1. Divisions of the nervous system
CNS
PNS
EFFERENT
AFFERENT
Somatic
ANS
Somatic
Visceral
Skeletal
muscle
-voluntary
Cardiac &
smooth muscles
Glands
-involuntary
Skeletal
muscle, tendons
joints
Cardiac &
smooth muscles
Glands

2. PNS Terminology Ganglia – neuron cell bodies
Peripheral nerves – neuronal axons
PNS neuroglia
Satellite cells
Enclose neuron cell bodies in ganglia
Schwann cells
Cover peripheral axons

3. Efferent Division of the PNS
the somatic nervous system and part of the autonomic nervous system
the somatic – control of skeletal muscle
the ANS – involuntary control over cardiac and smooth muscle + gland secretion

4. -cranial nerves – 12 pairs
I - Olfactory
II - Optic
III - Oculomotor
IV-Trochlear
V - Trigeminal
VI - Abducens
VII - Facial
VIII - Acoustic
IX - Glossopharyngeal
X - Vagus
XI - Accessory
XII - Hypoglossal
-cranial nerves – 12 pairs
-considered part of the peripheral nervous system (PNS)
-olfactory & optic contain only sensory axons = sensory nerves
-remaining are motor or mixed nerves (both motor and sensory axons)

5. Spinal Nerve
after passing through intervertebral foramina the spinal nerve branches = ramus/rami
Dorsal ramus
Sensory/motor innervation to skin and muscles of back
Ventral ramus
-Ventrolateral body surface, body wall structures, muscles of the upper and lower limbs
in addition to these rami - the spinal nerves also give off a meningeal branch - reenters the vertebral canal and supplies the vertebrae, vertebral ligaments and meninges

6. rami communicantes = branches from the spinal nerve
-defined as a connection between a spinal nerve and the sympathetic trunk of the ANS
-two types:
gray rami communicantes – unmyelinated post-ganglionic axons
white rami communicantes – myelinated preganglionic axons
sympathetic trunk

7. Somatic Nervous System
considered the voluntary aspect of the PNS
but the muscles of posture and balance are controlled involuntarily by the lower brain centers (brain stem, cerebellum)
cell bodies located in the ventral gray horn of the spinal cord
the axon of a motor neuron extends from the CNS continuously to its skeletal muscle target
ANS usually requires two neurons
terminals release acetylcholine – contraction
can only stimulate its target
whereas the ANS can either stimulate or inhibit its target

8. Somatic Nervous System
- somatic/motor
commands emerge from
the ventral horn and travel
through the:
dorsal ramus to target the muscles of the back
ventral ramus to target the muscles of the limps and body wall

9. Somatic Nervous System
motor neurons receive incoming information from many converging presynaptic neurons
both excitatory and inhibitory on these motor neurons
some information are part of reflexes originating in the spinal cord
other information can come in from areas of the brain via the descending white matter tracts
motor areas of the cerebral cortex, the basal nuclei and the cerebellum
synapse with the motor neurons in the ventral horn and regulate their activity
activation – impulse sent to muscles
inhibition – no impulse, no contraction
level of activity of a motor neuron is the balance between the EPSPs/activation and the IPSPs/inhibition of the incoming synapsing neurons
therefore motor neurons are considered the final common pathway
considered the only way any other part of the nervous system can influence muscle activity

10. Somatic Motor pathways
all excitatory and inhibitory signals that control movement converge on the motor neurons that extend from the brain stem and SC to innervate the skeletal muscles
called lower motor neurons (LMNs)
have their cell bodies in the brain stem and SC (anterior gray horn)
their axons extend through the cranial and spinal nerves to skeletal muscle
only LMNs provide output from the CNS to skeletal muscle fibers = final common pathway
damage to the LMNs produces flaccid paralysis on the same side as the damage – loss of reflex action, motor tone and voluntary contraction
neurons in four distinct circuits control movement by providing input to these LMNs
1. local circuit neurons
2. upper motor neurons (UMNs)
3. basal ganglial neurons
4. cerebellar neurons

11. Somatic Motor pathways
1. local circuit
input arrives at LMNs from nearby interneurons called local circuit neurons
receive input from somatic sensory receptors and higher centers of the brain
help coordinate rhythmic activities in muscle groups
2. UMNs
Interneurons that provide input to the local circuit and LMNs
essential for planning, initiating and directing sequences of voluntary movements
extend from the brain to the LMNs via two types of somatic motor pathways
1. direct motor pathways: nerve impulses for precise voluntary movement
lateral corticospinal, anterior corticospinal and corticobulbar
cell bodies are located in motor cortex and travel down the spinal cord (corticospinal tracts) or through the brain stem (corticobulbar)
about 90% decussate within the medulla oblongata (lateral corticospinal)
2. indirect motor pathways: or extrapyramidal pathways
nerve impulses follow complicated circuits that involve the cortex, basal ganglia, thalamus and brain stem

12. Somatic Motor pathways
3. Basal ganglia
assist movement by providing input to the UMNs
also suppresses unwanted movements by inhibiting thalmic activity
the production of dopamine by the substantia nigra also effects muscle tone
major pathway (cortex – basal ganglia – thalamus – cortex – UMN - LMN)
Globus pallidus and substantia nigra involved
this circuit may function in initiating and terminating movements
caudate nucleus and putamen receive imput from sensory, association and motor areas of the cortex and from the substantia nigra
UMNs of this pathway form the reticulospinal, rubrospinal and vestibulospinal tracts
4. Cerebellar
function involves four activities
1. monitoring intentions for movement
2. monitoring actual movement
3. comparing the command (intention and movement) with sensory information
4. provides correction – to UMNs
travels via the thalamus to the UMNs in the cerebral cortex
or can go directly to the UMNs that originate in the brain stem

13. Medical application: Lou Gehrig’s Disease
-Amyotrophic lateral sclerosis: Lou Gehrig’s disease
-unknown cause
-attacks motor areas of the cortex, axons of motor neurons
in the spinal cord and motor neuron cell bodies
-muscle weakness and atrophy
-begins in regions of the SC that affect hands and arms and
then spreads
-specific destruction of the axons of UMNs in the corticospinal (direct UMN)
and rubrospinal (indirect UMN) tracts plus the cell bodies of LMNs
-about 15% of cases are inherited = familial ALS
-non-inherited cases have implicating factors
-buildup in the synaptic cleft of the NT glutamate – released by
motor neurons because the gene controlling the recycling of this
NT is mutated
-excess glutamate causes motor neuron malfunction and death
-drug – riluzole – may help by reducing damage to these neurons
by decreasing glutamate concentration
-also roles for free radicals, autoimmune, viral infections???

14. The Neuromuscular Junction
end of neuron (synaptic terminal or axon bulb) in very close association
with a muscle fiber/cell
distance between the bulb and the folded sarcolemma = synaptic cleft
nerve impulse leads to release of neurotransmitter (acetylcholine)
this release will result in activation of the muscle cell and contraction
therefore the NMJ is ALWAYS excitatory
the only way inhibition can take place is through the inhibition of the neuron “connecting” with the muscle

15. Medical Application black widow botulism curare myasthenia gravis
triggers an explosive release of ACh
also at other sites other than the NMJ (i.e. neurons that release ACh = cholinergic neurons)
prolonged depolarization of target
paralysis of the diaphragm – respiratory failure
botulism
blocks release of ACh from the neuron at the NMJ
from Clostridium botulinum bacteria – toxin
death due to respiratory failure
curare
reversibly binds to the muscle cell
but doesn’t trigger the opening of Na channels – no contraction
ACh antagonist
myasthenia gravis
disease of the NMJ - autoimmune
extreme muscle weakness
antibodies are produced against the AcH receptors at the NMJ (sodium channel)
so AcH cannot bind to the muscle cell and trigger a contraction
as a result Acetylcholinesterase destroys the released AcH before it has a chance to interact at the NMJ
treatment – neostigmine – AchE inhibitor
this temporarily increasing the chance ACh can find and bind its receptor at the NMJ – Na influx etc….. contraction

16. Motor Units Each skeletal fiber has only ONE NMJ
MU = Somatic neuron + all the skeletal muscle fibers it innervates
Number and size indicate precision of muscle control
Muscle twitch
Single momentary contraction
Response to a single stimulus
All-or-none theory
Either contracts completely or not at all
Motor units in a whole muscle fire asynchronously
some fibers are active others are relaxed
delays muscle fatigue so contraction can be sustained
Muscle fibers of different motor units are intermingled so that net distribution of force applied to the tendon remains constant even when individual muscle groups cycle between contraction and relaxation.

17. ANS involuntary motor commands and sensory information
supplies cardiac and smooth muscle, glands (i.e. viscera)
comprised of two neurons
preganglionic and postganglionic
preganglionic synapses with the cell body of the postganglionic within the ganglion
therefore the collection of their cell bodies forms the ganglion itself!!!
the pregang and postgang neurotransmitters can differ
the postganglionic neuron is unmyelinated

18. ANS two divisions that innervate the same organs
efferent branch regulates “visceral” activities (motor commands, involuntary, organs)
also has an afferent branch that receives sensory information from these areas – called the visceral division of the CNS

20. Parasympathetic Division
cell bodies of the preG neurons are located in the four cranial nerves III, VII, IX and X (brain stem) and in the lateral gray horns of the sacral spinal nerves 2 through 4
emerge as part of the cranial or spinal nerve
parasympathetic ganglia: called terminal ganglia
located close to the wall of a visceral organ
the preG fibers are very long because they must extend from the CNS to an organ
synapse with postG within the terminal ganglia
four major TGs – located close to the organ they innervate
otic, submandibular, pterygopalatine, ciliary

21. Sympathetic Division
cell bodies of the preG neurons are located in the lateral gray horns of T1 to L2
sympathetic ganglia
site of the synapse between the preG and postG neurons
two groups:
1. sympathetic trunk ganglia:
-vertical row lateral to the vertebral column
-short preG lead into these ganglia
-3 cervical, 11 or 12 thoracic, 4 or 5 lumbar and 4 or 5 sacral
-3 cervical have specific names (superior, middle, inferior)
2. prevertebral ganglia:
-close to the large abdominal arteries
-postG neurons innervate the abdominal organs
-three major prevertebral ganglia: celiac, superior mesenteric and inferior mesenteric
axons exit the lateral gray horn through the ventral (anterior) root of the thoracic spinal nerve along with somatic motor nerve axons
and parasympathetic preG axons
form part of the spinal nerve
they then enter a white rami communicantes and pass to the nearest sympathetic trunk ganglion– visceral motor commands
celiac
ganglion
*** whether it is sympathetic or parasympathetic – the preG neurons release AcH

22. Sympathetic Dominance
fight or flight
protective response
elevated heart rate, blood pressure, respiration rate
increase blood flow to skeletal muscles, lungs, heart, brain
decrease blood flow to digestive, reproductive and urinary organs

23. Parasympathetic Dominance
“rest and digest” response
dominates in quiet, stress-free situations
resets the system after sympathetic stimulation
e.g. slow the heart rate and lower blood pressure

24. ANS Neurotransmitters
specific neurons release specific NTs – have distinct names
cholinergic neurons and AcH
include all preG neurons from sympathetic and parasympathetic neurons
sympathetic postG that innervate the sweat glands
all parasympathetic postG neurons
two types of receptors
1. nicotinic
2. muscarinic
adrenergic neurons and NE
most sympathetic postG
1. alpha – a1 and a2
2. beta – b1 and b2 and b3

25. ANS receptors
the NTs released by the ANS can either stimulate or inhibit its target – depends on the receptors located in the target
1. Cholinergic receptors – respond to AcH
a. nicotinic – named because they are activated by nicotine
found in the ganglia of the symp. and parasymp. division (all ANS ganglia)
respond to AcH release from symp and parasymp preG fibers
binding opens channels for the movement of Na and K
more Na enters the target neurons within the ganglion – depolarization and initiation of an AP by the postG neurons
nicotinic R
muscarinic R
adrenergic R

26. b. muscarinic receptors
can bind either Ach or muscarene (Amanita muscaria mushroom)
expressed on tissues “downstream” of post-ganglionic neurons – at the target tissue
e.g. neuromuscular junction (ligand-gated sodium channel)
nicotinic R
muscarinic R
adrenergic R

27. 2. Adrenergic receptors – respond to NE/Epi
alpha and beta classes – a1, a2, b1, b2, b3
distributed in a specific pattern and respond to either NE or Epi or both
respond to activation by activating G proteins -> second messangers (cAMP or Ca)
therefore they are called G protein coupled receptors
nicotinic R
muscarinic R
adrenergic R

28. Somatic
ANS

29. Reflex arc
Neural “wiring” of reflex
Requires 5 functional components: 1. sensory receptor, 2. sensory neuron, 3. intergrating center (SC or BS), 4. motor neuron, & 5. effector

30. Classification of Reflexes
By development
Innate, acquired
Where information is processed
Spinal, cranial
Motor response
Somatic, visceral
Complexity of neural circuit
Monosynaptic

31. Stretch reflex is monosynaptic - causes contraction in response to stretch
Regulates skeletal muscle length and tone
all monosynaptic reflexes are ipsilateral reflexes - input and output on same side
only one synapse in the CNS - between ad single sensory and motor neuron
Sensory receptors are found in muscle spindles
e.g. Patellar reflex – muscle spindles in the quadriceps muscles, hit with a mallet stretches the quadriceps and its tendon - results in contraction
Spinal Reflexes

32. Spinal Reflexes Tendon reflexes - polysynaptic
controls muscle tension by causing muscle relaxation before muscle contraction rips tendons
Generally polysynaptic - more than one CNS synapse involved between more than two different neurons
sensory synapses with 2 interneurons - one inhibitory IN synapses with motor neurons and causes inhibition and relaxation of one set of muscles, the other stimulatory IN synapses with motor neurons and causes contraction of the antagonistic muscle

33. withdrawl crossed extensor
-Postural reflexes - maintain upright position
e.g flexor (withdrawl) reflex - polysynaptic
sensory input -> interneuron -> motor neuron which contracts muscles and pulls limb away
PLUS synapses with motor neurons in adjacent SC segments -> contracts muscle
known as an intersegmental reflex arc
IN ADDITION - the sensory input can cross to the other side of the SC (via the gray commisure) where it synapses with and interneuron and motor neuron to contract the antagonistic muscle group and maintains balance = Intersegmental and Crossed extensor reflexes involved
withdrawl
crossed
extensor

34. Reflexes – Laboratory Exercise
achilles tendon
also called the ankle-jerk reflex
occurs when the Achilles tendon is tapped while the foot is dorsi-flexed – results in plantar flexion (pointing of toes)
checks if the S1 and S2 nerve roots are intact
Absence: sciatic nerve pathology or disc herniations at L5-S1 level.
Diminshed: hypothyroidism or peripheral neuropathy
patellar tendon
also called knee jerk reflex
deep tendon or stretch reflex
tests the function of the femoral nerve and spinal cord segments L2-L4.
Absence or decrease of this reflex is known as Westphal's sign
receptor damage, peripheral nerve disease, involving the dorsal(sensory) columns of the spinal cord
cerebellar lesions
lesions present within the motor cortex of the brain
complete interruption of sensory and/or motor impulse transmission in the femoral nerve
is often known as a characteristic finding in tabes dorsalis, a type of neuro-syphilis
triceps
elicits involuntary contraction of the triceps brachii muscle
initiated by the Cervical spinal nerve 7 nerve root
tested as part of the neurologica examination to assess the sensory and motor pathways within the C7 and C8 spinal nerves.
Absence: essential to try again with reinforcement, with the patient clenching his or her teeth just as the reflex hammer strikes.
Hyper-reflexia: Indicates a potential upper motor neuron lesion.

35. biceps:
examines the function of the C5 reflex arc and to a lesser degree the C6 reflex arc
activates the stretch receptors inside the biceps brachii muscle which communicates mainly with the C5 spinal nerve and partially with the C6 spinal nerve
induces a reflex contraction of the biceps muscle and jerk of the forearm
strong contraction = 'Brisk' reflex = lesion of upper motor neuron
absent reflex = 'diminished‘ reflex = lower motor neuroe lesions.
change to the biceps reflex indicates pathology at the level of C5/6 or at some point above it in the spinal cord or brain
Babinski
Joseph Babinski
identifies disease of the spinal cord and brain
also exists as a primitive reflex in infants. When non-pathological it is
Babinski's sign refers to its pathological form
three responses possible:
Flexion: the toes curve inward and the foot everts - seen in healthy adults.
Indifferent: there is no response.
Extension of the hallux other toes fan out - the Babinski's sign indicating damage to the central nervous system (usually a lesion on a neuron or neurons)
BUT: Babinski response is normal while asleep and after a long period of walking.