01:146:295 Lecture Notes - Lecture 19: Ganglion Cell, Receptive Field, Metabotropic Glutamate Receptor 6

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violetseal1

17 Jun 2020

School

Rutgers University

Department

Cell Biology and Neuroscience

Course

01:146:295

Professor

J.Schjott

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Document Summary

These are small cells within the retina that do not fire action potential (actions potentials not necessary because of short distance between them and other cells). When they are depolarized, they release neurotransmitters on the ganglion. They are 2 different kinds of bipolar cells the on and off bipolar cells. On and off bipolar cell receive the same neurotransmitters the difference is they type of glutamate receptors they possess. The off bipolar cells have ampa glutamate receptors (ionotropic receptors). When glutamate binds to this receptor it causes an influx of na+ causing the cell to depolarize. The photoreceptors only release glutamate in the dark, therefore it can only bind to its receptor on the bipolar cells in the dark. It is called an off bipolar cell because it depolarizes when the light is off. The on bipolar cells depolarize when light is on.

Related Questions

Exercise #5: The Nervous system and Perception

Task #1: Color vision

Introduction

In the human retina, there are two kinds of light-sensitive cells: rods and cones. These cells are located on the outside of the retina, away from the vitreous humor and against the choroid layer, and are covered by a later of bipolar and ganglion cells as well as neurons. Light enters the posterior chamber through the lens and must pass through several cell layers before it is absorbed by the rods and cones.

Cones are involved in color vision at daylight intensities. Generator potentials in a cone excite one neuron, giving high-level resolution vision. Cones will not cause neural firing at low light intensities and are, therefore, nonfunctional at night.

Rods provoke black-and-white vision at low light intensities. A bipolar cell associates with several rods, so that generator potentials sum in their effect. This assures neuronal firing at low light intensities and provides a highly sensitive vision but with less resolution.

Receptor convergence. A ganglion cell, which receives input from a number of rods, spread out over the retina, cannot pinpoint the source of a light stimulus as well as a ganglion cell, which is stimulated by a single photoreceptor. In the case of a ganglion cell receiving the added input of several rods, light hitting any one of the rods can cause a neural spike in the ganglion cell, but the brain has no way to know which rod was excited. It is therefore harder to pinpoint the location of light stimuli on the retina when the stimulus is detected by rods (as compared to cones). The result is that our ability to see detail, or our resolving power, is considerably lower under dim light conditions than under bright light conditions.

Dark adaptation. If you go from a lighted area to a very dark room, you will not be able to see. After about ten minutes, however, you begin to be able to see again. This occurs because the rhodopsin pigment, which gets broken down when it absorbs light, is continually re-synthesized in the rods. When there is very little light, very little rhodopsin gets broken down and the amount of rhodopsin gradually builds up, making the rod much more sensitive to dim light.

When light strikes a receptor cell, it triggers a photo-chemical reaction that leads to neuronal firing. If a rod or cone receives high-intensity light, the visual pigments will be temporarily bleached and will not absorb any more light. Within a matter of a few seconds, enzyme systems in the cells will restore the visual pigment to its light-absorbing form. This can be easily demonstrated. If, after viewing a bright light, the eye is quickly shut or turned to a dark wall, the bright image will persist as a positive afterimage because the high generator potential causes the continued firing of neurons. If the eye is cast on a lighter background after a few seconds, a negative afterimage, or a dark image of the object will appear. This is because the still bleached cells are not receptive to the light coming from the light background.

According to the Young-Helmholtz theory of color vision, there are three types of cone cells, which respond respectively to red, green, and blue light.

All other colors are perceived as the brain interprets impulses coming from a mix of these receptors. If an object of one color is viewed for a long period of time at high light intensity, the cones for that color will become bleached. The afterimage of the object will be seen in the complementary color.

The Exercise 6 PowerPoint will demonstrate afterimages to you. Use the slide show option to project the square of red light on your entire screen in a dark room. After staring intensely at the square for 30 seconds or so, without shifting your gaze, click enter to change the slide to a soft white. Continue staring at the screen as the change is made. What do you see? What was the color of the afterimage?

Repeat this experiment using a blue square. Before doing the experiment, hypothesize what color the afterimage will be according to the Young-Helmholtz theory.

Hypothesis to be tested: (2 pts)

What did you see when the experiment was conducted? (2 pts)

Was you hypotheses accepted or rejected? (1 pt)

Explain the colors seen in these afterimages using the Young-Helmholtz theory. (5 pts)

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11.Which sequence of events is required for the brain to interpret sound?
I. Vibration of the basilar membrane relative to the tectorial membrane causes cilia on hair cells to bend and triggers depolarization.

II. Hair cells stimulate the production of action potentials in sensory neurons that project to the brain.

III. Ganglion cell axons transmit action potentials to the occipital lobe.

A. II then I B.III then I then II. C.III then I D.I then II E.I then II then III

12. Which animal became numerous and widespread by using sonar to enable a high level activity in the dark?

A.bats B.whales C.owls D.dolphins E.shrews

13.In the vertebrate eye, what structure is light focused onto?

A.pupil B.lens C.retina D.sclera E.iris

14.Which is NOT a part of the vertebrate eye?

A. cornea B. retina C. iris D. cochlea E. pupil

15. In the vertebrate eye, what structure controls the amount of light that reaches the retina?
A. fovea. B. cornea. C. iris D. lens E. sclera

16.What are the short retinal photoreceptors responsible for color vision called?

A.rods B.cones C.bipolar cells. D.glial cells. E.ganglion cells

17. What sensory equipment is required for an animal to have binocular vision?

A.eyes located to the sides of the head B.forward-facing eyes C.a camera-type eye with multiple lenses

D. infrared vision E.ultraviolet vision

18. Choose the receptor that is NOT correctly matched with its function.

A.proprioceptor - monitors stretch of muscle fibers

B.baroreceptor - monitors hydrostatic pressure in blood vessels

C.nociceptor - transmits signals that the brain interprets as pain

D.chemoreceptor - perceives taste and smell stimuli

E.peripheral chemoreceptor - monitors the pH of the cerebrospinal fluid

19. Where is the visual image in focus for a nearsighted individual?

A.behind the retina B.in front of the retina C.on the retina, but it appears blurred

D.at the lens, forming a shadow on the retina E.on the retina, but it is upside down

20. Since the optic nerve must pass through the retinal layer, we all have a blind spot devoid of light receptors. This normally goes unnoticed, since the brain attempts to compensate for missing sensory information by filling it in based on surrounding patterns. Which step of the sensory pathway is represented by perceptual filling-in of the physiological blind spot?

A. interpretation B. stimulus. C. transduction into receptor potential D.action potential transmission

Tetraethylammonium (TEA) is a drug that blocks voltage-gated potassium channels. What effect would this have on an action potential?

(a)Prevent the rising phase

(b)Prevent the cell from reaching the threshold to trigger an action potential

(c)Prevent or prolong the falling phase

(d)None of the above

The hyperpolarization phase of the action potential is due to:

(a)The opening of voltage-gated Cl- channels

(b)Prolonged opening of voltage gated K+ channels

(c)The closure of resting Na+ channels

(d)Rapid inactivation of voltage-gated K+ channels

The period when it is difficult to initiate another action potential for several milliseconds due to voltage-gated sodium channel inactivation is referred to as the:

(a)Relative refractory period

(b)Absolute refractory period

(c)Resting period

(d)Hyperpolarization period

In the human central nervous system, Gap junctions are found:

(a)Only between neurons

(b)Only between astrocytes

(c)In both neurons and astrocytes

(d)In all cells

Small molecule transmitters such as acetylcholine are synthesized in:

(a)The nerve terminal

B) The cell body and transported to the nerve terminal

C) Synaptic vesicles

D) Endoplasmic reticulum

Prior to Otto Loewiâs classical experiment, which of the following was not known:

(a)stimulation of the vagus nerve slows the heart

(b)extracts of frog heart, made following vagal nerve stimulation, slow the heart

(c)some acetylcholine effects are similar to those produced by muscarine

(d)vagal nerve stimulation releases a substance which slows the heart

Which of the following is most important in determining if neurotransmission is excitatory or inhibitory?

(a)The structure of the synapse

(b)The neurotransmitter released by the presynaptic neuron

(c)The neurotransmitter receptor

(d)The strength of the stimulus

Benzodiazepines such as Valium allosterically regulate GABA receptors by:

(a)Binding at receptor sites other than the transmitter binding site

(b)Binding at the transmitter (GABA) binding site on the receptor

(c)Blocking the action of the endogenous transmitter

(d)Mimicking the action of the endogenous transmitter

GABA-A receptors are ligand-gated Cl- channels. The equilibrium potential of Cl- is -65 mV. At the neuronal resting membrane potential of -65 mV, GABA binding to the GABA-A receptor would result in the opening the Cl- channel, resulting in:

(a)no net flow of Cl- ions

(b)Cl- inflow and hyperpolarization

(c)Cl- outflow and depolarization

(d)Cl- outflow and hyperpolarization

At the mammalian neuromuscular junction, the released neurotransmitter acts on:

(a)muscarinic receptors

(b)nicotinic receptors

(c)adrenergic receptors

(d)Beta receptors

Neurotransmitters are packaged into synaptic vesicles by:

(a)endocytosis following transmitter release

(b)presynaptic membrane transporters

(c)vesicular transporters

(d)all of the above

. Which of the following are NOT types of ion channels?

Voltage-gated

(a)Ligand-gated

(b)G protein coupled receptor (GPCR)-gated

(c)Leak channels

(d)NONE of the above

NMDA receptors are unique in that their ion channel is:

(a)Ligand-gated

(b)Voltage-gated

(c)Ligand- and voltage-gated ion channels

(d)GPCR-gated

. Which of the following is INCORRECT regarding Catecholamine neurotransmitters

(a)Includes Dopamine, Norepinerphrine, and Epinephrine

(b)Contain a Catechol Ring

(c)Synthesized from Tryptophan

(d)Are produced by neurons whose cell bodies are located in the upper brainstem

The largest and most diverse group of receptors in eukaryotes is:

(a)Ligand gated receptors

(b)Glutamate receptors

(c)G-Protein coupled receptors

(d)Allosteric receptors

The most abundant G-protein coupled receptor in the brain is:

(a)Glutamate receptors

(b)Acetylcholine receptors

(c)Cannabinoid receptors

(d)Dopamine receptors

Which of the following drugs DOES NOT block voltage-gated Na+ channels

(a)Lidocaine

(b)Riluzole

(c)Reserpine

(d)Tetrodotoxin

Sarin, a nerve gas, exerts its toxicity by:

(a)blocking nicotinic receptors

(b)inhibiting choline acetyltransferase

(c)inhibiting acetylcholinesterase

(d)inhibiting voltage-gated Na+ channels

Botulinum Toxin (BoTox) interferes with transmitter release by:

(a)cleaving protein(s) involved in transmitter release

(b)blocking voltage-gated Ca2+ channels

(c)blocking voltage-gated Na+ channels

(d)blocking voltage-gated K+ channels

Atropine is:

(a)An agonist of the acetylcholine ionotropic receptor

(b)An antagonist of the acetylcholine ionotropic receptor

(c)An agonist of the acetylcholine metabotropic receptor

(d)An antagonist of the acetylcholine metabotropic receptor

01:146:295 Lecture Notes - Lecture 19: Ganglion Cell, Receptive Field, Metabotropic Glutamate Receptor 6

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