Exam 3 Neuro III Flashcards
What is the refractory index? What happens if light strikes a perpendicular surface vs angled?
RI = speed of light in air / speed of light in the translucent material.
If light strikes perpendicular surface, only the speed changes. If the surface is angles, then rays bend if there is a difference in refraction of the two media.
What are diopters a measure of? What is the unit? What is the refractive power of the eye and which area of the high specifically and why?
the more a lens can bend lift rays, the greater it’s refractive power, measured in diopters. 1 diopter = 1 meter/focal length.
Eye = 59 diopters, 2/3s comes from the cornea (anterior cornea). This is bc the RI of the cornea differs markedly from air, while the RIs of the aqueous humor, lens, and vitreous humor are not that different from air’s.
What is presbyopia and why does it happen as we age
Difficult viewing near objects. As we age the lens becomes less elastic and loses ability to form sphere (thicken) as needed for focusing on near objects.
Contrast myopia and hyperopia
Myopia aka nearsightedness, image is focused in front of retina, eye might be too “long”.
Corrected w concave lens.
Hyperopia aka farsightedness. Image is focused behind the retina, “shortened” eyeball.
Corrected w convex lens
2° cataract vs traumatic cataract vs congenital vs radiation cataract
Secondary - form after surgery from other eye probs eg glaucoma, or form due to etc health probs eg diabetes, steroid use.
Traumatic - after eye injury.
Congenital - babies or children develop the cataracts very small and may not affect vision. But might need lens removal.
Radiation - develop after exposure to radiation.
Describe outer, middle and inner layers of the eye
Outer- cornea (refraction), conjunctiva, sclera.
Middle - choroid and iris (papillary dilator = sympathetic innervation, sphincter muscle = parasympathetic innervation).
Outer- neural coat & retina, macula contains fovea (focal point depression).
What are the two components of interocular fluid? Describe them/formationfiltration.
Interocular fluid: aqueous humor and vitreous fluid. The aqueous humor lies in front of lens, freely flowing and continuously produced and reabsorbed. The vitreous fluid is gelatinous mass which allows materials to diffuse but does not flow.
Aqueous humor is formed by active secretion of Na+, which pulls Cl- and HCO3-. These solutes generate and osmotic gradient which pulls fluid (water) from the capillaries.
Fluid flows through pupil into ‘antechamber of eye’, makes it way to place between cornea and iris. There the humor is absorbed into the trabeculae meshwork, and taken away via the canal of Schlemm, ultimately back into blood system.
Describe the fovea.
The fovea is area in center of retiina, 1 mm2, which is specialized for detailed vision. Center fovia has high concentration of cones, while rest of retina dominated by rods.
Describe the structure of a photoreceptor (outer segment, inner segment and synaptic terminal).
Structure of the photoreceptor:
outer segment = made up of discs or folds of membrane. Light-sensitive photochemical located here - rhodopsin in rods, or one of three color photocemicals in cones.
inner segment= cytoplasmic organelles, mitochondria, nucleus
synaptic terminal = synaptic contact with subsequent cells.
Describe the four main characteristics of rods.
Rods 1) Extremely sensitive to light: night vision: outer segment is longer. contains more photopigment. can capture more light. rod is activated by 1 photon. 2) Black & white vision: 1 photopigment. rhodopsin (429nm). 3) Distribution: primarily outside of fovea. 4) High Convergence: many rods synapse on 1 bipolar cell. many bipolar cells synapse on 1 ganglion cell (makes for highly sensitive detector of light but poor spatial resolution).
Describe the 4 main characteristics of cones.
Cones 1) Low light sensitivity: day vision. outer segment is shorter. contains less photopigment. can capture less light. cone is activated by 100+ photons. 2) Color vision: 3 photopigments; blue opsin (419 nm), green opsin (531 nm), red opsin (559 nm). 3) Distribution: primarily located in the fovea. 4) Low convergence: 1 cone synapses on 1 bipolar cell. 1 bipolar cell synapses on 1 ganglion cell (makes for weak light detection but high spatial resolution)
Degree of activation of cones by different monochromatic lights.
Loss of red cones: ?
Loss of green cones: ?
Why is this more common in males? How can it occur in females?
A specific cone will respond to varying degrees to different colored light.
Red-Green color Blindness- if you are missing either red or green cones, you will have trouble distinguishing between green-yellow-orange-red, since these are covered by the green and red cones.
Red-green blindness is X-linked, so phenotype is expressed in males, females are carriers.
If a woman is color blind, what are the chances that her son will be color blind? That her daughter will be color blind?
.
Explain the photochemistry of vision.
Rods and cones have chemicals which decompose in light. Rods have rhodopsin, cones have cone pigments. Outer segment of rod projecting into RPE has concentration of 40% rhodopsin, which is a combination of the protein scotopsin (opsin) and retinal , acarotenoid pigment.
Light energy is absorbed by rhodopsin in the rods, changes from cis to trans form. The all-trans form no longer fits well with scotopsin and they begin to separate to make bathorhodopsin, then lumirhodopsin, metarhodopsin I, then metarhodopsin II, and finally into all trans retinal and scotopsin. It is Metarhodopsin II (activated rhodopsin) which induces the electrical potential. All-trans retinal converts to 11-cis retinal, recombines with scotopsin.
Role of vitamin A: all-trans retinol can be converted to all-trans retinal, then converted by isomerase into cis-retina.
Excitation by light exposure: light causes the photopigments to become hyperpolarized; decomposing rhodopsin decreases Na+ current in outer segment of rod. K leaks out through non=gated channels. The Na-K ATPase maintains gradients.
Activated rhodopsin stimulates the G-protein trasnducin, which activates a cGMP phosphodiesterase. This in turn breaks down cGMP, thereby closes cGMP-gated Na+ channels. Rhodopsin kinase inactivates the activated rhodopsin.
Compare the polarization of photoreceptor cells in dark vs light conditions.
Photoreceptor cells are hyperpolarized by light.
In darkness, receptor cells are ‘depolarized’ (In depolarized state, Ca2+ channels are OPEN and transmitter release rate is high.) > exposure to light causes graded hyperpolarization based on intensity, (saturates at @-65 to -70mV). Hyperpolarization reduces Ca2+ current, reducing transmitter release.
Cation channels regulated by cGMP. In the dark, high cGMP levels keep channels open/cell depolarized.
In light, cGMP levels fall > closing cation channels and hyperpolarize the cell.
Photoreceptors project to____.
Horizontal cells project to ___, are always ___.
Bipolar cells project to ____, may be ___or ____.
Amacrine cells project to ____.
Ganglion cells make up the ____.
Photoreceptors project to bipolar and horizontal cells.
horizontal cells project to bipolar cells, always inhibitory, provide lateral inhibition.
Bipolar cells project to ganglion and amacrine cells, may be excitatory or inhibitory.
Amacrine cells project to bipolar cells and ganglion cells
Ganglion cells make up the retinal output, make up the optic nerve.
Descriube the W, X, and Y ganglion cells that make up the optic nerve. Speed, info inputs/outputs, vision.
W Ganglion cells- small and slow, receive information from rods, dendrites spread widely, sense directional movement, dark vision.
X ganglion cells- medium size and speed, most numerous, small dendritic field, fine detail vision.
Y ganglion cells- largest and fastest, large dendritic fields, poor localization but rapid detection of change and movement.
Photoreceptors have circular receptive fields.. Subsequent to these are bipolar cells which are ‘on-center’ or ‘off-center’. Explain.
On-center cell is depolarized with light in the center of receptive field, and hyperpolarized within the annulus. Off-center is hyperpolarized with light in the center of receptive field and depolarized within the annulus.
Most of the information in the visual field comes from what? Of what is this largely a function?
Most of the information in the visual field comes from detection among ganglion cells of the differences in level of illumination: luminance contrast. This is largely a function of on and off centers and surrounds.
Explain the sequence of events involved in receptive field vision.
- Light on the photoreceptor hyperpolarizes the cell, reducing neurotransmitter (glutamate) release.
- On-center bipolar cell has mGluR6 receptors (GPCRs). Receptor binding activates intracellular cascade which closes cGMP –gated Na+ channels, has hyperpolarizing effect. Decrease in transmitter from the photoreceptor will depolarize this cell (releases it from hyperpolarizing effect of transmitter).
- Off-center bipolar cell has ionotropic receptors, receptor binding depolarizes cell.
- Bipolar cells release transmitter in response to depolarization (they don’t fire APs, have graded potentials).
- Light in CENTER hyperpolarizes photoreceptor, which DEPOLARIZES on-center bipolar cell, which will release excitatory transmitter on ‘on-center’ ganglion cell.
What is lateral inhibition?
Further contributing to the generation of contrast is lateral inhibition. Horizontal cells connect laterally with photoreceptors. These are inhibitory cells. In the case depicted in the figure, the center photoreceptor is stimulated by a point of light, while the side photoreceptors in this case are in the dark. The direct pathway from photoreceptor to bipolar to ganglion is activated. This would produce contrast- if all three receptors were activated, then they would neutralize each other through the lateral inhibitory circuit.
Why do we experience a continuous visual field?
The visual fields of the two eyes are blended by the minority of fibers crossing at the chiasm- for ex. the left eye’s nasal field is blended with the right eye’s temporal field. The end result is that we experience a continuous visual field.
Note how the topographical arrangement of the retinal cells is preserved throughout the projection including the visual cortex.
Muscle control of eye movements: describe the 3 pairs of muscles. What cranial nerves project to them?
A. Muscle control of eye movements: 3 pairs of muscles; 1) medial and lateral recti- move side to side,
2) superior and inferior recti, move eyes up and down, and
3) superior and inferior obliques, rotate eyes to align visual fields.
Cranial Nerves: 3rd Oculomotor Nerve, 4th Trochlear Nerve, and 6th Abducens Nerve.
Humans fixate on objects via voluntary fixation or involuntary fixation. From where do the voluntary and involuntary signals originate?
What are the three continous types of movements of the eye and what do they achieve when they converge? What are saccades? What is “pursuit movement’?
The voluntary fixation signal originates in premotor areas of cortex (dysfunction of these areas makes it difficult to unlock the eyes from a fixation point). Involuntary signals start in secondary visual areas of occipital cortex.
Three continous types of movements: 1) a continuous tremor, 2) a slow drift, and 3) sudden flicking movements. These movements correct and keep a fixation point on the fovia.
Watching a constantly changing scene (riding in a car) requires jumping from one fixation point to another several times per second- these jumps are known as saccades. Fixating on a moving target = “pursuit movement”. These and orientation movements to visual disturbances appear to require the superior colliculi, mediated via the medial longitudinal fasciculus.
The separate visual images of the eyes have to fuse to produce a unified visual field. What is the origin of strabismus?
The separate visual images of the eyes have to fuse to produce a unified visual field. There are specific neurons in the visual cortex which respond when the visual images are not “in register”, which induces the appropriate corrective movements of the eyes. Lack of coordination however can produce strabismus (crossed eyes). In some patients the persons attends alternatively to one eye then the other, while other patients will attend to only one eye and ignore the other.
Describe outer ear and middle ear anatomy.
outer ear- the external auditory meatus leads to the tympanic membrane- the ear drum.
middle ear - which is the ossicles (malleus, incus, and stapes). These connect the tympanic membrane with the oval window.
Inner ear anatomy (including the labyrinths).
The inner ear - in a cavity within the temporal bone containing the COCHLEA and vestibular apparatus.
Bony Labyrinth - made up of the bony exterior of the vestibule, semicircular canals, and cochlea.
Membranous Labyrinth - the membranes making up the interior structures of the vestibule, semicircular canals, and cochlea.
Cochlea formation/anatomy.
Cochlea = formed by division of bony labyrnith into two structures- the scala vestibuli (connects with the vestibule) and the scala tympani.These connect at the end of the cochlea’s coil at the helicotrema. These are separated by a component of the membranous labyrinth- the scala media.
The scala media (aka cochlear duct) is filled with endolymph (high K solution). Organ of Corti (the sense organ for hearing, hair cells w/ stereocilia) is located in the scala media.
The scala tympani and vestibuli are filled with perilymph.
How do we hear? (5)
- Sound waves (pressure waves) vibrate the tympanic membrane, which causes the ossicular chain to vibrate at the same frequencies.
- This in turn oscillates the oval window, transferring the vibrations to the fluids in the cochlea.
- This produces a ‘traveling wave’ of oscillation in the basilar membrane.
- Displacement of the basilar membrane moves the hair cells > shearing force on the stereocilia. When the shorter ones are bent towards the longest, there is an increase in K conductance (hair cell depolarizes). If the shorter cilia are bent away, the cell is hyperpolarized. This depolarization is the receptor potential.
What is the relationship between response and location along the membrane? How are the frequencies distinguished?
The greatest response for a particular place along the membrane corresponds to specific frequencies (high frequencies at the base where it is narrowest, low frequencies at the apex where it is widest).
Explain the sequence of events involved in stereocilia hearing. Why is this particularly odd/unique in regards to the K+ conductance.
- The endolymph is high in K. When the stereocilia are sheared towards the large cilia, K channels open and K rushes into the hair cell, depolarizing it. This activates voltage-gated Ca channels, which open allowing Ca to flow into the cell.
- The increase in extracellular Ca induces vesicle fusion and transmitter release onto the afferent nerve. The increase in Ca also opens Ca-dependent K channels in the body of the hair cell.
- This end of the cell is in K-poor perilymph, so opening K channels induces an outflow of K, which serves to re-polarize the cell. *This is a curious example of K both depolarizing and hyperpolarizing the same cell.
Age-related hearing loss is believed due to what three main things? Which frequencies are lost 1st?
1) exposure to loud sounds, causing loss of hair cells (or exposure to chronic sound),
2) exposure to ototoxic chemicals (eg antibiotics).
3. degradation of the stria vascularis, which reduces the ability to maintian the high K+ environment in the endolymph. This in turn reduces the ability to excite hair cells.
Hearing loss starts in the higher frequencies and progresses to the lower frequencies.
(broadly) Describe hearing through the cochlea. What constant physiological theme is at play here?
Pressure waves are transmitted to the cochlea via the mechanism of the middle ear. In the cochlea, a traveling wave is generated which is maximized to a particular place along the cochlea according to the sound frequency (lower frequencies at the apex, where it is wider, and higher frequencies at the base where it is narrower). This is a consistent theme throughout sensory physiology, topographical arrangement. In this case a tonographic arrangement.
Simplified auditory neural pathway schematic? (5)
Simplified auditory pathway schematic:
1: Spiral ganglion of Corti to dorsal and medial cochlear nuclei.
2: most fibers cross midline, project to Superior Olivary Nuclei.
3: Pass through lateral lemniscus- some terminate on Nucleus Lateral Lemniscus, most continue to inferior colliculus.
4: Project to medial geniculate.
5: Project in auditory radiation to auditory cortex.
Notes:
- the auditory system entails parallel pathways, and information from each ear reaches both sides of the brain & brainstem.
- the midline is crossed at several layers.
-many fibers send collaterals to the reticular activating system and cerebellum- this is basis of startle response.
Where is the PRIMARY AUDITORY CORTEX located and what does it do?
What is the function(s) of the SECONDARY AUDITORY CORTEX?
PRIMARY AUDITORY CORTEX located in the Temporal Lobe). Integrates the auditory information for perception (TONOTOPY). Thalamic projections carry sound information to the auditory cortex, which is also tonographically arranged such that it is laid out to match the physical layout of the cochlea.
SECONDARY AUDITORY CORTEX: analysis of complex sound in humans, contains areas that are responsible for comprehension of human language (Wernicke’s area).
Describe the typical audiogram pattern seen in age-related hearing loss patients. What sounds are primarily affected?
Typical downward sloping pattern, reflecting hearing loss at progressively higher sound frequencies is seen in age-related hearing loss. The patterns of bone and air conduction would be very similar. The shallow U-shaped pattern (“speech banana”) shows how high-frequency hearing loss primarily affects the ability to hear consonant sounds.
