LIFS1902 Nervous System Revision Notes

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LIFS1902 Revision Notes - Nervous System

Nervous system: Central nervous system (CNS) – brain and spinal cord
Peripheral nervous system (PNS) – neurons carrying informa on
to/from CNS.
Uses both electrical and chemical ways for efficient communica on throughout the body.
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Types of cells in nervous system.
Neurons (or nerve cells) – transmit electrical currents called nerve impulses.
and
Glia (glial cells or neuroglia) – the other non-neuronal cells in the nervous system.
These include:
Microglia – CNS-resident macrophages

Oligodendrocytes – found in CNS – form the myelin sheath.


Schwann cells – found in the PNS – form the myelin sheath.
Ependymal cells – line the fluid-filled spaces and secrete cerebral spinal fluid (CSF)
Astrocytes – provide nutrients; have end feet that contact with blood capillaries and form
the blood-brain barrier. These cells have their own territory, and they can release
gliotransmi ers (e.g., glutamate).
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Neurons consist of:
Cell body (also called soma), which contains nucleus and other cell organelles such as
mitochondria and Golgi.

Dendrites – typically < 2 mm in length


Axon – leads from neuronal cell body to the dendrites or cell body of another neuron, or to
another effector cell such as a muscle or gland. Axons vary in length but can be > 1 meter
long (e.g. in scia c nerve).
The axons of some neurons are protected and insulated by a myelin sheath.
Gaps in myelin sheath called nodes of Ranvier.
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Three classes of neurons


1) Sensory neurons – afferent or ‘carry forward’ neurons (found in PNS) – carry signals
from sensory receptors (e.g., in eye) to brain. Most sensory neurons have the cell
body in structures called the dorsal root ganglion.
2) Interneurons – connector neurons (found in CNS) – integrate all signals coming in
from the sensory neurons.
3) Motor neurons – efferent or ‘carry away’ neurons (found in PNS) – carry signals from
brain to effector cells such as skeletal muscle.

Neuron another name for a nerve cell.


Nerve = bundle of axons (nerve fibers) in the PNS
Tract = bundle of nerve fibers in the CNS
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Nervous system physiology
Difficult to study in mammalian neurons as largest axons only have diameter of ~20 µm.
Rela vely easy to study in the giant axons of the Atlan c squid, which are 0.5 to 1.5 mm in
diameter.
Membrane poten al or voltage across membrane is measured with a voltmeter and
visualised with an oscilloscope.
Voltmeter has 2 electrodes – recording electrode (placed inside cell) and reference electrode
(placed outside cell).
Res ng poten al is -65 to -70 mV
Charge difference (or polarity) due to difference in the distribu on of ions on inside and
outside of cell.
Outside axon – higher concentra on of Na+
Inside axon - higher concentra on of K+
This unequal distribu on is maintained by sodium-potassium pumps, which ac vely
transport Na+ out of the axon and K+ into the axon.
Nega ve res ng poten al due to there always being more posi ve ions outside the cell than
inside AND the presence of nega vely charged proteins inside.
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Ac on Poten al
An ac on poten al is ini ated when the membrane poten al rapidly changes from nega ve
to posi ve.
Nerve s mulated >> voltage gated Na+ channels in localised area open >> Na+ enters cell.
This movement of posi ve ions called depolariza on.
If enough Na+ enters to increase membrane poten al from -70 mV to -55 mV (threshold),
then this is point of no return for an ac on poten al to start.
Depolariza on con nues (more Na+ enters cell) and membrane poten al increases to +35
mV.
The influx of Na+ in one loca on s mulates neighbouring voltage-gated Na+ channels to
open so ac on poten al moves along axon.
Ac on poten al ends when voltage-gated K+ channels open and K+ leaves cell. This is called
repolariza on.
Sodium-potassium pump then returns the ions to the res ng loca ons.
Before res ng poten al (-70 mV) restored, the membrane poten al briefly goes beyond this
(e.g., to -85 mV). This is called the refractory period.
During refractory period, no new ac on poten al can be generated as Na+ channels are
inac vated.
Scien sts who worked on the squid giant axon and demonstrated the ac on poten al were
Alan Hodgkin and Andrew Huxley. Won Nobel Prize in Physiology or Medicine in 1963.
In myelinated axons, depolariza on (movement of Na+) can only occur at Nodes of Ranvier.
Ac on poten als only occur along axons (not dendrites or cell bodies) and they start at axon
hillock (trigger zone).

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Types of ion channels found in neurons
Res ng (leak) K+ channels – found in axon (passive movement of K+)
Voltage-gated Na+ or K+ channels - found in axon
Ligand-gated channel - found in dendrites and cell body before axon hillock. Not involved in
ac on poten als
Na+/K+ pump – found in axon (ac ve transport – needs ATP).
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Ac on poten al is the same for any s mulus but differences in pain level due to:

1) Number of neurons s mulated


2) The frequency of the ac on poten als
Anaesthe cs (e.g., lidocaine) block Na+ channels and stop them from opening, which stops
nerve transmission to pain centers of brain.
Fugu toxin is a tetrodotoxin that blocks Na+ channels so ac on poten als cannot be
transmi ed. Deadly.

Ac on poten als in myelinated and unmyelinated axons.


Unmyelinated – AP travels down en re length one small por on at a me – quite slow
Myelinated – AP jumps from one Node of Ranvier to the next (via saltatory conduc on) –
much faster.

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Mul ple sclerosis


Autoimmune disease
Immune cells a ack myelin sheath in neurons of CNS (and PNS).
Myelin becomes damaged and leads to regions of inflamma on.
More common in women than men and typical age of diagnosis – 20 to 40 years.
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Neuron to neuron and neuron to cell communica on
Neurons communicate with other neurons or with other cell types (muscle or gland cells) at
a synapse.
Ac on poten al passes along axon of sending (pre-synap c) cell >> Synapse >> Receiving
(post-synap c) cell.
Most synapses are chemical – use chemical messengers – neurotransmi ers, which are
stored in the pre-synap c terminal in synap c vesicles.
A few synapses are electrical – ions flow between cells via gap junc ons. Synap c cle must
be very narrow – just 3.5 nm across. Gap junc ons made of 2 connexons, each of which is
made up of 6 connexin proteins.
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A synapse consists of:

1) Presynap c terminal (bouton) – end of sending cell.


2) Synap c cle
3) Post-synap c terminal – part of receiving cell.

Transmission across synapse


Ac on poten al arrives at presynap c axon terminal >> Ca2+ enters via voltage-gated Ca2+
channels >> Synap c vesicles fuse with presynap c membrane >> Neurotransmi ers in
vesicles released via exocytosis >> Diffuse across synap c cle >> Bind to ligand-gated
receptors on post-synap c membrane.

Excitatory neurotransmi ers s mulate influx of Na+ and an ac on poten al in this new cell.
e.g., glutamate and acetylcholine
Inhibitory neurotransmi ers open more K+ channels and prevent an ac on poten al.
e.g., GABA

One post-synap c neuron might receive input from both excitatory and inhibitory neurons.
All signals undergo synap c integra on to see if membrane poten al increases to threshold
and s mulates new ac on poten al.

A er release from presynap c terminal, neurotransmi ers can be removed as follows:


1) Broken down by enzymes – e.g., acetylcholinesterase breaks down acetylcholine.
2) Reuptake and recycle back into presynap c neurons. – e.g., dopamine and serotonin.
Cocaine prevents the reuptake of dopamine, so this neurotransmi er accumulates in the
synap c cle and leads to an amplified signal, manifested as a feeling of euphoria.

Examples of neurotransmi ers


1) Acetylcholine – binds to acetylcholine receptors on skeletal muscle >> has an
excitatory effect >> s mulates muscle contrac on. In this case the synap c cle is
called the neuromuscular junc on. Acetylcholine enzyma cally broken down with
acetylcholinesterase.
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2) Dopamine – excitatory and inhibitory effects. Send signals to other neurons in brain.
Dysfunc on of various dopamine pathways leads to various diseases/disorders:
Parkinson’s disease, ADHD, substance abuse disorders, restless legs syndrome.
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Parkinson’s disease
Caused by lack of dopamine due to the death of dopaminergic neurons in substan a nigra
region of brain.
Dopamine required for smooth coordinated movement so Parkinson’s characterised by
movement disorders.
This is a progressive degenera ve disorder – gets worse over me.
Typically starts between ages 60 – 60 years but might be earlier.
Treatment: L-dopa (Levodopa), which is converted to dopamine in brain.

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