Parts of the Nervous System

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Neuroscience and Mental Health · S Tran
Session 1: Neurological Disorders and
their Main Causes
Learning Objectives
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Define the following terms used to describe the Nervous System and explain
how they interact with each other:
Central Nervous System
Peripheral Nervous System
Autonomic nervous System
Somatic Nervous System
List the major causes of neurological disorders and give examples.
State the difference in the regenerative capacity of injured axons between the
CNS and PNS.
Describe the main components of a standard neurological examination.
Outline the main electrophysiological and imaging techniques used in
neurological diagnosis, noting the main advantages and disadvantages.
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Parts of the Nervous System
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Central Nervous System = Brain + Spinal Cord
o ‘Housekeeping’ Functions. – Processing sensory + motor information
o Supports higher functions: perceptions, cognition, emotion & memory.
Peripheral Nervous System = Peripheral nerves + Ganglia
o Provides sensory & motor innervations to the body
Autonomic Nervous System = parts of the CNS + PNS.
o Controls visceral function & homeostasis e.g. peristalsis & bladder release
o Internal organs, blood vessels, glands, eye structures, genitalia.
Somatic Nervous System
o Controls motor and sensory function for body wall
Causes of Neurological Disorders:
A. Trauma
o Spinal Cord Injury
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Can cause paralysis
B. Cerebrovascular Accident
o Cerbrovascular Infarct / Stroke
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Degeneration of neural tissue as no backup energy reserves like muscle
C. Neoplasia
o Meningioma
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Pressure is an issue
Normally metastasis,
If primary then it’s normally connective tissue or glial
D. Infection
o Bacterial Meningitis
E. Metabolic Disorders
o Diabetic Neuropathy e.g. Hypoglyceamia
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Can result in comas
In peripheral nerves  Injury  tingling sensation
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Neuroscience and Mental Health · S Tran
F. Genetic Defects
o Huntington’s Disease
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Degeneration of caudate and putamen nuclei
Basal gangular are for movement
o Down’s syndrome
G. Environmental
o Heavy Metal encepholopathies e.g. Lead Poisioning
o Alcohol  fetal alcohol syndrome
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? Mobile Phones
Recreation Drugs etc
H. Immunological
o Multiple Sclerosis
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Degeneration of
neurones
Differences in regeneration
capacity of the NS
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No replacement of neurones
No axonal regeneration of CNS
High energy requirement – Low
Energy Reserves
Little space inside the cranial cavity
In PNS, Regeneration may be
functionally compromised
In CNS, regeneration is limited in
distance therefore not viable
Investigations
Neurological Examination
1. Level of consciousness
o Glasgow Coma Scale
2. Speech
o Talking to patient
3. Mental state and cognitive function
o Simple general knowledge/mathematical
questions
4. Sensory function
o Pain, temperature, pressure and position tested
5. Motor function
o Twichage, feet touch, evaluation of strength of
muscle groups
6. Cranial nerve function
o Eyelid strength, facial movement, gag reflex,
smell, taste, hearing
Electrophysiology:
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EEG: Electroencephalography measures the electrical potentials measured at scalp of
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underlying neurones Epilepsy & Coma.
EMG: Electromyography examines integrity of muscles e.g. motor neurone disease
NCS: Nerve Conduction Studies examines integrity of peripherphal nerves & lower motor
neurones
Imaging
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CT: Computerised Tomography uses x-ray sources. Shows hard tissue. Can’t be used too
often. Cheap and Quick.
MRI: Magnetic Resonance Imaging is based on the behaviour of hydrogen protons to a
externally applied magnetic field. Use for soft tissue differentiation. Time consuming. Can be
used to give a functioning image: Functional MRI.
Angiography demonstrates cerebral vessels radiographically after a contrast medium
injection.
Neuronal Dysfunction and Death
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Neuronal Dysfunction = Epilepsy (abnormal synchronous firing)
Neuronal Death = Parkinson’s disease
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Neuroscience and Mental Health · S Tran
Session 2: Cells of the NS
Learning Objectives
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Draw and label a diagram of a typical neuron, identifying soma, dendrites, axon and
terminals.
Define the role of each cellular component in the specialised function of the neuron.
Outline the organisation and functions of intracellular transport in the neuron.
Define the functional subtypes of neurons and list the ways in which they are organised
collectively in the nervous system.
Describe the organisation of synapses.
Name the main classes of neuroglia and explain their functions in the nervous system.
Structure of a Neuron
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Axon – Long extension of a neuron that carries nerve impulses away from the body of the cell.
Axon Terminals - The hair-like ends of the axon
Cell Body/Soma - The cell body of the neuron; it contains the nucleus
Dendrites - The branching structure of a neuron that receives messages on the Soma.
Myelin Sheath - The fatty substance that surrounds and protects some nerve fibers
Node of Ranvier – Gaps in the myelin sheath, allows salutatory conduction to occur
Nucleus - Organelle in the cell body of the neuron that contains the genetic material of the cell
Schwann's Cells - Cells that produce myelin - they are located within the myelin sheath.
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Function of parts of the Neuron
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The neuron is the basic structural and functional unit of the nervous system, it is the
information processing unit, responsible for the generation and conduction of the electrical
signals
Neurons communicate with one another via chemicals released at the synapse.
(neurotransmitters)
Neurons are supported by neuroglia, comprising of several different cell types. (NB.
Neuroglia outnumber neurons by approx. 9:1)
A. Cell Body (Soma)
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Metabolic centre of the cell
Large nucleus with prominent nucleolus due to large amounts of mRNA
Abundant rough ER – protein synthesis
Well developed Golgi
Large number of mitochondria – for the generation of electric impulse
Numerous lysosomes
Highly organised cytoskeleton – because they can be quite long cells
Highly organised metabolically active cell.
B. Dendrites.
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Major area of reception of incoming information
Spread from the cell body and branch frequently
Greatly increase the surface area of the neuron.
Dendritic spines receive majority of synapses (spines = protrusions on the dendrites)
Large pyramidal neurons may have as many as 30,000/40,000 spines
C. Axon.
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Conducts impulses away from the cell body
Emerges as the axon hillock
Action potential generated at hillock
Usually only one axon per cell but can branch extensively
Microtubules and neurofilaments are prominent
Myelinated or unmyelinated
Axon membrane exposed only at nodes of Ranvier.
D. Terminals.
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Close to the target the axon forms a number of terminal branches (terminal arbor).
Specialised structures called synaptic terminals.
Boutons or varicosities
E. Neuronal cytoskeleton.
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In the human adult axons range in length from micrometers to up to a meter
Highly organised cytoskeleton is required
Neurofilaments play a critical role in determining axon calibre
Microtubules are very abundant in the nervous system
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Intracellular Transport in a Neuron
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Axonal transport is the process by which the neuron replenishes components of the axon
and the nerve terminal. Axonal membrane is constantly being replaced by new components
arriving from the cell body as are the macromolecular components of the nerve terminal
needed for synaptic transmission.
Anterograde transport - transport of materials needed for neurotransmission and survival
away from cell body.
A. Fast Anterograde
a. synaptic vesicles, transmitters, mitochondria
b. 400mm/day
c. uses microtubular network and requires oxidative metabolism
d. uses specific molecular motors
B. Slow Anterograde
a. delivery of cytoskeletal and cytoplasmic constituents (via bulk
cytoplasmic flow of cytoplasmic constituents
Retrograde transport - The process by which material returns from the terminals to the cell
body either for degradation or recycle.
a. transport rate approx. 200mm/day
b. transport of substance from extracellular space
c. trophic growth factors, neurotropic viruses
d. uses different molecular motors
e. Particles are driven along microtubules by a microtubule-associated ATPase –
dynein
f. The composition of the material is similar to that of the anterograde fast
component and is packaged in large membrane-bound organelles
Morphological subtypes of neurons
A. Pseudounipolar Neurons
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Dorsal root ganglia sensory neurons have two fused processes and both axonal in structure.
DRG neurons give rise to no dendrites and receive no synapses
single axon acts as a continuous cable carrying action potentials from the peripheral
receptor organ to the central terminal in the spinal cord without passing through the cell
body
found in the spinal cord ganglia
B. Bipolar neurons
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Cerebral cortex, retina.
Bipolar neurons of the retina have one dendritic process and an axon coming off the cell
body
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C. Golgi type I multipolar neurons
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D.
Highly branched dendritic trees
Cells whose axons extend long distances
Pyramidal cells of the cerebral cortex
All of the cortical output is mediated through pyramidal neurons which are the major
excitatory neurons
Pyramidal cells can be subdivided into numerous classes based on morphology, laminar
location and connectivity
Purkinje cells of the cerebellum
Anterior horn cells of the spinal cord
Golgi type II multipolar neurons – highly branched dendritic trees
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Cells with short axons terminating quite close to the cell body of origin.
Stellate cells of the cerebral cortex and cerebellum
Spiny stellate cells represent the other major excitatory input to cortical pyramidal cells
Small multipolar cells with local dendritic and axonal arborizations
use glutamate or aspartate as transmitter.
(NB. multipolar, meaning they have more than two cell processes with only one being an
axon and the remaining processes being dendrites)
Functional subtypes of neurons
A. Sensory neurons
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Commonly pseudounipolar with one major process which divides into two branches, one
running to the CNS and one to a sensory receptor.
Conduct impulses from sensory receptors to the spinal cord and brain.
Dorsal root ganglia neurons.
B. Motor neurons
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Conduct impulses from the brain and spinal cord to effectors - muscles and glands.
Generally multipolar with large cell body.
Spinal motor neurons.
C. Interneurons (vast majority)
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Neurons whose cell bodies and processes remain within the CNS.
Majority of neurons in the CNS.
Can be large multipolar neurons or small bipolar local circuit neurons.
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Interneurons are responsible for the modification, coordination, integration, facilitation and
inhibition that must occur between sensory input and motor output.
Functional Organisation (Groups) of Neurons
1. Nucleus
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Group of encapsulated neuronal cell bodies within the CNS
Usually consist of functionally similar cells
o E.g. brain stem nuclei and deep cerebellar nuclei
2. Laminae
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Layers of neurons of similar type and function
o E.g. cerebral cortex and cerebellum
3. Ganglion
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groups of neuronal cell bodies in the peripheral nervous system and encapsulated to
form a ganglion
o E.g. dorsal root ganglia and sympathetic ganglia
4. Fibre Tracts
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Groups or bundles of axons (mixture of myelinated and unmyelinated) in the CNS
White matter tracts
o e.g. corpus callosum- links the right hemisphere of brain to the left side
5. Nerves
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Discrete bundles of axons outside the CNS (exceptions)
Often mixed sensory/motor
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Terminal portions of axons form synapses onto other neurons allowing communication through
chemical transmitters.
There is a diversity of chemical transmitters
Neurons receive multiple synaptic inputs.
Competing inputs are integrated in the postsynaptic neuron.
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Synapses
 Axo-dendritic (on the dendrites) - these are
often excitatory
 Axo-somatic (on the cell body) - these are
often inhibitory
 Axo-axonic (terminating on the axon at either
the hillock or the terminal) – ? Modulatory
 Gray’s type I synapses – vesicles clear and
rounded excitatory
 Gray’s type II synapses- vesicles oval or
flattened – inhibitory
Neuroglia
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Support cells of CNS (glia=glue) Important for neuron function.
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A. Astroglia (astrocytes)
a. Structure:
o Largest population (numberwise) in the CNS
o Divided morphologically into:
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Fibrous astrocytes
ii.
Protoplasmic astrocytes
iii.
Radial Glia
o Intimate association with blood vessesl, ventricle, leptomeninges, neuronal soma,
synpases & nodes of Ranvier.
o Most prominent cytoplasmic component is numerous intermediate filament bundles
o Gap junctions
b. Function:
i. Scaffold for other cell types
ii. Formation of the blood brain barrier & brain-CSF barrier via endfeet.
iii. Transporting substances between the circulation and neurons
iv. Removal & degeneration of neurotransmitters
v. K+ Buffering
vi. Release of Neuotrophic factors
vii. Repond to injury by dividng, migrating into areas of injury – Scar formation.
viii. Glioma Formation
B. Oligodendroglia (oligodendrocytes)
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Myelin forming cells in CNS
Interfascicular olgodendroglia – found in axon tracts
Sometimes found in association with neuronal cell bodies
a. Structure:
o Nuclei are small & spherical
o Few thin processes
o Prominent Golgi
o No Intermediate filament
b. Function:
i. Elaboration & maintainence of myelin sheath
ii. One oligodenroglia is capable of producing numerous
myelin internodes (~40)
iii. Up to 50 myelin lamellae are common
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iv. Dark and light bands seen at EM
v. Olgodendroglia are very susceptible to nutritional state, toxins and infection
vi. Meylin disease states – diasterous neurological consequence e.g. Multiple
Sclerosis, Adenoleucodystrophy
C. Microglia Cells
a. Structure:
o Derived during early development from blood monocytes that invaded the brain.
o Dense lysosomes, lipid droplets & residual bodies  phagocytosing cells.
b. Function:
i. Phagocytoses of foreign material
ii. Antigen-presenting cells
iii. Widespread network throughout the brain
iv. Role in tissue modelling
v. Synapse stripping.
D. Ependymal Cells
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Epithelial type cells, which line the ventricle & central canal of the cord
Apical microvilli & cilia
Prominent gap junctions between ependymal cells
Not connected by tight junctions.
E. Peripheral Glia
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Schwann Cells
Axons of peripheral neurons are eveloped by Schwann Cells
Myelin Producing Cells of the PNS
1:1 Relationship with axon
Also perform astroglial functions
Promotes repair.
2. Satellite Cells
 Cell bodies of neurons in the spinal ganglia are surrounded by metabolically supportive cells.
 Perform function of astrocytes in the grey matter of the CNS
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Neuroscience and Mental Health · S Tran
Session 3: Resting Potential
Learning Objectives
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Define the following:
o Diffusion of an ion
o Permeability of a cell membrane
o Electrochemical gradient of an ion.
Describe how a resting membrane potential can arise from a difference in
concentration of an ion across a selectively permeable membrane (use diagrams).
Define electrochemical equilibrium for an ion.
What is the equilibrium potential for an ion?
The Nernst equation is Ex+ = (RT/ZF) ln (Co/Ci). You should know that Ex+ is the
equilibrium potential of ion X+, R is the gas constant, T is absolute temperature, Z is
the charge on the ion, and F is Faraday’s number 96,500 coulombs of charge/mol of a
singly charged ion.
Substituting the values of the constants and T= 37oC, and converting to log10, gives
(for an ion with charge +1)
Ex+ = 61 log (Co/Ci)
You need not memorize the Nernst equation, but you are expected to be able to use it
(and get the signs right!). For example, given this equation and Co and Ci, you
should be able to calculate the equilibrium potential for the ion, or given the
equilibrium potential and one of the concentrations, you should be able to calculate
the other concentration.
What are typical values for the concentration of K+ and for Na+ inside and outside a
normal neuron?
What is a typical value for the resting potential of a neuron?
K+ concentration has a much stronger effect on the resting potential than Na+
concentration does. Explain the basis of this difference.
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Definitions
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Flux: number of ions that cross a unit area per unit time
Diffusion equilibrium: no net flux
Potential (emf) : electrical force between ions that repel like charges and attract opposite
charges (Units: mV)
Current: movement of ions due to the influence of potential (Units: Amps)
Resistance of a material: a measure of how hard it is for current o flow through it (Units:
Ohms)
Electrochemical equilibrium: concentration gradient is balance by the electrical gradient
across the membrane
Equilibrium potential Ex+: the electrical potential that prevents diffusion down the ion’s
concentration gradient.
Resting potential
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Zero reference point is OUTSIDE the cell
Inside the cell is negative compared to ref.
All cells have a membrane potential
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Importnat in excitable cells for cell function
Membrane separates charges because:
o Membrane is selectively permable
o Concentration of at least one permanent ion is different on each side
The ENa+ is +72 mV whereas EK+ is -90mV
Na+ in plasma: 150 mmol/l and outside: 10 mmol/l
K+ in plasma: 5 mmoll and outside: 150 mmol/l
Graded Potentials
Action
Potential
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Occurs in axons
Equilibrium potentials for
Na+ is +72 mV
Equilibrium potentials for
K+ is -90 mV
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1
2
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1. Resting Potential
a. Voltage gated Na+ Channels and Voltage-gated K channels are closed.
b. Na-K pump maintains the resting potential
2. Foot of the Action potential (Exaggerated here)
a. Stimulus depolarises the membrane potential (towards positive)
3. Upstroke Phrase
a.
PNa  because the voltage-gated Na channels open quickly
i. This starts at the threshold potential
ii. Na ions enter the cell down their electrochemical gradient
b. PK  as voltage-gated K channels start to slowly open
i. K ions leave the cell down their electrochemical gradient but fewer than Na
ion entering.
ii. As upstroke progresses, more and more Voltage-gated K channels open.
c. Membrane potential moves towards the Na Equilibrium potential.
4. Repolarisation phase
a.
b.
PNa  because voltage-gated Na channels close. Na entry stops.
PK  as more voltage-gated K channels open & remain open
i. K ions leave the cell down their electrochemical gradient
c. Membrane potential moves towards the K equilibrium potential
d. Absolute refractory period: A new action potential cannot be triggered even with a
very strong stimulus (Inactivation gates closed)
5. After-hyperpolarisation phase
a.
PK is greater at rest because the voltage-gated K channels are still open
i. K ions continue to leave the cell
ii. Membrane potential moves closer to the K equilibrium potential until the
voltage-gated K channels close
b. Membrane potential returns to resting potential.
c. Relative refractory period: stronger than normal stimulus can trigger an action
potential (Inactivation gate is open)
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Regenerative Relationship between PNa and Membrane potential
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Threshold must be reached before depolarisation.
o Positive Feedback Behaviour
All or Nothing Reponse: Once threshold is reached, a full sized action potential is produced.
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Cycle continues until the voltage-gated Na Channels INACTIVE, which means they close
and become voltage INsensitive.
The membrane remains in a refractory (unresponsive) state until the voltage-gated Na
channel recovers from inactivation and becomes voltage-sensitive again.
Key Points on Ions Movement
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Na ions enter the cell, K ions leave
Only a very small number of ions cross the membrane and change the membrane potential
The concentration change is extremely small, less than 0.1%
Ion pumps are NOT directly involved in ion movement during the action potential only
between.
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Conduction Velocity
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Large diameter, myelinated axons – 120m/s
Small diameter, non-myelinated axons – 1 m/s
Increases with axon diameter (less resistance to current flow inside the large diameter axon)
Is higher in myelinated due to nodes of Ranvier
Reduced by axon diameter (regrowth), demyelination (MS, diphtheria), cold, anoxia,
compression and drugs (some anaesthetics)
Propagation
Local current flow
depolarizes adjacent
region toward threshold
Direction of propagation of action
potential
Active area at peak
of action potential
Remainder of axon at resting potential
Adjacent area at
resting potential
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Session 4: Neurotransmitters
Learning Objectives
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Define the essential components required for neurotransmitter release
Understand the differences between excitatory and inhibitory transmission
Define at least two mechanisms for the termination of neurotransmitter action at
the synapse
Describe how modulation of the synaptic properties of GABA can be used
pharmacologically to treat epilepsy
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Neurotransmission
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Restricted to specialised structures – Synapses.
~20nm
Types of neurotransmitters:
o Amino acids (e.g. glutamate & gamma amino butyric acid (GABA),
o Amines (noradrenaline & dopamine
o Neuropeptides (opioid peptides)
Mediate rapid (μs-ms ) or slower effects (ms-s)
Vary in CNS tissue concentrations: mM to nM
Neurotransmitter Release
1. Action potential reaches PRE-synaptic terminal & depolarises it. Calcium channels open.
2. Ca2+ ions enter pre-synaptic terminal through their voltage gated channels. Allows
neurotransmitter vesicles to fuse with the pre-synaptic membrane & release their content
into the synaptic gap.
3. Vesicles then are invaginated back into pre-synaptic terminal & are recycled.
4. Neurotransmitters diffuse
across the synapses to the
POST-synaptic terminal
receptor (Protein/lipid
gated channels). This
allows inflow of Na+ ions
 depolarisations occurs
(in an excitory synapse)
Depolarisation in pre-synaptic
 Ca2+ channels open  Ca2+
ions enters  NT vesicles
fusion & exocytosis  Recyling
of Vesicles & Receptor Action
 Na+ Influx  Depolarisation
in post synaptic
Inactivation occurs by:
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Enzyme destruction of NT in cleft
Re-uptake of NT by PRE-synaptic terminal
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Uptake of NT by glial cells
Diffusion out of the cleft
Agonists – Enhance/Mimics neurotransmitter’s effects
Antagonists – Binds & blocks receptors
Synaptic Transmission
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Quantum: the minimum quantity of transmitter released and detected at the postsynaptic
membrane ( = content of a a synaptic vesicle)
Quantal hypothesis: Quanta ~ 4000-10,000 molecules of transmitter
Synaptic vesicles
Small clear (Ach) 200 μs
Large dense cored (neuropeptides and proteins) 50 ms
Toxins:
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TETANUS toxin: C. Tenani causes paralysis.
Zn2+ dependent endopetidase inhibit
transmitter release
BOTULNUM toxin: C.notulinum causes falcid
paralysis
α-LARTROTOXIN black widow spider stimulates
transmitter release to depletion.
Speed of synaptic potentials at post-synaptic terminal:
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Fast: Uses ion channels (pentameric complexes)
to bring about change in membrane potential
e.g. Na+, Ca2+, K+ & Clo CNS: Glutaminergic & GABAergic synapses. NMJ: Acetylcholine (Ach) at nicotinic
receptors.
Slow: G-protein receptors and second messengers e.g. cAMP, IP3 via amplification cascades.
o CNS & PNS: Ach at muscarinic receptors, Dopamine (DA), Noradrenaline (NA), 5hydroxytryptamine (5HT) & neuropeptides e.g. enkephalin.
Ion channel linked receptors
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Rapid activation μ to msec.
Diversity and rapid information flow
o Nicotinic cholinergic receptors (nAChR)
o Glutamate (GLUR)
o GABA (GABAR)
o Glycine (GlyR)
o 5-hydroxytryptamine (5HT3 receptors)
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Excitatory vs Inhibitory
Excitatory: Post-synaptic membrane depolarises due to
transmitter (e.g. GLUR/glutaminergic) uses Na+
Inhibitory: Post-synaptic membrane hyperpolarises due to
transmitter (e.g. GABAergic) uses Cl-
Glutamate receptors:
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AMPA receptors – α-amino-3-hydroxy-5-methyl-isoazole
propinoic acid
o Majority of FAST excitatory synapses
o Rapid onset, offset and desensitisation
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NMDA receptors – N-methyl-D aspartate
o Slow component of excitatory transmission
o Serves as coincidence detectors which underlie learning mechanisms
GLUR and (Excitatory amino acid transporter) EAAT in glial cells with glutamine synthetase
o Glutamate  Glutamine
Epilepsy
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One of the commonest neurological conditions
50 million people worldwide
Characterised by recurrent seizures due to abnormal neuronal excitability
Despite advances in modulating seizure generation and propagation, the disease is disabling
30% are refractory to treatment
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Inhibitory CNS synapses mediated
by GABA
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Glucose  TCA cycle  α-ketoglutamate
 glutamate  GABA ( Succinate
semialdehyde)  Cl- ions opening
Glutamate  GABA via Glutamic acid
decarboxylase GAD (B6)
GABA  Succinate semialdehyde via GABA
transaminase GABA-T
Research has found drugs targeting GABA synapses
have been beneficial for epilepsy.
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With epilepsy, there is either a decrease in GABA-mediated inhibition or an increase in
glumate-mediated excitation, which results in brain seizures
This can be treated by enhancement of GABA-mediated inhibition and suppression of
glutamate-mediated excitation using glutamate receptor antagonists.
Benzodiazepines (such as clonazepam, clobazam and diazepam) enhance GABA action
Vigabatrin inhibits GABA transaminase
Phenobarbital enhances GABA action and inhibits synaptic excitation
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Session 5: Organisation of CNS
Learning Objectives
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Draw a diagram to explain the relationship between the following major divisions of the CNS:
spinal cord, brainstem, cerebellum, diencephalon, cerebral hemispheres.
Define the functions of the dorsal and ventral horns of the spinal cord and explain how the
dorsal and ventral roots and spinal nerves relate to them.
Define the 3 components of the brainstem and state the main functions of the brainstem.
Describe the functions of the 2 main structures in the diencephalon.
State the functions of the basal ganglia and the cerebellum.
Draw on a diagram of the cerebral hemisphere, the cortical lobes and primary cortical areas.
Recognise the main structures of the brain in a diagram or MRI.
Describe the 3 layers of the meninges and explain their role in protecting the brain.
Explain how the major divisions of the brain relate to the cranial fossae in the base of the skull.
Explain the relationship between the spinal segments, spinal nerves and vertebrae and state at
what level a lumbar puncture can be performed safely.
Identify the components of the ventricular system and relate them to the divisions of the CNS.
Explain the composition, circulation and functions of CSF.
State the average total volume and flow rate of CSF.
Define hydrocephalus and outline how it may be treated.
Distinguish between an epidural (extradural) and subdural haemorrhage.
The Central Nervous System

The central nervous system is made up of the brain and the spinal cord.
Cerebral Hemispheres
Forebrain
Diencephalon
Brain
Midbrain
Pons
Hindbrain
Medulla
Cerebellum
Spinal Cord:
o
o
Supplies motor, sensory adn autonomic (sympathetic & parasympathic) innervations
to the body through spinal nerves
Mediates reflexes
Brain Stem
o
o
o
Consists of the medulla, pons and midbrain
Controls vital functions e.g. respiration and consciousness
Cranial nerve function
pg. 20
Neuroscience and Mental Health · S Tran
Cerebellum
o
Co-ordinates movement
Diencephalon
o
o
Thalamus – relay between lower structures and cerebral cortex
Hypothalamus – control of homeostasis. Interface between CNS, ANS and endocrine
system
Cerebal Hemispheres
o
o
Cerebral cortex – involved in all function, Primary areas and association cortex
Basal ganglia – control of movement
Dorsal and Ventral Horns of spinal cord





Grey matter on each side is subdivided into
regions called HORNS.
The ANTERIOR (VENTRAL) gray horns contain
cell bodies of somatic motor neurons and
motor nuclei, which provide nerve impulses for
contraction of skeletal muscles.
The POSTERIOR (DORSAL) gray horns contain
somatic and autonomic sensory nuclei.
A typical spinal nerve has two connections to
the cord: a posterior and anterior root.
The posterior & anterior unite to form a spinal
nerve at the inter-vetebral foramen. Sensory +
motor axons make the spinal nerve a mixed
nerve.
pg. 21
Neuroscience and Mental Health · S Tran
Brainstem
Comprised of the midbrain, the pons and medulla.
Medulla
 A continuation of spinal cord that forms the inferior part of the brain.
 The medulla contains sensory and motor neurones  many nuclei – affiliates with 5/12 cranial
nerves, the cardiovascular centre and part of the respiratory centre.
Pons
 Pons is a bridge that connects the cerebellum by transverse neurons and is also part of the
sensory and motor tracts; it is also involved in the respiratory centre.
 The pons lie directly superior to the medulla and anterior to the cerebellum
Midbrain
 The midbrain extends from the pons to the diencephalon. The cerebral aqueduct passes through
the midbrain connecting the third and fourth ventricle below.
 Midbrain contains tracts and nuclei, containing neurons for muscle activity, input from
proprioceptors.
Basal ganglia and the Cerebellum
Basal ganglia
 The basal ganglia receives input from the cerebral cortex and provides output back to motor
parts of the cortex
 Helps with the initiation and termination of movement
 Helps initiate some cognitive process, such as attention, memory and planning
 May act with the limbic system to regulate emotional behaviour.
Cerebellum
 The cerebellum is posterior to the medulla and pons and inferior to the posterior portion of the
cerebrum.
 A main function of the cerebellum is to evaluate how well movement initiated by motor
cerebrum are carried out.
 Sends feedback to motor areas of the cerebral cortex to help correct the errors
 The main brain region that regulates posture and balance.
Cortical Lobes:
Cortical Areas:
pg. 22
Neuroscience and Mental Health · S Tran
The Meninges

Membrane enclosing the brain
and spinal cord- for protection
 Dura mater – tough membrane
attached to bone or forming
partitions (dural folds) with
venous sinuses in their margins.
 Archnoid Membrane – thin
membrane attached to the
underside of the dura, it
contains delicate collagen fibres
and elastic tissue
 Pia mater – delicate transparent
membrane closely adherent to surface of brain and spinal cord
 Between arachnoid membrane and pia mater, there is the sub-arachnoid space
 CSF circulates once around the CNS before being absorbed back into the blood stream.
Clinical significance: Cerebro-spinal fluid flows in the subarachnoid space and therefore
obstruction by meningitis may cause hydrocephalus or bleeding between layers may cause a type of
stroke.
The Cranial Fossa


Split into anterior fossa, middle fossa & posterior fossa.
In the base of the skull, the sphenoid bone and the large hole at the back of the base of the skull
called the foramen magnum can be seen
o The Frontal Lobe lies in the anterior cranial fossa
o The Temporal Lobe lies in the middle cranial fossa
o The Cerebellum lies in the posterior cranial fossa
o The Pituitary Gland lies directly above the body of the sphenoid bone
o The Brain Stem passes through the Foramen Magnum
The inferior aspect of the brain and inside base of the skull
pg. 23
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The Vertebrae and Spinal Nerves





There are 31 vertebrae in total:
o 7 Cervical
o 12 Thoracic
o 5 Lumbar
o 5 Sacral
o 2 Coccyx
There are also 31 pairs of spinal nerves:
o 8 Cervical
o 12 Thoracic
o 5 Lumbar
o 5 Sacral
o 1 Coccyx
First cervical nerve comes out above C1 and last spinal nerve comes out
between the coccyx vertebrae.
Big differences in size between the spinal cord and the length of the
vertebrae, this is because the spinal cord stops developing but the
vertebrae carry on growing in adolescence.
Spinal Cord ends at L1/L2, but CSF still flows to the bottom of the
spinal column, therefore below L2 is a good place to extract CSF for
analysis (Between L4 and L5)
Ventricular System


Compromises of the spaces between the brain parts, filled with CSF.
Function: to hold the brain in its usual position and to protect the brain.
Different parts of the ventricular system relates to the divisions of the
CNS:
o Lateral Ventricle – Cerebral hemispheres
o Third Ventricle –Diencephalon
o The Aqueduct – Midbrain
o Fourth Ventricle – Pons and Medulla.
Cebero-spinal Fluid (CSF)




Colourless liquid that protects the brain and
spinal cord from chemical and physical damage
Carries oxygen, glucose and other needed
chemicals from the blood to neurons and
neuroglia.
Provides mechanical protection – it acts as a
shock absorber that protects the delicate tissue
of the brain and spinal cord from jolts, which would otherwise cause them to the bony wall &
vertebral cavities.
Buoys the brain; the brain effectively floats in CSF
pg. 24
Neuroscience and Mental Health · S Tran





Provides an optimal chemical environment for accurate neuronal signalling, as ionic
composition changes can seriously disrupt production of action potentials
Medium for exchange of nutrients and waste products between the blood and nervous tissue
Formed in the choroid plexuses of each lateral ventricle  third ventricle (where more CSF is
added by choroid plexus on the roof)  aqueduct  fourth ventricle  circulation in
subarachnoid space  reabsorbed back into the blood through arachnoid villi that project into
the dural venous sinuses.
Average total volume of CSF is ~ 150 ml
Flow rate of CSF is ~ 500ml/day
Hydrocephalus




Accumulation of excess CSF in the ventricles  increased CSF pressure
Two main causes:
o Communicating-block in the CSF absorption or flow: meningititis, headinjury or subarachnoid haemorrhage
o Non-communicating-block caused by aqueduct stenosis, or by a ventricular or
paraventricular tumour
Relieved by draining excess CSF by implanting a shunt into lateral ventricle to divert into the
superior vena cava or abdominal cavity or treated by removing causative agent (ventricular
tumour)
Symptoms:
o Increased Head Circumference
o Loss of Upper Gaze in Children
o Adults: Headaches, Drowsiness & Blackouts
Meningitis





Definition: Inflammation of the meninges (covering the brain)
Symptoms: Fever, Tiredness, Headache, Irritability. More serious: Confusion, Fits,
Photophobia, Severe Headaches & Drowsiness.
Viral Meningitis – less severe, but depends on infective agent e.g. enterovirus, EBV. Presents
with Headache, Vomiting and Neck Stiffness
Bacterial Meningitis – Neisseria Meningtidis, Haemophilus influenza or streptococcus
pneumonae. Present with headaches, photophobia and painful eye movement.
Sampling of CSF needed to differentiate. Bacterial causes increase in white blood cell count,
protein levels and decreased glucose levels because blood vessel permeability increase. Viral
– normal glucose levels.
Epidural (Extradural) and Subdural Haemorrhage
 Epidural/Extradural haemorrhage – due to damaged meningeal artery between skull &
dura after head trauma
 Subdural haemorrhage – usually due to a damaged vein between dura and arachnoid
membrane
 Both cause a space-occupying lesion in the confined space of the cranium and hence
neurological deficits.
pg. 25
Neuroscience and Mental Health · S Tran
 Distinguishing: Rate of bleeding & onset of symptoms. Epidural is arterial bleeding  faster
and earlier symptoms. Subdural is venous bleeding  slower and slow onset of symptoms.
pg. 26
Neuroscience and Mental Health · S Tran
anterior
posterior
pg. 27
Neuroscience and Mental Health · S Tran
Session 6: Peripheral Nervous System
Learning Objectives






Describe the structural and functional components of a normal peripheral nerve.
List the factors that affect conduction velocity of peripheral axons.
Define the terms: dermatome, myotome, ramus, plexus, and explain their significance
with regard to innervation of the body.
State the spinal levels which contribute to the nerves of the upper and lower limb.
Compare and contrast the effects of injury and disease on peripheral nerve function.
Outline the main diagnostic techniques for peripheral nerve disorders.
The Peripheral Nervous System



Nerves emerging from the brain & spinal cord that innervate peripheral organs.
Receptor  Dorsal Roots  CNS  Ventral Root  Effector
Divided into afferent and efferent
o Afferent: Transmit information from receptors into the CNS
o Efferent: Transmit information from CNS to the effectors
 Somatic motor neurons: innervates skeletal muscle
 Autonomic neurons (pre- & post-ganglionic): Innervates glands &viscera.
Cells of a Peripheral Nerve
a. Neurons
a. Cell bodies (Somata) located in CNS (motor) or periphal ganglia
(sensory/autonomic) and their axons/processes project to peripheral targets
b. Glial Cells
a. Swann Cells wrap around axon, & satellite glial cells found in
sensory/autonomic ganglia.
c. Connective and vascular tissue components
Spinal Nerves




31 pairs of spinal nerves
Spinal nerve supply a band of skin & muscle.
Have a ventral root (motor) and a dorsal root (sensory) which meet inside the vertebral
canal at the level of the dorsal root ganglion
Rami branches of the spinal nerves, the different types are:
i.
Dorsal ramus: innervates skin & muscles on the back
ii.
Ventral ramus: innervates skin, muscle of chest, limbs and pelvic area.
iii.
Rami comunicantes: contain axons of pre-ganglionic sympathetic motor neurons
(white ramus) and postganglionic sympathetic neurons innervating visceral
structures.
Connective tissue sheaths:

Epineurium
o Loose connective tissue surrounding the whole nerve
o Strong Collagenous fibres oriented in the long axis of the nerve
pg. 28
Neuroscience and Mental Health · S Tran





o Carries major blood vessels supplying teh nerve
Perineurium
o Dense connective tissue surround a fascicle (concentric layers of flttaened
fibreoblast-like cells and collagenous fibres)
o Diffusion barrier (blood-nerve barrier) which helps preserve the ionic milieu
of the axon
Endoneurium
o Loose connective tissue surrounding individual axons.
The larger the diameter, the faster the axonal conduction velocity
PN contain a mixture of fibres of different diameters and conduction velocity (CV)
Compound action potential recorded from a nerve contains several peaks reflecting
different CVs due to diameter and myelination.
Myelinated Fibres
o Schwann cell membranes wrap around a single axon in a spiral fashion (100 layers) of
myelin. Each cell covers only a small segment of the axon (internode)
o Node of Ranvier – devoid of myelin
o Saltatory conduction – APs jump from one node to the next
Unmyelinated Fibres
o Several nerve fibres lie within invagination of Schawnn Cells
o Axonal diameter (~1 µm) is much less than of myelinated (1.5-2.0 µm)
o Continuous conduction: AP causes depolarisation of immediately adjacent membrane.
Plexuses




C5-T1 (Brachial Plexus) = Upper Limbs
L2-S2 (Lumbo-sacral Plexus)= Lower Limbs
Ventral rami of the spinal nerves (except T2-T12) form network of nerves called plexuses.
Convergence of axons of different spinal nerves to form a peripheral nerve
Dermatome




31 pairs of spinal nerves are named according to associated spinal vertebra. Each one
innervates the skin and musculature of a circumscribed region of the body.
Dermatome: the skin area innervated by a given spinal nerve – Important in establishing the
location of a lesion to the spinal cord, dorsal root or peripheral nerve.
Each spinal nerve also innervates half of the adjacent dermatome too, so a lesion to a single
nerve causes a decrease in sensitivity and not a complete loss.
Can point to damaged region of the spinal cord
pg. 29
Neuroscience and Mental Health · S Tran

Peripheral nerve injury or nerve compression may result in complete sensory and mtoor lsos
over the area supplied by the nerve
Nerve Dysfunction


Nerve Conduction Velocity studies can determine whether a peripheral neuropathy is
present and whether it’s demyelinating or axonal.
Nerve biopsy of a small peripheral nerve (e.g. sural nerve in the leg) can be used to study the
pathogenesis of the disease
Injury and Compression to the PNS



Medial nerve can be compressed & damaged as it passes a narrow tunnel in the wrist 
wasting of the thumb muscles (carpal tunnel syndrome)
Peripheral nerve injury or nerve compression can result in complete sensory & motor loss
over the area supplied by the nerve. Examples are:
i.
Ulnar nerve: lies near the surface of the elbow & is easily damaged  wasting of
hand muscles and loss of sensation over the little finger.
ii.
Sciatic nerve: injured in the buttock by badly placed injections  paralysis of the
foot % loss of sensation over the front and back of the lower leg and foot.
PNS neurons have the capacity to regenerate the axon but severity of the damage affects
the functional recovery. Regeneration occurs in these stages:
1. After a crush lesion or complete axotomy, the axons and myelin sheath distal to the
jury break up within 48h and macrophages phagocytose the axon & myelin debris –
Wallerian Degeneration
2. Cell bodies of the neuron undergo metabolic changes known as chromatolysis
3. Proximal axons needs to make contact with Schwann cells & find their former
endoneurial sheaths in the distal part. Failure results in a neuroma (trapped nerves)
4. Regeneration of the axons (2-5mm/day) and will reinnervaste their targets within 1
month to over a year.
pg. 30
Neuroscience and Mental Health · S Tran


Factors that affect recovery are the
severity of damage and the distance of
regeneration.
Diagram summarising the events occurring
during axonal degeneration and
regeneration following nerve injury:
A. Normal nerve.
B. One week after axonal damage.
Schwann cells containing myelin debris
(‘onion bulbs’) are seen surrounding the
degenerated axons. Distally, Schwann
cells undergo mitosis forming a scaffold
for regeneration.
C. Axon sprouts begin to regenerate into
the distal stump.
D. Schwann cells enfold and begin to
remyelinate the regenerating axons.
E. Connection with the target organ (e.g.
muscle) is re-established. Note the
contrast in the response of Schwann
cells proximal and distal to the lesion.
pg. 31
Neuroscience and Mental Health · S Tran
Session 7 & 8: ANS
Learning Objectives
 Describe the sympathetic and parasympathetic pathways and their central/spinal connections.
 Identify the neurotransmitter substances released at different levels within the autonomic
nervous system and describe the principal steps involved in their biosynthesis and
metabolism.
 Describe the influence of the sympathetic and parasympathetic nervous system on the
principal systems/organs of the body (e.g. cardiovascular system, lung, gut, exocrine glands)
and understand the concept of dual innervation and autonomic tone (giving examples).
 Give an example of an autonomic reflex and describe the principal pathways involved.
 Classify the cholinoceptors found within the autonomic nervous system and identify the
principal loci of (a) the nicotinic cholinoceptors and (b) the muscarinic cholinoceptors. Note
that the nicotinic receptors are ion-gated and the muscarinic receptors are G-protein coupled.
 Identify the principal loci of adrenoceptors in the autonomic nervous system. Classify these
-classes and note that they are G-protein coupled.
 Describe how autonomic activity can be estimated with physiological and biochemical
examples.
 Describe the main abnormalities in autonomic failure differentiating between localised and
generalised disorders.







Describe the basic anatomy of ANS innervation in terms of pre-ganglionic neurons, ganglia
and post-ganglionic fibres. Contrast the anatomical location of sympathetic and
parasympathetic ganglia.
Describe the thoracolumbar (sympathetic) and craniosacral (parasympathetic) central origins
of the ANS.
Understand the terms sympathetic trunk, plexus and subsidiary ganglia.
Identify the rich sympathetic plexuses that surround the major organs and blood vessels
Understand the pre-ganglionic nature of the thoracic and lumbar splanchnic nerves and their
synapses in subsidiary ganglia e.g. coeliac ganglion.
Understand the importance of the sacral parasympathetic outflow for innervation of
structures within the pelvis e.g. the bladder.
Identify which of the cranial nerves contain parasympathetic pre-ganglionic fibres.
Fig. A1. PRINCIPAL EFFERENT OUTPUTS FROM THE CENTRAL NERVOUS SYSTEM (CNS)
CENTRAL NERVOUS SYSTEM
AUTONOMIC NERVOUS
SOMATIC NERVOUS SYSTEM
NEUROENDOCRINE SYSTEM
SYSTEM
Exocrine glands
Skeletal muscle,
Growth, Metabolism,
Smooth muscle
including the Diaphragm and
Reproduction, Development,
Cardiac muscle
Respiratory muscle
Salt & water balance,
Metabolism
Host defence
pg. 32
Host defence
Neuroscience and Mental Health · S Tran
Autonomic Nervous System



One of the principle efferent paths of communication between the CNS and periphery
Comprises of two fibres: pre-ganglionic and post ganglionic.
Can be split into 2 components, anatomically, functionally and neurochemically different.
Fig. A2. THE AUTONOMIC NERVOUS SYSTEM
SYMPATHETIC
PARASYMPATHETIC
“Fight and flight”
“Rest and digest”
Sympathetic Nervous System






Prepares the body for responses to a stressful situation  The “Fight or Flight” response
Key role in the regulation of a number of body
functions including blood pressure, body
temperature & metabolism.
Arises in the thoracic and lumbar regions.
Pre-ganglionic are short whereas post-ganglionic are
long.
Located in a chain close to the vertebral column
(paraventerbral ganglia) and also closer to the target
tissue (celiac ganglion)
Connection allows for mass activation of the
sympathetic system.
 Also
includes
modified
ganglions to
the adrenal
medulla, which releases it product directly into the
blood stream
Parasympathetic Nervous System



Controls a number of functions in non-stressful
conditions i.e. gasto-intestinal motility and
secretion
Opposes sympathetic system e.g. on heart rate via
bronchiolar diameter
Arises in the cranial and sacral region of the spinal
cord.
pg. 33
Neuroscience and Mental Health · S Tran


The pre-ganglionic are long whereas the post-ganglionic are short.
Parasympathetic ganglia are therefore located in or very close to the target tissue
Neurotransmitters


Acetylcholine - Choline ester; a charged molecule with a quaternary ammonium group
Noradrenaline & Adrenaline – Catechloamines




Parasympathetic system are cholinergic – Ach
Sympathetic system the pre-ganglionic fibres are cholinergic – Ach
Majority of post-ganglionic fibres of the sympathetic system are (nor)adrenergic – NA
Adrenal medulla forms part of the sympathetic system: innervated by pre-ganglionic
cholinergic fibres which trigger the release of neurohormones ( 80% adrenaline, 20%
noradrenaline) into the blood circulation.  Chromaffin Cells
Some instances, post-ganglionic sympathetic fibres use acetylcholine.
Fast transmission. ACh use nicontinic receptors – ligand gated channels.
G-protein coupled recptors are used at effector hence are ‘slower’.
o Muscarinic receptors – ACh.
o Adrenoceptors (α & β) – NA/Adrenaline.



pg. 34
ACETYLCHOLINE
ACh = acetylcholine
Neuroscience and Mental Health · S Tran
Biosynthesis, storage and
release of Acetylcholine
Acetyl Co A
+
Choline
Choline acetyl
transferase
ACh + Co A
ACh
A
po ctio
te n
nt
ia
l
Ca++
ACh
4
Choline
+
Acetate
1
ACh
2
ACh
e
ras
e
t
3
es
l in
o
h
lc
ety
Ac
Effector cell
Receptor
Fig. C5: SYNTHESIS, RELEASE, REUPTAKE AND
METABOLISM
Biosynthesis, storage andOF
release
of noradrenaline
NORADRENALINE
Tyrosine
Tyrosine
hydroxylase
DOPA
Tyrosine
Metabolites
DOPA decarboxylase
Dopamine
Act
ion
pot
ent
ial
Dopamine
Dopamine b
hydroxylase
Noradrenaline
Monoamine
oxidase A
(MAO-A)
Noradrenaline
Uptake 1
Noradrenaline
Ca ++
Uptake 2
Noradrenaline
Adrenoceptor
Degredation
(COMT)
pg. 35
Neuroscience and Mental Health · S Tran
FIG. 6: SYNTHESIS,
STORAGE
AND RELEASE OF ADRENALINE
Biosynthesis,
storage and release
of Adrenaline
Tyrosine
Tyrosine
hydroxylase
DOPA
Tyrosine
DOPA-decarboxylase
Dopamine
Dopamine
Dopamine b
hydroxylase
Noradrenaline
Adrenal medulla
chromaffin cell
Ca2+
Noradrenaline
Phenylethanolamine
methyl transferase
Adrenaline
Adrenaline
Adrenaline
Ca2+
Adrenaline
capillary
pg. 36
Neuroscience and Mental Health · S Tran
o
o
Dual Innervations is where an organ is innervated by the sympathetic and parasympathetic
branches
Opposing systems result in an overall balanced effect.
Heart:


Sympathetic
o Increase force of contraction of cardiac muscles (inotropic effect)
o Increase heart rate (chronotropic effect)
o Hence increase cardiac output as CO = HR x SV (stroke volume)
Parasympathetic - Vagus
o Depresses the heart rate from the myogenic 100bpm to 60-70bpm.
Vasoconstriction


Sympathetic
o Arteries and veins but mainly arterioles
o Great influence on total peripheral resistance
o Increases cardiac output as CO = mBP/TPR
o Increases arterial blood pressure (as CO and TPR increased)
o During Exercise, stress and activity, when the sympathetic system is dominant it
constricts vessels to non-essential organs: kidneys, GI tract and dilates vessels to the
skeletal muscle, cardiac muscle, liver and adipose tissue.
Parasympathetic
Vasodilution

Due to decreased sympathetic tone however:
o Increased sympathetic activity to some blood vessels (skeletal muscle) which are
cholinergic or adrenergic beta receptors cause vasodilation
o Local effect of vasodilator such as CO2 and increased [H+], nitric oxide, histamine
o Increased parasympathetic stimulation may cause vasodilation to certain blood
vessels to discrete glands/organs (e.g. penis)
pg. 37
Neuroscience and Mental Health · S Tran
Organ/System
Effect of sympathetic
Effect of parasympathetic
Cardiovascular
↑ Increases cardiac output (ionotropic
effect SV and chronotropic effect HR);
increased TPR
↓vasodilatation (due to decreased
sympathetic tone)
↑ - Slows HR; vasodilatation of certain
blood vessels to discrete glands and
organs (e.g. penis)
Gastrointestinal
Decreases motility and tone; stimulates
contraction of sphincters; inhibits
secretory activity
Increases motility and tone; relaxation
of sphincters; stimulates secretory
activity
Eye muscles
Relaxes ciliary muscle, lens flattens for
distant vision; contracts radial muscle
(pupil dilation)
Contracts ciliary muscle, lens bulges for
near vision; contracts pupillary
sphincter (pupil contraction)
Bladder
↓ Relaxation of the sphincter vesicae
(via hypogastric nerve)
Main influence; ↑ contraction of
detrussor muscle and relaxation of
sphincter vesicae (via pelvic nerve)
Lungs
Penis
↑ Dilates bronchi and bronchioles (↑
O2 delivery)
↑ penile flaccidity; ejaculation
↑ Erection
Autonomic Reflexes


When nerve impulses pass over an autonomic reflex arc. These reflexes play a key role in
regulating controlled conditions
e.g. blood pressure, heart rate, force of ventricular contraction, blood vessel diameter,
respiration and digestion or even the diameter of the pupil of the eye
Cholinoceptors


Nicotinic Cholinoceptors
o Ligand gated ion channels  Fast
o At all autonomic ganglia
o Found also in the adrenal medulla
Muscarinic Receptors
o G-Protein coupled  Amplification
o Found on effector organs with parasympathetic innervations
o Also sweat glands of the sympathetic system
Adrenoceptors

Found on effector cells of the SYMPATHETIC nervous system
o Alpha (α)
 Radial muscle in eye, salivary glands, sphincter muscles of stomach and
bladder
o Beta (β)
 Cardiac muscle, smooth muscle or airways, liver.
pg. 38
Neuroscience and Mental Health · S Tran

Alpha(α)1 and Beta(β)1 produce excitation, whilst α2 and β2 receptors generally cause
inhibition. Another type β3 is only found on brown adipose tissue  thermogenesis.
Effects of the Autonomic System


Mass Sympathetic Discharge  Alarm & Stress:
o Increased arterial blood pressure
o Increased blood flow to active muscle (↓ to other areas e.g splanchnic bed)
o Increased blood glucose concentration
o Increased Respiration
o Increased Awareness
Acute Stress Reponse:
o Tachycardia
o Splanchnic Bed Vasoconstriction
o Sweating
o Pupil Dilation
o Increased Metabolic Rate
o Increase Glucose
o Increased Mental Awareness
Autonomic Failure
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Systemic: Phaeochromocytoma (PCC) (Mass of the chromaffin cells in the adrenals)
Causes excessive release of adrenaline and noradrenaline
Symptoms:
o Headache
o Palpitations
o Raised Blood Pressure
o Tachycardia
o Other Adrenergic Effects
Localised: Damage to the spine and loss of autonomic functions below that point.
Other
Pupil Reactions
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Miosis (Constrict of eye pupil)  Parasympathetic Activation: Pilocarpine
Mydriasis (Dilation of eye pupil) Blockage of Parasympathetic: Atropine
Enteric System
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In walls of alimentary tract
o Myenteric (Auerbach’s) plexus
o Submucous (Meissner’s) plexus
Sensory – monitoring mechanical, chemical and hormonal activity of gut
Motor – gut motility, secretion, vessel tone
Can be overridden by sympathetic and parasympathetic systems
pg. 39
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