Exam 8

Question 1

Steps in phototransduction (light passes through 6 layers

Trace the path that light takes before stimulating the photoreceptor

Answer 1

Layers of retina:

1. Pigment layer: Absorbs light and converts all-trans-retinal to 11-cis-retinal
2. Photoreceptor layer: outer portion of rods and cones that contain light sensitive pigments
3. Outer nuclear layer: cell bodies and nuclei of rods and cones
4. Outer plexiform layer: Synapses of photoreceptors cell axons terminals with dendrites of retianl interneurons (bipolar and horizontal)
5. Inner nuclear layer: cell bodies of retinal interneurons. Bipolar (B), Horizontal (H), Amacrine (A).
6. Inner plexiform layer: Synapses of retinal interneuron axon terminals with dendrites of ganglion cells

7. Ganglion cell layer: Cell bodies of ganglion cells (g). These are the output cells of the retina

8. Optic nerve layer: axons of ganglion cells traversing the inner retina on their way to the optic disc. They are later bundled into the true optic nerve

Phototransduction

1. Light causes the photoisomerization of 11-cis-retinal to all-trans-retinal (retinal is an aldehyde of vitamin A)
2. All-trans-retinal causes conformational change from opsin (GCPR) to Metarhodopsin II
3. Metarhodopsin II activates G-protein subunit ‘Transducin”
4. Transducin activates a phosphodiesterase which lowers cGMP in cell causing conversion to 5’-cGMP
5. Decrease in cGMP causes the sodium and calcium channels in the photoreceptor membrane to close
6. An outward potassium channel remains open, so potassium influx continues
   - Cell becomes HYPERPOLARIZED and releases Glutamate from its axon terminal (where it synapses with bipolar and horizontal cells.

Hyperpolarization of photoreceptor membrane potential responses:

A. Decrease of release of glutamate = Decrease excitatory response in ionotropic receptors = Hyperpolarization of bipolar and horizontal cells (inhibition)

B. Decrease release of glutamate = Decrease inhibitatory glutamate response (metabotropic receptor) = Depolarization of bipolar and horizontal cells (excitation)

Question 2

Where is the tapetum lucidum and what function does it perform?

List several reasons why veterinary species see better in dim light?

do Dogs have color vision? is it the same as in humans?

Answer 2

Present in scotopic animals to increase photon reception in very low light conditions. Located in the choroid layer with no pigmented layer above it.

Increased number of rods, increased rod/cone ratio, presence of tapetum

Yes, but limited to 2 cone types (B,Y). Humans have three cone types (R,B,G)

Question 3

What happens to rods or cones when they are exposed to light versus darkened conditions?

Key points about phototransduction and retinal signal transmission

Answer 3

Cones: have greater member infolds, they require greater number of photos to stimulate them. They have few converged cones in one bipolar cell. Rhodopsin more diffused in outer member folds

Rods: have rhodopsin, which has greater sensitivity to light, so less number of photos is required to stimulate them. They also have tons of converged rods in one bipolar cell. Rhodopsin packed into discs for rods

• Light cuases hyperpolarization (inhibition) of both rods and cones
• Inhibited photoreceptors can cause downstream excitation of some (but not all) bipolar cells
• At rest bipolar cells are semi-depolarized, light hits them they become hyperpolarized

GLUTAMATE

• Amount of glutamate released by photoreceoptor cells (and bipolar cells) is proportional to the amount of depolarization or hyperpolarization
• This graded response of these cells allows different levels of luminance
• Gradual increase in glutamate release = progressively darker conditions: there is no photopigment conversion of metarhodopsin II, cGMP keeps the sodium/calcium channels open, the resulting depolarization increases glutamate release.Ionotropic Glutamate receptors will be inhibited when less glutamate is released by photoreceptors (Light conditions) and excited when glutamare release increases.
• Gradual decrease in glutamate release = progressively brighter conditions: there is photopigment conversion to metarhodopsin II, and G-protein mediated reduction in cGMP. Lack of cGMP keeps sodium/calcium channels closed, the resulting hyperpolarization decreases Glutamate release. Metabotropic Glutamate receptors will be excited when less glutmate is released (light conditions)

Question 4

Ganglion Cells

Horizontal Retinal Cells

Amacrine Cells

Scotopic vs. Photopic Vision

Answer 4

Action potentials from Ganglion cells transmitted along the optic nerve layer to the optic nerve itself.

Retina cells (H): mediate lateral interactions between photoreceptor cells and bipolar cells (provide sensitivity to luminance = contrast)

Amacrine cells: Mediate lateral interactions between bipolar cells and ganglion cells. Inhibitory in the inner nuclear layer

• Photopic: humans suited to visual detection in light conditions. Mostly cones. No tapetum lucidum.
• Scotopic: ideally suited for dim light or darkened conditions. Mostly Rods. Tapetum lucidum.

Tapetum: is an area within the choroid containing reflective material, epethillium without pigmentation. Reflects light back to the photoreceptor layer so that it can make use of light as much as possible.

Question 5

Post-retinal visual pathways for conscious visual perception

Pupillary light reflex

Answer 5

• Optic nerve, optic chiams, optic tracts, Lateral geniculate nucleui, optic radiation, visual cortex in occipital lobe
• Ganglion cell axons from the nasal (medial) retina enter the optic nerve then cross over the optic chiasm to enter the contralateral optic tract.
• Ganglion cell axons from the temporal (lateral) retina enter the optic nerve, but at the optic chiasm do not cross over. Instead these fibers enter the ipsilateral optic tract.
• The medial retina predominance of optic nerve fibers transmit visual signals. Loss of optic pathways that recieve this visual input results in clinical blindness

PLR fibers (20%) go to Pretectal nucleus and move to rostral colliculus, bypasses the Lateral geniculate nucleus.

Vision fibers (80%) go to the Lateral geniculus nucleus in thalamus.

Question 6

The peripheral auditory system or Choclear portion of CN VIII

Answer 6

Peripheral auditory system similar to peripheral vestibular system

Membranous cochlea housed within the bony cochlea of inner ear

Contains perilymph and endolymph

-Bony cochlea, Spiral lamina (ridge that separates internal bone): separated into two compartments

*Compartment dorsal to the duct is the scala vestibuli (Oval window)

*Compartment ventral to the duct is the scala tympani (Round window)

*Round window stops sound waves from reflecting

-Cochlear duct: between Scala vestibuli (Vestibular membrane), Scala tympani (Basilar membrane).

*Contains endolymph (high in K+)

Question 7

Organ of Corti and connections with Cochlear Nerve

Hearing and Organ of Corti Physiology

Answer 7

Group of hairs resting on the basilar membrane. They are in contact with peripheral axon endings of frist order cochlear neurons of CN VIII

Hair cells have stereocilia embeded in a gelatinous membrane

Cell bodies are within the ‘Spiral Ganglia’

Hearing

Sound waves vibrate tympanum and ear ossicles

Oval window vibrates, Scala Vestibuli perilymph vibrates, Vestibular membrane vibrates

• Endolymph vibrations transmitted to basilar membrane. The tectorial membrane is eventually stimulated
• Vibrations in the Scala Vestibuli perilymph can also be transmitted to the Scala Tympani via Helicotrema

Scala Tympani perilymph vibrations are transmitted directly to the basilar membrane

Basilar membrane resonates:

• At the Cochlear Apex: optimally at low sound frequencies
• At the Cochlear Base: optimally at high sound frequencies

*Hair cells move. Sterocilia on hair cells bend within the tectorial membrane and are activated.

Amplitude: energy, loud sounds

Question 8

Sound transduction

The auditory pathway

The descending auditory pathway

Auditory Reflex pathway

Answer 8

Endolymph is high in K+

Bending sterocilia opens up K+ channels

K+ enters hair cell and depolarizes it

Voltage gated calcium channels are activated

Neurotransmitter Glutamate is released

K moves from the base of the hair cell to the perilymph.

Auditory pathway (starts from ear)

1. Left or right auditory cortex
2. Medial Geniculate Body
3. Inferior Colliculus
4. Lateral lemniscus
5. Superior Olivary Complex
6. Dorsal Cochlear Nucleus
7. Ventral Cochlear Nucleus
8. Left or right ear.

Descending auditory pathway

Auditory cortex, Medial geniculate nucleus, Caudal colliculus, Cochlear nuclei, Dorsal nucleus, Medulla Oblongata, Facial nerve CN VII, Afferent fibers, Efferent fibers, Sensory hair cells.

Auditory Reflex Pathway

Hiar cells, auditory nerve, Cochlear nuclei, Trapezoid body, superior Olivary Complex, Acustic reflex, Trigeminal Motor Nucleus, Facial Motor Nucleus, Lateral lemniscus, Infeior colliculus, Medial Geniculate NUcleus, Primary Auditory Complex.

Question 9

The BEAR in animals

Answer 9

Six wavefroms produced

1. generated by distal cochlear axon and spiral ganglion cell body
2. ’’ proximal cochlear nerve just as it enters the cochlear nucleus
3. II-VI Combination of relay nuclei in the auditory pathway within the brain stem

Question 10

Olfatory and Taste

Olfatory Transduction

Answer 10

For taste the sensory receptor is a specialized epethilial cell that transduces chemical signals and then sends electrical signals to primary afferent neuron

Sensory receptors for smell

• GPCRs
• Ionotropic, utilized by chemoreceptors
• Olfatory epethilium: Basal Cells divide and produce new ones thorughout life (Stem Cells)
• Olfatory receptor cells are primary afferent.
• Axons travel through the cribriform plate. Unmyelinated fibers so they are slow at conducting
• Synapse with second order neurons in olfatory bulb called Mitral Cells
• Basal cells are stem neural cells

- Bone Morphogenic Protein regulares the renewal olfatory process (growth factors)

Olfatory Transduction

• Odorant binds to GPCR on the olfatory receptor cells
• Adenylyl cyclase activated and converst ATP cAMP
• cAMP opens sodium, potassium, and calcium channels
• Membrane depolarized
• Action potential generated in olfatory neuron’s axon

Primary olfatory (bipolar) neurons are the ‘sense organ’ that project through the cribriform plate to mitral cells in the olfatory bulb

• 1000 olfatory receptors axons converge on one second order neuron
• Mitral cells = ordor map

Olfatory signals travel to primary olfatory cortex bypassing the thalamus

Question 11

Olfatory Pathway

Answer 11

Main intracortical connections are towards the Neocortex, hippocampus, thalamus, and the hypothalamus, as well as to the neocortex and contralateral olfatory cortex.

The axons arising from the vomeronasal organ (VNSO) from the vomeronasal nerve and project to the accessory olfatory bulb (AOB)

Question 12

Taste Buds

Encoding the transmission of different tastes

Answer 12

Taste buds are the sensory organs for taste

• Located in tongue, palate, pharynx, larynx
• Receptor cells are specialized epethilial cells
• Taste buds have microvilli that contain the taste chemoreceptors

Bitter: back of tongue. GCPRs stimulate IP3, calcium, etc.

Sweet: mostly front of tongue. GCPRs stimulate IP3, calcium, etc.

Salty: around the front edges mostlySour: in the center of the tongue. Ionotropic epethelial sodium channels ENAC channels

Sour: mostly middle of tongue. Ionotropic epethelial sodium channels ENAC channels

Encoding different tastes

CN IX, X, VII

Peripheral olfatory neuron axons enter the brainstem and will eventaully reach second order neurons in the Solitary Nucleus of the Medulla Oblongata.

Second order neurons send axonal projections to third order neurons in the thalamus

Fourth order neurons are in the ‘taste cortex”

Question 13

Somatic Motor System

Answer 13

Requires coordination of cerebral cortex, basal nuclei, and cerebellum

UMN centers in brain: Cerebral cortex and brainstem

• Fascilitates muscle strength for weight support and posture.
• Initiate and regulate locomotor abilities
• Does not include reflexive limb movement if the animal is recumbent
• Partial inhibition of tendon reflexes when animals are laterally recumbent
• -Partial inhibition of extensor muscle tone when animals are laterally recumbent*

LMNs in spinal cord and brainstem: includes peripheral motor nerves and the muscles they innervate

Pyramidal Tracts Conscious control

Extrapyramidal tracts Subconscious reflex control, mostly out of brain stem

Planning voluntary movements:

• Cerebral cortex
• Basal Nuclei
• Thalamus

Postural reflexes coordination of head, body and eyes.

• Brain Stem
• Vestibular Nuclei
• Cerebellum

Spinal Reflexes pattern generation

Spinal Cord

Skeletal Muscle

Muscle Spindle

Question 14

Upper Motor Neuron System

Answer 14

Origen of the Motor Cortex Tracts

Cerebral cortext : Ventral Corticospinal tract (Ventral funiculus of Spinal Cord)

Lateral Corticospinal tract (Lateral funiculus of spinal cord)

Corticonuclear tract

Costicopontine tract

Vestibular Nuclei: Medial Vestibulospinal tract

Pontine Reticular Formation: Pontine reticulospinal tract.

Midbrain: Rubrospinal tract (Red Nucleus)

Pons: Pontine, Reticulospinal tract

Medulla Oblongata: Medullary reticulospinal tract

Question 15

Corticospinal Tract (pyramidal system)

Answer 15

Portion of the motor cortex with DIRECT connections with the spinal cord pre-motor neurons or LMNs

Originates in the motor cortex (caudal frontal/rostral parietal lobe)

• Pyramidal, pyramidal decussation (before spinal cord)
• Lateral corticospinal tract (Contralateral), Ventral corticospinal tract (Ipsilateral), Ventral horn motor neuron (spinal cord)
• Both lateral and ventral corticospinal tracts cross over to innervate contralateral LMN.

Cranial nerve motor nuclei

CN III, IV, VI : somatic nucleus Midbrain (Crus cerebri)

CN V Pons

CN VII Medulla Oblongata

CN IX, X, XI Medulla Oblongata

CN XII Medulla Oblongata

Question 16

Extrapyramidal UMN system

Answer 16

Portion of the Motor cortex with no direct connections with the spinal cord pre-motor neurons or LMNs

• Instead motor cortex projects to UMN centers in the brainstem
• Brainstem UMN centers then send axonal projections to the spinal cord

Both premotor and supplementary motor areas receive inputs from sensory cortical areas and may either send outputs to the primary motor cortex or to brainstem UMN centers

Question 17

Corticopontine Tract

Extrapyramidal UMN system

Answer 17

Projections to the contralateral cerebellum

Left Cerebral Cortex to Corticopontine Tract (right) Goes to pontine nuclei, middle cerebellar peduncle, right cerebellum, thalamus and cortex.

-Sensory, propioception, motor information

Extrapyramidal Brain Stem Centers

Red Nucleus rubrospinal tract (Midbrain)

Reticular Formation Pontine reticulospinal tract, Medullary reticulospinal tract

Other: Olivary nucleus, Vestibular nuclei, Tectum nuclei.

RUBROSPINAL System:

• Red nucleus in midbrain
• Recieves output of cortex, basal nuclei, cerebellum
• Monitors cerebral and cerebellar efferents. Corrects errors in movements initiated by cerebral cortex.
• Controls flexor muscles and fine motor actions

PONTINE Reticulospinal system:

Fascilitates LMNs (Alpha and Gamma) of extensor mucles, inhibits Flexors. Very important for weight support and postural control.

Can function autonomosly is the absence of cortical inputs

MEDULLARY Reticulospinal system:

UMN nuclei are in reticular formation

• Key roles to maintain muscle tone necessary for support and against gravity, as well as posture adjustments and synergestic body movements.
• Modification of spinal reflex circuits.
• Fascilitatory to LMNs innervating distal Flexor muscles, Inhibits extensors LMNs. Receives some facilitatory input from the ipsilateral motor cortex. Withdrawl type of thing.

Olivary Nucleus:

-Red nucleus efferents to Olivary Nucleusn. to contralateral cerebellum.

Vestibular Nuclei: vestibulospinal tract Tectum nuclei- Tectospinal tract. Coordination of movement.

Question 18

Lower Motor Neurons

Alpha and Gamma

Answer 18

The LMN includes the cell body and its axon collaterals in the periphery. The entire cell.

Axons start at the ventral root, eventually become part of a motor nerve

• Most peripheral are mixed meaning they have motor axons and sensory axons.
• One LMN together with all of the muscle fibers it innervates is called a single motor unit
• The more motor neurons per unit, the more the muscle force

Alpha-motorneurons: Innervate extrafusal muscle fibers

Gamma motorneurons: Innervate the contractile poles of intrafusal muscle fibers (part of the muscle spindle)

Mixed function stimulate to contract or stretch.

• When poles of spindle contract, the spindle is stretched and spindle afferents are activated

Clinical signs of weakness “paresis”

• +/- loss of motor abilities since disconnects UMN pathways from muscle
• Loss of spinal reflex (motor arm defective)
• Muscle atrophy, loss of trophic support, no neural stimulation, decreased protein synthesis.

Acetylcholine is release to muscles to maintain muscle tone normally

Question 19

Integration of Motor Control

Motor Systems Influence on Alpha and Gamma LMNs

Answer 19

Basal Nuclei is first level process

Spinal Neurons are under the influence of cerebral cortex, basal nuclei, cerebellum, and brain stem nuclei.

Extrapyramidal tracts (reticulospinal, rubospinal) provide stable background for optimal pyramidal motor performance and maintain muscle tone.

Cerebellum: Caudal cerebellar peduncle, middle cerebellar peduncle, rostral cerebellar peduncle.

Basal Nuclei or Basal Ganglia

-Located in the deeper, more ventral forebrain regions

Includes: Caudate nucleus, Putamen, Globus Pallidus, Other nuclei.

Primary motor cortex: primary source of projections to the brainstem UMN

Premotor Cortex: Orients the body in preparation for execution of a particular motor task

Supplementary motor cortex: Planning and organizing complex sequences of discrete movements

UMNs Coactivate both types of LMNs during movement

alpha-motorneuron causes contraction of extrafusal mucle fibers

Gamma motorneurons cuases strectching of muscle spindles (via contraction of poles of intrafusal muscle fibers)

Question 20

Central Pattern Generators

Answer 20

“Spinal Walk”

• Injury that disconnects UMNs from LMNs due to transection at the thorocolumnar junction
• Pelvic limbs affected
• Difficulty initiating walking, robot-like movement
• Ataxia is present (innability to coordinate movement)

CPGs are local networks of LMNs, excitatory and inhibitory interneurons are interconnected and can function autonomosly

Feedback neural loops on each side of the spinal cord can generate extension of one leg and concurrent flexion of the opposite leg

• No sensory input required, but sensory input may allow a reflexive stepping pattern to be initiated and provide some improvement in coordination
• Presence in neurologically-intact animal indicates plasticity of CPG synapses depending on the presence or absence of UMN

Question 21

The Mesencephalic Locomotor Region (MLR)

The Cerebellum and movement that is about to occur

Answer 21

CPGs need brain inputs to initate and help regulate stepping in neurologically inteact animal.

Selection: Forebrain, Basal Ganglia

Initiation: Brainstem, DLR, MLR, RS

Pattern generation: Spinal cord

The cerebellum receives information about a movement that is about to occur via:

• Olivary nuclei in brainstem: receives inputs from extrapyramidal UMN nuclei. Sends outputs to the cerebellum
• Pontine nuclei in brainstem: Receive inputs from motor cortex. Sned outputs to the cerebellum

Propioceptors:

• Spinocuneocerebellar Tract
• Dorsal spinocerebellar Tract

Cerebellum and movements in progress

-Spinocerebellar pathways: changes in muscle length, stretch, tension associated with contraction (from spindles and GTOs)

Limb and trunk position in space

-Vestibular pathways: spatial orientation, acceleration

Clinical signs of UMN disease:

• Spinal cord lesions that disconnect LMN from motor commands
• Loss of excitation of LMNs that are important for weight support and locomotion
• Degrees of weakness (paresis) and loss of motor abilities
• Very similar to LMN disease
• Patellar and triceps reflexes may or may not be hyperreflexic
• A complete reflex arc is till intact
• Muscle will not atrophy
• Limb extensor tone may increase with lateral recumbancy

Question 22

The vestibular system

Answer 22

Head motion-Angular acceleration: Semicircular canals, CNS, Visual Propioceptive Tactile inputs, Forebrain: Perceives orientation, Spinal cord and cerebellumL Postural control. Oculomotor System: Eye movements

Head motion-Linear Acceleration, Head Position-Gravity: Saccule and Utricle

Peripheral component:

• Located in the cochlear structures
• Sends connections to central vestibular system in the brainstem
• Membranous labyrinth (encased in bony labyrith)
• 3 semicircular canals, Utricle, and Saccule

Hair-cells (just receptor cells, the neurons are the vestibular neurons) in all three compartments are the sense organs: they are depolarized in one direction and repolarized in the other direction. K+ mechanical channels. Kinocilium

Crista ampullaris in semicircular cannals

Macula in utricle and saccule

Bipolar Bestibular neurons are activated or inhibited

Question 23

The Utricle and The Saccule

The Semicircular Cannal

Answer 23

They both contain Macula, which is a specialized receptor organ similar to crista ampullaris.

-Hair cells with sterocilia embedded in gelatinous otholithic membrane

Otholithic membrane covers the sterocilia. Contains crystalline structures called

Statoconia is displaced in one direction and activates the hair cells

Semicircular Cannal

Crista ampullaris at one end of each cannal: contains hair cells with sterocilia embedded in an overlying gelatinous cupula

-Head movement causes endolymph movement, which deflects the cupula

Stereocilia of hair cells bend endolymph ‘appears’ to move in opposite direction of head.

The semicircular canals are at right angles of each other

Each is paired to a semicircular canal on the opposite side

-Movement in one plane stimulates receptors on one side and decreases the activity of the receptors on the opposite side.

Question 24

First and second order vestibular neurons

Answer 24

Peripheral vestibular axons in contact with the base of hair cells

Bipolar cell body in vestibular ganglion

Central axon travels to lateral surface of rostral medulla

Axons synapse on second order vestibular neuron in a vestibular nucleus or go directly to the cerebellum

Vestibular Pathways

CN III, IV, VI.

-Propioceptors, Vestibular organ, Caudal cerebellar peduncle (Vestibular Nerve), Vestibular nuclei, Cerebellum (Flocculonodular lobe), Lateral and medial vestibulospinal tracts. Lower motor neurons, skeletal muscle. Or Vestibular nuclei, Medial longitudinal fasciculus, Extraocular muscles.

Question 25

Central Vestibular System Tracts

Answer 25

Lateral Vestibulospinal Tract

• From lateral vestibular nuclei, cerebellum
• Fascilitates LMNs going to Ipsilateral extensor mm. in limbs over entire spinal cord.

*If dog falls to the Right, Ipsilateral extensors respond*

-Inhibits LMNs going Ipsilateral flexors and contralateral extensor muscles

Medial Vestibulospinal Tract

• From medial vestibular nuclei
• Goes to Ipsilateral motor nucleus of accessory nerve XI and cervical spinal motor nuclei
• Moves head to maintain equilibrium

Ascending Medial Longitudinal Fasciculus

Rises from medial vestibular nucleus

• It is in brainstem, goes to CN III, IV, VI.
• This pathway coordinates head eye movement during changes in head position
• Keeps eye fixed on a stationary target when the head and body are rotation or moving

Vomitting Center

In reticular formation of the brainstem

Contralateral medial geniculate nucleus

To Thalamus to temporal cortex for conscious perception of vestibular stimuli.

-Can stimulate Emetic Center, Chemoreceptor trigger zone

Question 26

Clinical Signs of Vestibular Dysfunction

Answer 26

In a normal animal at rest, there is tonic activity (sustained response to stimuli) of vestibular receptors in both ears compartments.

-This tonic activity is transmitted to central vestibular structures

*Disease on one side results in absent vestibular signals entering from that side, but tonic activity from the vestibular system on other side, intact side persists.

• Damaged side has reduced signals, the tilt is toward the damaged side
• Rapid eye movement away from the side of the lesion, slow toward the lesion NYSTAGMUS