizure-depolarization and the dependence of the response amplitude on axonal membrane potential suggested that the seizure-depolarization was an excitatory synaptic potential. However, the failure of the seizure-depolarization amplitude to continue to grow at membrane potentials greater than 30 mV negative to the resting potential was not consistent with this interpretation. 4. A synaptic conductance change as the cause of the seizure-depolarization was ruled out by setting the axonal membrane potential at different levels with injected current and monitoring the input resistance of the axon before and during seizure-depolarizations. It was found that no change in input resistance occurred during the seizure-depolarization when the axon was hyperpolarized more than approximately 30 mV, the same potential at which the growth in the response amplitude ceased. From analysis of these data and the passive current-voltage properties of Muller axons it is concluded that the seizure-depolarization is not a chemical synaptic potential, but rather the result of the passive injection of depolarizing current into the axons. 5. The source of the depolarizing current which flows into Muller axons during seizures is probably paroxysmal action-potential activity in spinal motoneurons and interneurons, many of which are electrically coupled to Muller axons.

scholarly journals Ion Transport and Membrane Potential in CNS Myelinated Axons I. Normoxic Conditions

1997 ◽  
Vol 78 (4) ◽  
pp. 2086-2094 ◽  
Author(s):  
Lisa Leppanen ◽  
Peter K. Stys
Keyword(s):  
Membrane Potential ◽  
Optic Nerve ◽  
Ion Transport ◽  
Transport Systems ◽  
Resting Membrane Potential ◽  
High Dose ◽  
Myelinated Axons ◽  
Gap Technique ◽  
Influx Pathways ◽  
Dose Dependent

Leppanen, Lisa and Peter K. Stys. Ion transport and membrane potential in CNS myelinated axons. I. Normoxic conditions. J. Neurophysiol. 78: 2086–2094, 1997. Compound resting membrane potential was recorded by the grease gap technique during normoxic conditions (37°C) in rat optic nerve, a representative CNS myelinated tract. Mean potential was −47 ± 3 (SD) mV and remained stable for 2–3 h. Input impedance of a single optic nerve axon was calculated to be ≈5 GΩ. Contribution of the Na+ pump to resting axonal potential is estimated at −7 mV. Ouabain (10 μM to 10 mM) evoked a dose-dependent depolarization that was maximal at ≥1 mM, depolarizing the nerves to ∼35–40% of control after 60 min. Inhibiting energy metabolism (CN− and iodoacetate) during high-dose ouabain (1–10 mM) exposure caused an additional depolarization, suggesting additional ATP-dependent, ouabain-insensitive ion transport systems. Perfusion with zero-Na+ (choline substituted) caused a transient hyperpolarization, that was greater than with tetrodotoxin (TTX; 1 μM) alone, indicating both TTX-sensitive and -insensitive Na+ influx pathways in resting rat optic nerve axons. Resting probability (P)K:PNa is calculated at 20:1. In contrast to choline-substituted solution, Li+-substituted zero-Na+ perfusate caused a rapid depolarization due to Na+ pump inhibition and the ability of Li+ to permeate the Na+ channel. TTX reduced, but did not prevent, ouabain- or zero-Na+/Li+–induced depolarization. We conclude that the primary Na+ influx path in resting rat optic nerve axons is the TTX-sensitive Na+ channel, with evidence for additional TTX-insensitive routes permeable to Na+ and Li+. In addition, maintenance of membrane potential is critically dependent on continuous Na+ pump activity due to the relatively high exchange of Na+ (via the above mentioned routes) and K+ across the membrane of resting optic axons.

scholarly journals The Mechanism of Discharge Pattern Formation in Crayfish Interneurons

1965 ◽  
Vol 48 (3) ◽  
pp. 435-453 ◽  
Author(s):  
Kimihisa Takeda ◽  
Donald Kennedy
Keyword(s):  
Membrane Potential ◽  
Discharge Rate ◽  
Frequency Curve ◽  
Current Frequency ◽  
Inhibitory Processes ◽  
Optimal Current ◽  
Current Threshold ◽  
Time Courses ◽  
Repetitive Discharge

Excitatory and inhibitory processes which result in the generation of output impulses were analyzed in single crayfish interneurons by using intracellular recording and membrane polarizing techniques. Individual spikes which are initiated orthodromically in axon branches summate temporally and spatially to generate a main axon spike; temporally dispersed branch spikes often pace repetitive discharge of the main axon. Hyperpolarizing IPSP's sometimes suppress axonal discharge to most of these inputs, but in other cases may interact selectively with some of them. The IPSP's reverse their polarity at a hyperpolarized level of membrane potential; they sometimes exhibit two discrete time courses indicating two different input sources. Outward direct current at the main axon near branches causes repetitive discharges which may last, with optimal current intensities, for 1 to 15 seconds. The relation of discharge frequency to current intensity is linear for an early spike interval, but above 100 to 200 impulses/sec. it begins to show saturation. In one unit the current-frequency curve exhibited two linear portions, suggesting the presence of two spike-generating sites in the axon. Current threshold measurements, using test stimuli of different durations, showed that both accommodation and "early" or "residual" refractoriness contribute to the determination of discharge rate at different frequencies.

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