scholarly journals Genetic access to neurons in the accessory optic system reveals a role for Sema6A in midbrain circuitry mediating motion perception

2018 ◽  
Vol 527 (1) ◽  
pp. 282-296 ◽  
Author(s):  
Brendan N. Lilley ◽  
Shai Sabbah ◽  
John L. Hunyara ◽  
Katherine D. Gribble ◽  
Timour Al-Khindi ◽  
...  
Keyword(s):  
Motion Perception ◽  
Optic System ◽  
Accessory Optic System

Connectivity of the turtle accessory optic system

2003 ◽  
Vol 989 (1) ◽  
pp. 76-90 ◽  
Author(s):  
Amy E Weber ◽  
John Martin ◽  
Michael Ariel
Keyword(s):  
Optic System ◽  
Accessory Optic System

Retinal ganglion cells projecting to the rabbit accessory optic system

1980 ◽  
Vol 190 (1) ◽  
pp. 49-61 ◽  
Author(s):  
Clyde W. Oyster ◽  
John I. Simpson ◽  
Ellen S. Takahashi ◽  
Robert E. Soodak
Keyword(s):  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Retinal Ganglion ◽  
Optic System ◽  
Accessory Optic System

Displaced ganglion cells and the accessory optic system of pigeon

1981 ◽  
Vol 195 (2) ◽  
pp. 279-288 ◽  
Author(s):  
Katherine V. Fite ◽  
Nicholas Brecha ◽  
Harvey J. Karten ◽  
Stephen P. Hunt
Keyword(s):  
Ganglion Cells ◽  
Optic System ◽  
Accessory Optic System

Membrane Properties and Monosynaptic Retinal Excitation of Neurons in the Turtle Accessory Optic System

1997 ◽  
Vol 78 (2) ◽  
pp. 614-627 ◽  
Author(s):  
Naoki Kogo ◽  
Michael Ariel
Keyword(s):  
Receptive Field ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Membrane Properties ◽  
Retinal Ganglion ◽  
Optic System ◽  
Accessory Optic System ◽  
Postsynaptic Potentials ◽  
Synaptic Inputs ◽  
Bon Cells

Kogo, Naoki and Michael Ariel. Membrane properties and monosynaptic retinal excitation of neurons in the turtle accessory optic system. J. Neurophysiol. 78: 614–627, 1997. Using an eye-attached isolated brain stem preparation of a turtle, Pseudemys scripta elegans, in conjunction with whole cell patch techniques, we recorded intracellular activity of accessory optic system neurons in the basal optic nucleus (BON). This technique offered long-lasting stable recordings of individual synaptic events. In the reduced preparation (most of the dorsal structures were removed), large spontaneous excitatory synaptic inputs [excitatory postsynaptic potentials (EPSPs)] were frequently recorded. Spontaneous inhibitory postsynaptic potentials were rarely observed except in few cases. Most EPSPs disappeared after injection of lidocaine into the retina. A few EPSPs of small size remained, suggesting that these EPSPs either were from intracranial sources or may have been miniature spontaneous synaptic potentials from retinal ganglion cell axon terminals. Population EPSPs were synchronously evoked by electrical stimulation of the contralateral optic nerve. Their constant onset latency and their ability to follow short-interval paired stimulation indicated that much of the population EPSP's response was monosynaptic. Visually evoked BON spikes and EPSP inputs to BON showed direction sensitivity when a moving pattern was projected onto the entire contralateral retina. With the use of smaller moving patterns, the receptive field of an individual BON cell was identified. A small spot of light, projected within the receptive field, guided the placement of a bipolar stimulation electrode to activate retinal ganglion cells that provided input to that BON cell. EPSPs evoked by this retinal microstimulation showed features of unitary EPSPs. Those EPSPs had distinct low current thresholds. Recruitment of other inputs was only evident when the stimulation level was increased substantially above threshold. The average size of evoked unitary EPSPs was 7.8 mV, confirming the large size of synaptic inputs of this system relative to nonsynaptic noise. EPSP shape was plotted (rise time vs. amplitude), with the use of either evoked unitary EPSPs or spontaneous EPSPs. Unlike samples of spontaneous EPSPs, data from many unitary EPSPs formed distinct clusters in these scatterplots, indicating that these EPSPs had a unique shape among the whole population of EPSPs. In most BON cells studied, hyperpolarization-activated channels caused a slow depolarization sag that reached a plateau within 0.5–1 s. This property suggests that BON cells may be more complicated than a simple site for convergence of direction-sensitive retinal ganglion cells to form a central retinal slip signal for control of oculomotor reflexes.

Shunting Inhibition in Accessory Optic System Neurons

2005 ◽  
Vol 93 (4) ◽  
pp. 1959-1969 ◽  
Author(s):  
Michael Ariel ◽  
Naoki Kogo
Keyword(s):  
Nonlinear Interaction ◽  
Visual Processing ◽  
Inhibitory Response ◽  
Optic System ◽  
Accessory Optic System ◽  
Excitatory Response ◽  
Electrical Microstimulation ◽  
Preferred Direction ◽  
Conductance Changes ◽  
Whole Cell Recordings

The interaction of excitatory and inhibitory inputs to the accessory optic system was studied with whole cell recordings in the turtle basal optic nucleus. Previous studies have shown that visual patterns, drifting in the same preferred direction, evoke excitatory and inhibitory postsynaptic events simultaneously. Analysis of the reversal potentials for these events and their pharmacological profile suggest that they are mediated by AMPA and GABAA receptors, respectively. Here, neurons were recorded to study nonlinear interaction between excitatory and inhibitory responses evoked by electrical microstimulation of the retina and pretectum, respectively. The responses to coincident activation of excitatory and inhibitory inputs exhibited membrane shunting in that the excitatory response amplitude, adjusted for changes in driving force, was attenuated during the onset of the inhibitory response. This nonlinear interaction was seen in many but not all stimulus pairings. In some cases, attenuation was followed by an augmentation of the excitatory response. For comparison, the size of the excitatory response was evaluated during a hyperpolarizing current pulse that directly modulated voltage-sensitive channels of a slow rectifying Ih current. Injection of hyperpolarizing current did not cause the attenuation of the excitatory synaptic responses. We conclude that there is a nonlinear interaction between these excitatory and inhibitory synaptic currents that is not due to hyperpolarization itself, but probably is a result of their own synaptic conductance changes, i.e., shunting. Since these events are evoked by identical visual stimuli, this interaction may play a role in visual processing.

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