Download Chapter 11 Efferent Division: Autonomic and Somatic Motor Control

Chapter 11
Efferent Division:
Autonomic and Somatic Motor Control
Part 2
On Friday, go back to part one and go over slide 50
Some definitions
Endocrine gland
– A ductless gland or a single cell which secretes a
hormone
Exocrine gland
– Releases secretions through a duct
Figure 11-10a The adrenal medulla secretes epinephrine into the blood
Adrenal
gland
Kidney
(a)
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The Adrenal Gland
Adrenal cortex
– Endocrine gland
– Epidermal origin
– Secretes steroid hormones
Adrenal medulla
– The interior or core of the adrenal gland
– Neurosecretory structure
– Developed from same embryological tissue as the
sympathetic neurons
Figure 11-10b The adrenal medulla secretes epinephrine into the blood
Adrenal cortex is a
true endocrine gland.
Adrenal medulla is a
modified sympathetic
ganglion.
(b)
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Adrenal Medulla is a modified sympathetic ganglion
Preganglionic sympathetic neurons project from the
spinal cord to the medulla, where they synapse
The postganglionic neurons lack axons
The axon-less cell bodies (Chromaffin cells), secrete
the neurohormone, epinephrine directly into the blood
In response to alarm signals from the CNS, the
adrenal medulla releases large amounts of
epinephrine as part of the “Fight-or-Flight” response
Figure 11-10c The adrenal medulla secretes epinephrine into the blood
ACh
Spinal cord
Preganglionic
sympathetic
neuron
The chromaffin
cell is a modified
postganglionic
sympathetic
neuron.
(c)
Adrenal medulla
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Epinephrine is a
neurohormone that
enters the blood.
Blood vessel
To target
tissues
Parasympathetic Pathways
Parasympathetic neurons release Acetylcholine at their targets
Parasympathetic neuroeffector junctions have muscarinic
cholinergic receptors
Muscarinic receptors are all G protein-coupled receptors.
Receptor activation initiates second messenger pathways,
some of these open K+ or Ca++ channels
Tissue response varies with receptor subtype (5 subtypes)
Autonomic Agonists and Antagonists
Agonists:
– Molecules which combine with a receptor and
mimic a response
Antagonists:
– One substance opposes the action of another
Autonomic Agonists and Antagonists
Direct agonist or antagonist
– Combine with the target receptor
– Mimic or block neurotransmitter action
Indirect agonists and antagonists
– These act by altering
– Secretion of neurotransmitters
– Re-uptake of neurotransmitters
– Degradation of neurotransmitters
Examples of Autonomic Agonists and Antagonists
Cocaine
– An indirect agonist
– Blocks re-uptake of NE into adrenergic nerve
terminals; extends NE's excitatory effect
Anticholinesterases
– Includes the organophosphate insecticides
(parathion and malathion)
– Cholinesterase inhibitors
– Indirect agonists
– Block ACh degradation
– Extends the active life of each ACh molecule
Examples of Autonomic Agonists and Antagonists
Once alpha and beta adrenergic receptors had been
discovered, drugs were designed to block specific
ones:
Tamsulosin (Flomax) blocks alpha-1A adrenergic
receptors
Beta blockers are antagonists for Beta adrenergic
receptors
– Used to treat high blood pressure
Table 11-3
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Autonomic Nervous System Summary
P. 396, Summary of Sympathetic and Parasympathetic
branches
P. 397, Figure 11-11 Summary of Efferent Pathways
(next slide)
Table 11-4: Comparison of Sympathetic and
Parasympathetic Branches
Table 11-5: Comparison of Somatic and Autonomic
Branches
Figure 11-11, overview
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Table 11-4
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Table 11-5
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The Somatic Motor Division
Somatic motor pathways
– Control skeletal muscles
– Consists of a single neuron which originates in the
CNS
– The target is ALWAYS a skeletal muscle
– Somatic pathways are always excitatory
Figure 11-11 Summary of efferent pathways
SOMATIC MOTOR
PATHWAY
CNS
Parasympathetic
pathway
AUTONOMIC PATHWAYS
Sympathetic
pathways
CNS
CNS
Adrenal sympathetic
pathway
CNS
ACh
Adrenal
cortex
Nicotinic
receptor
Adrenal
medulla
Ganglia
E
ACh
Ganglion
Nicotinic
receptor
α receptor
NE
ACh
Muscarinic
receptor
Autonomic effectors:
• Smooth and cardiac muscles
• Some endocrine and exocrine
glands
• Some adipose tissue
Blood vessel
β 1 receptor
E
ACh
Nicotinic receptor
Skeletal
muscle
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β2
receptor
KEY
ACh = acetylcholine
E
= epinephrine
NE = norepinephrine
The Somatic Motor Division
Somatic motor pathways
– Cell bodies of somatic motor neurons are located
in either
• Ventral horn of spinal cord
• or
• The brain
The myelinated axons of these pathways may be a
meter or more long
– Examples: those that innervate the muscles of the
hand and the foot
Somatic motor neurons branch close to their targets
Each branch divides into a cluster of enlarged axon
terminals that lie on the surface of the skeletal muscle
fiber
This arrangement allows a single motor neuron to
control many muscle fibers at one time
Neuromuscular Junction (NMJ):
– The synapse of a somatic motor neuron + a
muscle fiber
Figure 11-12, part 1
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Neuromuscular Junction (NMJ)
3 main components to the NMJ
1. Motor neuron's presynaptic axon terminal
2. Synaptic Cleft
3. Postsynaptic membrane of the skeletal muscle fiber
Neuromuscular Junction (NMJ)
Also at the NMJ are Schwann cell extensions which
cover the axon terminals
Once thought that this was just additional insulation to
speed up the conduction of the AP
Now we know that that the Schwann cells secrete a
variety of chemical signal molecules
These chemicals play a vital role in the formation and
maintenance of the NMJ
Neuromuscular Junction (NMJ): Postsynaptic side
Motor End Plate
– The muscle cell membrane is modified into a
series of folds that look like shallow gutters
– Along the upper edge of each gutter, there is an
active zone filled with nicotinic ACh receptor
channels (nAChR)
Figure 11-12, part 2
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Figure 11-12, part 3
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Neuromuscular Junction (NMJ): Postsynaptic side
Motor End Plate (continued)
– Synaptic cleft is filled with a fibrous (collagen
matrix)
• Holds the motor end plate and axon terminal in
alignment
• Matrix also contains acetylcholinesterase which
rapidly deactivates ACh by degrading it into
acetyl and choline
Neuromuscular Junction (NMJ): Receptors
An AP arriving at the axon terminal will cause voltagegated CA++ channels to open
Calcium ion diffuses into the cell and triggers the
release of ACh which then diffuses across the synaptic
cleft
On the other side of the synaptic cleft, ACh binds with
a nicotinic receptor channel (nAChR) on the skeletal
muscle membrane
Figure 11-13a
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The nAChR channels of skeletal muscle are similar to
but not identical to the nicotinic ACh receptors found
on neurons
Their differences are highlighted by the snake toxin
alpha-bungarotoxin:
– This toxin binds to nicotinic skeletal muscle
receptors, but not to similar receptors in the
autonomic ganglia
Both muscle and neuronal receptor proteins have five
subunits encircling a central pore, but the SUBUNITS
in each receptor type are DIFFERENT
Nicotinic cholinergic receptors are chemically gated
ion channels
They have 2 binding sites for ACh
When ACh binds, the gate opens and allows
monovalent cations to flow through
In skeletal muscle, the monovalent cation is Na+
Figure 11-13b Events at the neuromuscular junction
Open channel
Closed channel
ACh
Na+
K+
(b)
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K+
Na+
Na+ entry into the muscle fiber depolarizes it,
triggering an AP which causes contraction of the
skeletal muscle cell
Acetylcholine acting on the skeletal muscle motor end
plate is always excitatory and always causes muscle
contraction
There is no antagonistic innervation to relax the
muscle
Relaxation occurs when somatic motor neurons are
inhibited by the CNS