Download PNS Terminology

Divisions of the nervous system
CNS
PNS
EFFERENT
Somatic
Skeletal
muscle
-voluntary
ANS
Cardiac &
smooth muscles
Glands
-involuntary
AFFERENT
Somatic
Visceral
Cardiac &
Skeletal
muscle, tendons smooth muscles
Glands
joints
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
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
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)
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
• rami communicantes = branches from
the spinal nerve
-defined as a connection between a spinal
nerve and the sympathetic trunk of
the ANS
-two types:
1. gray rami communicantes –
unmyelinated post-ganglionic axons
2. white rami communicantes –
myelinated preganglionic axons
sympathetic trunk
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
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
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
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
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1. local circuit neurons
2. upper motor neurons (UMNs)
3. basal ganglial neurons
4. cerebellar neurons
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•
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
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
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???
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
http://www.blackwellpublishing.com/matthews/neurotrans.html
Medical Application
•
black widow
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botulism
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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
blocks release of ACh from the neuron at the NMJ
from Clostridium botulinum bacteria – toxin
death due to respiratory failure
curare
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reversibly binds to the muscle cell
but doesn’t trigger the opening of Na channels – no contraction
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ACh antagonist
myasthenia gravis
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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
Motor Units
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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.
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
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
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
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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
Sympathetic Division
celiac
ganglion
*** whether it is sympathetic or
parasympathetic – the preG
neurons release AcH
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
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
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
– two types of receptors
• 1. alpha – a1 and a2
• 2. beta – b1 and b2 and b3
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
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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
adrenergic R
nicotinic R
muscarinic R
• 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)
adrenergic R
nicotinic R
muscarinic R
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
adrenergic R
nicotinic R
muscarinic R
• Somatic
• ANS
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
• By development
– Innate, acquired
• Where information is processed
– Spinal, cranial
• Motor response
– Somatic, visceral
• Complexity of neural circuit
– Monosynaptic
Classification of
Reflexes
• 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
•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
Spinal
Reflexes
-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
Reflexes – Laboratory Exercise
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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
– deep tendon or stretch reflex
– 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.
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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
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Babinski
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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.