Oligodendrocytes form myelin sheath by wrapping around the axon
Essential for efficient communication, for propagation of signals along axon
Multiple Sclerosis involves loss of myelin, disruption of efficient neural communication throughout the body

Synapses

Join axon terminals of one neuron to dendrites of another neuron for transmission of signals between neurons
Neural signals go one-way
- pre-synaptic = from cell body to axon terminal
- post-synaptic = from dendrite to cell body

Neurotransmitter

Chemical ‘messenger’
released from pre-synaptic terminal
acts of post-synaptic receptors

Neurotransmitter Release

Depolarisation of axon terminal (action potential) triggers release of neurotransmitter
Neurotransmitter acts on receptor on post-synaptic neuron to open ion channels and pass signals
- chemical signal neuron-to-neuron

Synaptic Vesicles

Stores neurotransmitter in synaptic terminal
Joins cell membrane wall to release neurotransmitter into synaptic cleft
recycled: neurotransmitter taken back into pre-synaptic terminal is re-packaged into vesicles

Neurotransmitter Receptors

Gates on post-synaptic side (neuron dendrite)
Neurotransmitter in syanptic cleft joins with receptor
Activates receptor to open ion channels on post-synaptic neuron
- Transmits signal by opening ion channels and changing membrane potential on synaptic neuron
Lock and key — each receptor only binds to a specific type of neurotransmitter
- only activate their specific type of receptor
- important for drug effects—drugs can act on specific receptors to cause specific effects

Re-uptake Pump

Clears neurotransmitter from synaptic cleft back into pre-synaptic terminal

Enzymes

Break down neurotransmitter in synaptic cleft

Both stop neurotransmitter signalling to post-synaptic neuron — closes ion channels (when neurotransmitter is gone) and turns off the signal

Dopamine — Parkinson’s Disease

loss of dopamine in the basal ganglia deep in the brain
primarily affects movement
treatment with l-dope replaces dopamine in the brain

Anti-Depressant Drugs — Serotonin

Act to keep serotonin in the synaptic cleft for longer which increases serotonin signalling

SSRIs

Selective serotonin re-uptake inhibitors (prozac, zoloft, lexapro, lovan, cipramil)

MAOIs

Monoamine oxidase inhibitors (Nardil, parnate)

Neurons — Electrical Signals

Action potential
Electrical signal pulse travels along the axon
Fixed size — either on or off, signal or no signal

Cell Membrane Wall

70% of the brain is water
Water surrounds the cells — extra-cellular fluid
Water fills the cells — intra-cellular fluid
Cell membrane forms barrier between extra-cellular and intra-cellular fluid

Ions and Electrical Potential across Cell Membrane

Sodium (Na+) and Potassium (K+) positively charged ions
Different concentrations outside and inside cell, across cell membrane
Gives difference in electrical charge (potential) across cell membrane

Membrane Potential — Resting Potential

Membrane Potential Definition = difference in the eletrical charge (voltage) between inside and outside cell, across cell membrane wall
Resting Potential Definition = at rest (not during action potential) more positive ions outside than inside the cell gives overall negative potential (voltage) inside compared with outside the cell

Ion channels in Cell Membrane

Ion channels in cell membrane wall open and close to pass or block movement of ions across cell membrane
- Ions move between intra- and extra-cellular fluid
- movement of ions changes electrical potential
Important types

Ion channel 1: Sodium Potassium Pump

Actively pumps Na+ and K+ across cell membrane
Overall pumps positive charge out of cell (3 Na+ out for every 2 K+ in)
- Positive change will naturally move towards negative area (opposites attract)
Maintains negative resting membrane potential (approximately -70mV)
Uses energy — about 25% of body total energy (70% of brain energy)

Action Potential

Transmissions of electrical signal along axon
Input from other neurons (via synapses on dendrites) increase membrane potential
If voltage exceeds threshold, triggers action potential
Depolarisation of cell: membrane potential goes back to zero
- occurs in less than 0.002 seconds
Repolarisation: membrane potential back to -70mV resting potential
- refractory period — more difficult for another action potential to occur
- further to threshold to trigger another action potential
Fixed Size and All-or-None principle:
- If threshold level is reached, action potential of a fixed sized will occur. The size of the action potential is always the same for that neuron.
- All-or-None: Either a full action potential is “fired” (if membrane potential reaches threshold) or there is no action potential. There are no “large” or “small” action potentials.
- The strength of the neuron signal is determined by the rate of repeated action potentials
Conduction along axon
- Starts at axon hillock: membrane at axon hillock has lowest threshold to trigger action potential
- Depolarisation spreads from site of action potential to neighbouring region of cell membrane: causes neighbouring region to pass threshold to trigger action potential
- Repolarisation and undershoot (refractory period) prevents action potential going backwards

Ion Channel 2: Voltage-dependent ion channels

Voltage dependent ion channel, closed at resting potential
Open when membrane potential reaches threshold voltage
Allows flow of ions across cell membrane
- positive ions can flow from outside into the cel (because positive charge will naturally move towards negative area)
Causes depolarisation of cell (voltage less negative = closer to zero)

Voltage-dependent ion channels: Na+ and K+

Different channels open and close at different membrane potentials (voltage dependent)
Depolarisation: Na+ channels open when voltage exceeds threshold
- Na+ flows into cell
- Less negative potential
Repolarisation: Na+ channels close and K+ channels open after depolarisation
- K+ flows out of cell
- plus Na/K pump
- more negative potential

Ligand-Gated Ion Channels

Neurotransmitter receptors open ion channels when neurotransmitter binds
Different neurotransmitters bind to and open different ion channels (Na+, K+, Cl-) to change membrane potential in different ways
Receptor binding
- Can cause depolarisation (less negative)
- Can cause hyperpolarisation (more negative)

EPSPs and IPSPs

Receptor Channels — activated by neurotransmitters

Excitatory

Receptor open channels that cause depolarisation
ESPS = excitatory post synaptic potential

Inhibitory

Receptor opens channels that cause hyperpolarisation
IPSP = inhibitory post-synaptic potential
further from threshold for action potential

Graded Potentials

Excitatory and Inhibitory inputs (via dendrites) combine together
- changes membrane potential on postsynaptic cell
Graded Potential on postsynaptic cell depends on strength of synapse connection (on dendrite)
- strong connection causes large change in membrane potential
- weak connection causes small change

When do Inputs trigger an Action Potential?

Membrane potential at axon hillock depends on sum and timing of inputs through dendrites
If enough excitatory inputs occur together close enough in time, membrane potential will exceed threshold level for action potential
if membrane potential exceeds threshold level (at axon hillock)
- triggers action potential, neuron sends signals along its axon

Integration of Signals

Neuron receives many, many inputs — has only one output
- what combination of inputs will cause this neuron to fire and pass on it’s signal
Brain is enormous integrator of information — adapts with learning (billions of neurons with millions of billions of connections)