Faculty Opinions recommendation of Resting and stimulated mouse rod photoreceptors show distinct patterns of vesicle release at ribbon synapses.

2021 ◽  
Author(s):  
Alapakkam Sampath
Keyword(s):  
Vesicle Release ◽  
Rod Photoreceptors ◽  
Ribbon Synapses

scholarly journals Location of Release Sites and Calcium-Activated Chloride Channels Relative to Calcium Channels at the Photoreceptor Ribbon Synapse

2011 ◽  
Vol 105 (1) ◽  
pp. 321-335 ◽  
Author(s):  
A. J. Mercer ◽  
K. Rabl ◽  
G. E. Riccardi ◽  
N. C. Brecha ◽  
S. L. Stella ◽  
...  
Keyword(s):  
Chloride Channels ◽  
Flash Photolysis ◽  
Ion Concentration ◽  
Ca Channel ◽  
Ca Channels ◽  
Vesicle Release ◽  
Voltage Range ◽  
Synaptic Release ◽  
Ribbon Synapses ◽  
Ca Currents

Vesicle release from photoreceptor ribbon synapses is regulated by L-type Ca2+ channels, which are in turn regulated by Cl− moving through calcium-activated chloride [Cl(Ca)] channels. We assessed the proximity of Ca2+ channels to release sites and Cl(Ca) channels in synaptic terminals of salamander photoreceptors by comparing fast (BAPTA) and slow (EGTA) intracellular Ca2+ buffers. BAPTA did not fully block synaptic release, indicating some release sites are <100 nm from Ca2+ channels. Comparing Cl(Ca) currents with predicted Ca2+ diffusion profiles suggested that Cl(Ca) and Ca2+ channels average a few hundred nanometers apart, but the inability of BAPTA to block Cl(Ca) currents completely suggested some channels are much closer together. Diffuse immunolabeling of terminals with an antibody to the putative Cl(Ca) channel TMEM16A supports the idea that Cl(Ca) channels are dispersed throughout the presynaptic terminal, in contrast with clustering of Ca2+ channels near ribbons. Cl(Ca) currents evoked by intracellular calcium ion concentration ([Ca2+]i) elevation through flash photolysis of DM-nitrophen exhibited EC50 values of 556 and 377 nM with Hill slopes of 1.8 and 2.4 in rods and cones, respectively. These relationships were used to estimate average submembrane [Ca2+]i in photoreceptor terminals. Consistent with control of exocytosis by [Ca2+] nanodomains near Ca2+ channels, average submembrane [Ca2+]i remained below the vesicle release threshold (∼400 nM) over much of the physiological voltage range for cones. Positioning Ca2+ channels near release sites may improve fidelity in converting voltage changes to synaptic release. A diffuse distribution of Cl(Ca) channels may allow Ca2+ influx at one site to influence relatively distant Ca2+ channels.

scholarly journals Synaptic vesicles burst into sight

2020 ◽  
Vol 152 (12) ◽  
Author(s):  
Ben Short
Keyword(s):  
Synaptic Vesicles ◽  
Vesicle Release ◽  
Low Light ◽  
Rod Photoreceptors ◽  
Small Voltage

JGP study shows that small voltage changes disrupt semi-regular bursts of vesicle release from rod photoreceptors, potentially facilitating low-light vision.

scholarly journals Clearing the way for synaptic vesicle release

2018 ◽  
Vol 150 (4) ◽  
pp. 511-511
Author(s):  
Caitlin Sedwick
Keyword(s):  
Synaptic Vesicle ◽  
Vesicle Release ◽  
Ribbon Synapses ◽  
Synaptic Vesicle Release ◽  
The Way

JGP study shows that endocytosis aids synaptic vesicle release at ribbon synapses.

scholarly journals Resting and stimulated mouse rod photoreceptors show distinct patterns of vesicle release at ribbon synapses

2020 ◽  
Vol 152 (12) ◽  
Author(s):  
Cassandra L. Hays ◽  
Asia L. Sladek ◽  
Wallace B. Thoreson
Keyword(s):  
Single Photon ◽  
Glutamate Release ◽  
Glutamate Transporter ◽  
Resting Potential ◽  
Single Photons ◽  
Spontaneous Release ◽  
Vesicle Release ◽  
Readily Releasable Pool ◽  
Ribbon Synapses ◽  
Voltage Dependent

The vertebrate visual system can detect and transmit signals from single photons. To understand how single-photon responses are transmitted, we characterized voltage-dependent properties of glutamate release in mouse rods. We measured presynaptic glutamate transporter anion current and found that rates of synaptic vesicle release increased with voltage-dependent Ca2+ current. Ca2+ influx and release rate also rose with temperature, attaining a rate of ∼11 vesicles/s/ribbon at −40 mV (35°C). By contrast, spontaneous release events at hyperpolarized potentials (−60 to −70 mV) were univesicular and occurred at random intervals. However, when rods were voltage clamped at −40 mV for many seconds to simulate maintained darkness, release occurred in coordinated bursts of 17 ± 7 quanta (mean ± SD; n = 22). Like fast release evoked by brief depolarizing stimuli, these bursts involved vesicles in the readily releasable pool of vesicles and were triggered by the opening of nearby ribbon-associated Ca2+ channels. Spontaneous release rates were elevated and bursts were absent after genetic elimination of the Ca2+ sensor synaptotagmin 1 (Syt1). This study shows that at the resting potential in darkness, rods release glutamate-filled vesicles from a pool at the base of synaptic ribbons at low rates but in Syt1-dependent bursts. The absence of bursting in cones suggests that this behavior may have a role in transmitting scotopic responses.

scholarly journals Multivesicular Release Increases the Efficiency of Information Transmission at Sensory Synapses

2021 ◽  
Author(s):  
Ben James ◽  
Pawel Piekarz ◽  
Jose Moya-Diaz ◽  
Leon Lagnado
Keyword(s):  
Time Constant ◽  
Information Transfer ◽  
Ganglion Cells ◽  
Classical Model ◽  
Sensory Information ◽  
Bipolar Cells ◽  
Spike Generation ◽  
Vesicle Release ◽  
Ribbon Synapses ◽  
The Impact

The statistics of vesicle release determine how information is transferred in neural circuits. The classical model is of Poisson synapses releasing vesicles independently but ribbon synapses transmit early sensory signals by multivesicular release (MVR) when two or more vesicles are coordinated as a single synaptic event. To investigate the impact of MVR on the spike code we used leaky integrate-and-fire models with inputs simulating the statistics of vesicle release measured experimentally from retinal bipolar cells. Comparing these with models of independent release we find that MVR increases spike generation and the efficiency of information transfer (bits per spike) over a range of conditions that mimic retinal ganglion cells of different time-constant receiving different number of synaptic inputs of different strengths. When a single input drives a neuron with short time-constant, as occurs when hair cells transmit auditory signals, MVR increases information transfer whenever spike generation requires depolarization greater than that caused by a single vesicle. This study demonstrates how presynaptic integration of vesicles by MVR can compensate for less effective summation post-synaptically to increase the efficiency with which sensory information is transmitted at the synapse.

scholarly journals Two mathematical frameworks for vesicle release from a ribbon synapse of a retinal bipolar cell

2020 ◽  
Author(s):  
Hassan Bassereh ◽  
Frank Rattay
Keyword(s):  
Intracellular Calcium ◽  
Voltage Clamp ◽  
Bipolar Cell ◽  
Reversal Potential ◽  
Bipolar Cells ◽  
Signal Delay ◽  
Vesicle Release ◽  
Ribbon Synapses ◽  
Retinal Implants ◽  
The Impact

Abstract Background: Bipolar cells communicate with amacrine and ganglion cells of the retina via both transient and sustained neurotransmitter release in ribbon synapses. Reconstructing the published quantitative release data from electrical soma stimulation (voltage clamp experiments) of rat rod bipolar cells were used to develop two simple models to predict the number of released vesicles as time series. In the experiment, the currents coming to the AII amacrine cell originating from releasing vesicles from the rod bipolar cell were recorded using paired-recordings in whole-cell voltage-clamp method. One of the models is based directly on terminal transmembrane voltage, so-called ‘modelV’, whereas the temporally exacter modelCa includes changes of intracellular calcium concentrations at terminals. Results: The intracellular calcium concentration method replicates a 0.43-ms signal delay for the transient release to pulsatile stimulation as a consequence of calcium channel dynamics in the presynaptic membrane, while the modelV has no signal delay. Both models produce the quite similar results in low stimuli amplitudes. However, for large stimulation intensities that may be done during extracellular stimulations in retinal implants, the modelCa predicts that the reversal potential of calcium limits the number of transiently released vesicles. Adding sodium and potassium ion channels to the axon of the cell enable to study the impact of spikes on the transient release in BC ribbons. A spike elicited by somatic stimulation causes the rapid release of all vesicles that are available for transient release, while a non-spiking BC with a similar morphometry needs stronger stimuli for any transient vesicle release. During extracellular stimulation, there was almost no difference in transient release between the active and passive cells because in both cases the terminal membrane of the cell senses the same potentials originating from the microelectrode. An exception was found for long pulses when the spike has the possibility to generate a higher terminal voltage than the passive cell. Simulated periodic 5 Hz stimulation showed a reduced transient release of 3 vesicles per stimulus, which is a recovery effect. Conclusions: We presented two mathematical concepts for vesicle release in ribbon synapses and explained decreasing efficiency in retinal implants for suprathreshold stimulation.

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