Exam 4

M ganglion cells

M ganglion cells

From peripheral rods - detect motion in periphery

High convergence 10-50 rods → 1 bipolar

Multiple bipolar → 1 M ganglion cell

P ganglion cells

From center/surround fields

Form + color detection

No convergence, high spacial resolution

Intrinsically Photosensitive Retinal Ganglion Cells

Detect light, but no conscious perception

No rods/cones - no rhodopsin - instead melanopsin

Why blind people still have circadian rhythm + pupillary reflex

From eye to optic tract

Ganglion axons form optic nerve (CN II)

Leave fovea at blind spot

Both sides reach optic chiasm

Temporal axons travel ipsilaterally into optic tract

Nasal axons travel contralaterally into optic tract

Recall nasal axons responsible for temporal optic field and temporal for nasal

Right optic tract = right temporal + left nasal axons = entire left visual field

Optic tract synapses onto

Hypothalamus - circadian rhythm

Superior colliculus - turning head to stimuli

Midbrain → pretectum - pupillary reflex

Lateral geniculate nucleus of thalamus → primary visual cortex

If light on left

Light falls onto left nasal + right temporal

Forveating

Looking through both foveas

If light in center, falls on both foveas at same location

Lateral geniculate nucleus of thalamus structure

6 sections

1&2 - M class 1 = contralateral, 2 = ipsilateral

3-6 - P class - 3&5 = ipsilateral, 4&6 = contralateral

Segregation important for depth perception

LGN has receptive fields like ganglion and a threshold for sending info to V1

LGN to V1

1&2 of LGN → 4Calpha of V1 (where/motion) n

3-6 of LGN → 4Cbeta of V1 (form + color)

*Still segregated by layers

Automatic gain control

LGN measures relative light intensity so light changes don’t feel too bright

Optic radiations

LGN sends optic radiations to V1 - relate to fovea

Top of fovea sees ground and bottom of fovea sees sky

So superior radiations see ground and run through upper bank

Inferior radiations see sky and run through lower bank

to V1

Layer 4C synapses onto

spiny or smooth stellate cells → Pyramidal cells

4C → 4B → layers 1&2 → V2, V3, etc

1&2 → 5&6 → SC, LGN, pons, etc

Pathway from 1&2 LGN

Dorsal pathway, magnocellualr inputs

The “where/mvmt” info

→ 4Calpha of V1 → V2 → middle temporal association area (MT) → Parietal lobe

Pathway from 3-6 LGN

Ventral pathway, parvocellular inputs

What/object pathway

→ 4Cbeta of V1 → V2 → V4 → Temporal lobe → Fusiform gyrus for faces

V1 - edges

V2 - general shape

Fusiform gyrus

Identify/associate an object

Complex visual connections, 1 cell receives unput from thousands of ganglion cells

Snakes simulate specific set of cells only for snakes before even know what a snake is

Specific cells for different parts/orientations of faces—respond to key face contrasts: ex: :)

V1 receptive fields

Not responsive to spots of light

Recognizes edges/light at angles - fundamental to how brain identifies objects

No response to horizontal bar - more vertical = more response

Ovular receptive field with bar in middle made of multiple overlapping cells/fields converging onto 1 pyramidal cell

Have simple cells for every orientation

Most firing at ideal angle but some firing at non ideal

Stellate → simple → pyramidal

Direction of mvmt

Stellate and simple cells responsible for sensing direction of light.

Inhibitory neurons connect stellate to simple cells so simple cells only fire if light moves in specific direction, otherwise inhibited

Ocular dominance in 4C

Ocular dominance columns in layer 4C. L or R eye column—changes every .5 mm

Segregation from LGN continues into 4C

Zero disparity cells

In V1

Fire only when analogous ganglion cells fire simultaneously on both retinas. Allows depth perception of objects in a straight line

Closer = light on temporal sides of retina

Further = light on nasal sides of retina

Different cells fire based on where on retina/depth

Binocular disparity cells

In V1

Fire when light strikes each retina at a different place

Cell for every possible conformation, also allow for depth perception`

V1 Structure

All angle pyramidal cells for both eyes and all color cells and all disparity cells in 1×1×2-4 mm cube of cortex

Takes output from LGN and breaks inro contrasting bars of light, then sends to higher order brain regions

Fovea gets largest SA of V1

Parasympathetic nervous system basics

Preganglionic neurons release Ach a ciliary ganglion onto post ganglionic neurons

Sympathetic nervous system basics

Preganglionic neurons release Ach, most post ganglionic use NE (sweat uses Ach)

Note: Preganglionic synapses directly onto adrenal gland

Prevertebral sympathetic ganglion

Celiac ganglion - stomach, liver pancreas

Superior mesenteric ganglion - colon

Inferior mesenteric ganglion - bladder, genitails

Lower extremities spinal nerves

Where does the sympathetic nervous system arise from?

Sympathetic preganglionic cell bodies arise from T1-L6 in the intermediolateral cell column in the gray matter between the dorsal and ventral horn.

Paraganglia leave through the ?lateral horn → through the white ramus → sympathetic trunk

@ Trunk:

Can go up to form cervical/chain ganglia

Leave through gray ramus to innervate blood vessels + skin

Synapse at trunk to lower motor neuron

Leave trunk and go to prevertebral ganglia

Prevertebral ganglia

close to organs they supply

Sympathetic chain ganglia

Chain of ganglia close to the cervical spinal cord

Where does the parasympathetic nervous system arise from?

From the cranial spine/brain stem

Edinger-westphal nucleus (in midbrain) → CN III (to ciliary ganglion for pupillary reflex)

Salivatory nuclei (upper medulla) → CN VII (facial nerve) + CN IX (saliva + tears)

Dorsal motor nucleus of vagus + Nucleus ambiguus (cardiac, larynx, pharynx) → CN X (HR, lung constriction)

And from the sacral spine (S1-S5) - intermediate gray zone b/t horns like the sympathetic nervous system - leaves spine to enter pelvic splanchnic nerve to synapse at ciliary ganglion

Regulation of HR

Carotid body (detects blood chemical comp) afferents in CN IX → nucleus of solitary tract

Baroreceptors (sense stretch by heart) afferents also → nucleus of solitary tract

Nucleus of solitary tract → nucleus ambiguus → cardiac plexus → SA node of heart

Also nucleus of solitary tract → preganglionic neurons in sympathetic nervous system → sympathetic chain ganglia → post ganglionic neuron → SA node

To inc/decrease HR/BP

To dec HR,

Carotid body or baroreceptors send APs to nulcues of solitary tract → APs to nucleus ambiguus → release Ach onto cardiac plexus → release Ach onto SA node → dec APs

NEED SYMPATHETIC INHIBITION AT THE SAME TIME

Nucleus of solitary tract → inhibits preganglionic neuron firing → inhibits post ganglionic neuron firing → decreases norepinephrine released onto heart

Regulation of core temp

Thermoreceptors all over body converge at comparator of hypothalamus

Preoptic area of thalamus sends APs to comparator based on set point

Comparator compares APs/sec from preoptic area and thermoreceptors to determine to inc or dec body temp and sends signals to rest of hypothalamus

During fever, pyrogens released by pathogens increase set point in preoptic area

Inc/dec core temp

Lateral + medial preoptic nuclei (anterior hypothalamus) - responsible for heat dissapation

Posterior area of hypothalamus - responsible for heat conservation

When we want to move

Motor cortex plans → sends info to basal ganglia and cerebellum

Basal ganglia and cerebellum send info back to excite the motor cortex enough to send info to motor neurons

Note that motor cortex dampens reflexes

Local circuit neurons

Receive sensory info and integrate w/ lower motor neurons near DRG

Motor neuron pools

Each major muscle = large poll of lower motor neurons coming from spinal cord

Organized spaciotopically - proximal regions more medial in spinal cord and distal regions more lateral in spinal cord

Flexor muscles more dorsal

Extensor muscles more ventral

Innervation

Single motor neuron innervates multiple muscle fibers, but single muscle fiber innervated by only 1 neuron. Lower innervation ratio for more precise mvmt

Eyes, ears: 1:10

Hands: 1:100

Posture: 1:180

Jumping: 1:1-2k

EPPs

Lower (alpha) motor neurons release Ach onto muscle fiber’s nicotinic ach receptor. Large SA in muscle fiber and very large EPSP from Ach

Muscle fiber types

Slow twitch - small forces over long time

Fast fatigue-resistant - large force for a long period, but not as long as slow twitch

Fast fatigable - large, explosive force but tire quickly

Graded recruitment

First recruit slow twitch, then fast fatigue-resistant, then fast fatigable

Slow twitch fibers have the smallest motor neurons (fast fatigable = largest neuron). Same ion channel density, but small neuron has smaller SA so higher R. V=IR, so small I produces large V in smaller neuron, firing AP, but doesn’t produce big enough V to fire AP in large neuron.

Muscle fiber summation

1 AP = 1 twitch. Multiple APs close together = twitches sum together to generate greater force

Unfused tetanus - so many APs, plateau of force, but can see individual twitches

Fused tetanus - so many APs, cannot see individual twitches

Proprioceptors

Sensory afferents give feedback about muscle + joint position

Extra + extrafusal muscle fibers

Extrafusal - produce tension, alpha motor neurons

Intrafusal - run parallel to extrafusal inside, wrapped in Ia spindle afferents

When extrafusal muscle stretches, stretches intrafusal and Ia spindles, generating AP

Ia afferents

Very fast APs, a lot of myelin

Output to lower motor neurons, local circuit neurons, dorsal nucleus of Clarke, somatosensory cortex (not conscious)

How keep arm at same height when pouring liquid?

Contract bicep + conscious initial setting of position

When add weight, extrafusal muscle fibers stretch so intrafusal muscle fibers stretch so Ia afferents send APs to DRG

Ias synapse onto flexor alpha motor neurons and send APs to activate more flexion. Ias also synapse onto inhibitory interneurons that synapse onto extensor alpha motor neurons and inhibit extension.

Gamma motor neurons

Control intrafusal muscle fibers/set tension

Usually contract intrafusal muscle fibers the same as extrafusal

If didn’t contract intrafusal, intrafusal couldn’t be stretched enough to send APs

Tension set up by gamma motor neurons determines threshold for adjustment

Glogi tendon organ

Series element between muscle and tenson

Has Ib afferent neurons + collagen fibrils in capsule

Measures shortening of muscle

Afferent output to same places and Ia neurons.

Does not respond to stretch

Acts in same way as Ia to prevent too much flexion

Nocioceptive reflexes

If step on glass, lift foot up + shift weight reflexively

APs from nociceptors → DRGs → local circuit neurons → excite flexor + inhibit extensor on one side and excite extensor + inhibit flexor on other side to lift up foot and shift weight

Tonic control while walking

Swing/flexion phase and stance/extension phase

When cat spinal cord cut, continues to walk and change pace

Can walk w/out input from brain

Central pattern generators in local spinal circuit that provide involuntary phasic control while walking

Medial motor neurons

Neurons to axial muscles that control posture

Colliculospinal/Tectospinal tract

Involuntary control of neck (turn head to sight/sound)

Superior (vision) + inferior (sound) colliculus (midbrain) → DEUSSATE in midbrain → down cervical spinal cord → branch bilaterally when synapse onto medial motor neuron in cervical spine

Reticulospinal tract

Colliculus → deussate in midbrain → synapse at pontine reticular formation → synapse bilaterally at target alertness/broader posture

Vestibulospinal tract

Begin in lateral and medial vestibular nuclei (medulla and pons) → synapse bilaterally at target → maintaining balance

Anterior/ventral corticospinal tract

Voluntary control of posture

Upper motor neurons in medial motor cortex → internal capsule → cerebral peduncle (midbrain) → pontine fiber bundles (middle pons) → synapse bilaterally (branch bilaterally at pyramidal deussation in spine) at lower motor neuron

Corticorecticulospinal tract

Involuntary, feed-forward posture - shift weight for movement before it happens

Primary motor cortex + medial + lateral premotor cortex → synapse bilaterally at reticular formation → synapse at lower motor neurons bilaterally

Lateral corticospinal tract

Voluntary movement of limbs

Movement planned in medial (internal cues) or lateral (external cues) premotor cortex → primary motor cortex → upper motor neurons → internal capsule → cerebral peduncle (midbrain) → pontine fiber bundles (middle pons) → pyramidal DECUSSATION at caudal medulla → synapse at ventral horn onto lower motor neurons

Motor cotex mapping

Somatotopic mapping like somatosensory cortex

Corticobulb tract

Voluntary face + neck movement

lateral portion of precentral gyrus → primary motor cortex → internal capsule → cerebral peduncle (midbrain) → middle pons →

synapse at contralateral trigeminal motor nucleus of CN V (jaw) or CN VII (face) (middle pons)

OR

pontine fiber bundles → middle medulla → synapse contralaterally at hypoglossal nucleus CN XII (tounge) or CN XI (trapezius + sternocleidomastoid muscles)

Facial expressions tract

Lower face:

Facial representation in primary motor cortex → pons → contralateral facial nucleus → facial nerve (VII)

Upper face:

Both sides of cortex have two paths

1 path: face representation in cingulate motor area → synapse ipsilaterally at facial nucleus

2nd path: face representation in cingulate motor area → synapse contralaterally at facial nerve

So damage on one side won’t affect upper face unless after facial nerve

Targeting limbs in voluntary movement

Small groups of upper motor neurons = many muscle fibers

Encode movement by using multiple lower motor neuron pools, not only one

Ex: money reaching 180 degrees uses 90 degrees, 135, 180, and 275 muscles

Sum multiple vectors to get desired movement

Motor areas

Basic movements use motor + somatosensory cortex

More complex movements add in supplementary motor area

Can also rehearse movement with supplementary motor area only

Basal ganglia

Suppress inappropriate motor programs

= Striatum = putamen (body) + caudate nucleus (head, neck, eyes)

Decides what to suppress from info from frontal association and motor association cortex

Ventral anterior + lateral complex of thalamus (VA/VL)

Relay info to motor cortex

Caudate nucleus

Inputs from multimodal association cortex, frontal lobe, and eye movement areas

Putamen

Inputs from somatosensory, visual, premotor, and motor cortex

Somatotopic mapping

Direct caudate pathway

Caudate → Substantia nigra pars reticulata (SNPR) → superior colliculus (SC)

Direct putamen pathway

Putamen → Globus pallidus internal segment (GPIS) → VA/VL thalamus → motor cortex

Indirect putamen pathway

Putamen → Globus pallidus external segment (GPES) → subthalamic nucleus (SN) → GPIS → VA/VL → motor cortex

Basal ganglia when we don’t want to move

No excitation of striatum → no GABA release onto SNPR or GPIS → SNPR and GPIS active → release GABA onto SC or VA/VL → SC or VA/VL inhibited

Basal ganglia when we do want to move

Excitation of the striatum → GABA release onto SNPR or GPIS → inhibition of SNPR or GPIS → no GABA release onto VA/VL or SC → VA/VL or SC active

Substantia nigra pars compacta (SNPC)

High density of dopaminergic neurons + communicate directly with striatum because cortical inputs alone not large excitement in striatum, need more excitement from SNPC

Acts on D1 and D2 pathway

D1 Pathway

SNPC releases dopamine into excitatory synapses in direct pathway. Increases activity in striatum → more GABA release onto SNPR or GPIS → less GABA release onto VA/VL or SC → more activity

D2 pathway

SNPC releases dopamine onto inhibitory synapses in indirect pathway. Decreases activity in striatum → decreased GABA on GPES → GPES active → GPES releases GABA onto SN → SN not active → does not excite GPIS → no inhibition of unwanted movement

Parkinson’s

Little wanted or unwanted movement

Degeneration of dopadenergic receptors in SNPC

Huntington’s disease

Degradation of striatum neurons onto GPES → can’t inhibit GPES → GPES active → GABA onto SN → SN inactive → GPIS inactive → unwanted movement + poor emotion regulation

How refine + coordinate movement?

Cerebellum integrates sensory info and coordinates precise timing of ongoing mvmt

Cerebellum Input Pathways

Info from primary, pre, and supplementary motor, and somatosensory cortex (to pontine nuclei → deussates and enters through middle peduncle) + info from clarke’s nucleus and cuneate nucleus (through inferior peduncle) to coordinate timing

Info from sensory motor association cortex (to pontine nuclei → deussates and enters through middle peduncle) to refine movement

Info from vestibular nuclei (through inferior peduncle) for balance

Info from inferior olive (through inferior peduncle) for motor learning

Cerebellum output pathways

Out through superior peduncle

To red nucleus to inferior olive or

to VL complex of thalamus to primary + premotor cortex

Motor pathway with cerebellum decussations

Motor cortex → internal capsule → pontine nuclei → DECUSSATE through middle cerebellar peduncle → cerebellum → deep cerebellar nuclei → superior cerebellar peduncle → DECUSSATE → VL complex of thalamus → primary + premotor cortex) → DECUSSATE again before lower motor neurons

Left cerebellum for left movement