Axonal and Synaptic Neural Transmission Flashcards
Ions involved
Anions (negative protein), Na+, K+, Cl-
Final resting potential
-70 mV
Na+ high conc. outside but with both forces pushing in.
Membrane and pump resists Na+ inward movement.
K+ and Cl- move both ways across membrane so reach steady state determine by diffusion and electrostatic pressure.
Some Na+ leaks back in but is expelled by pump.
Sodium-potassium pump
Keeps resting potential by pumping 3 Na+ ions out and 2 K+ in.
Active and requires ATP
What do neurotransmitters do?
Activate receptors on dendrites . soma
Ion channels open
Ions cross
Membrane potential changed
Potential changes spread through cell
If large enough, action potential triggered
What does a positive voltage mean
Depolarised
What would hyperpolarisation do to voltage
More negative
Excitatory neurotransmitters
Depolarises cell membrane (more positive)
Increases probability of action potential (more likely to cross threshold of -60mV)
Cause an Excitatory Post Synaptic Potential (EPSP)
Inhibitory neurotransmitters
Hyperpolarises cell membrane
Decreases probability of action potential (less likely to cross threshold of -60mV)
Causes Inhibitory Post Synaptic Potential (IPSP)
Spatial summation
Temporal summation
Passive conduction
Voltage changes spread away (decrementally) from point of origin
What part determines whether an action potential is generated?
Axon hillock
What happens after action potential generated?
When -60mV reached, voltage gated Na+ channels open and influx of Na+ into neuron.
Polarity becomes +30 mV in neuron.
Membrane potential reverses with neuron becoming positive.
Voltage gated Na+ channels close. K+ channels open and K+ rushes out of neuron.
This makes resting membrane potential more negative again to restore it to the resting membrane potential.
Myelination
Speeds up axonal conduction.
Where does myelin come from?
Oligodendrocytes in CNS and Schwann cells in PNS
Chemical Synapse
Action potential reaches terminal buttons on pre-synaptic side.
Voltage gated Ca2+ channels activated.
Ca2+ ions flood in.
Causes exocytosis, neurotransmitter molecules cross synaptic cleft.
Attach to receptors on post-synaptic membrane
What happens to the neurotransmitter on post-synaptic side?
Acetylcholinesterase breaks down acetylcholine.
Other enzymes break down other neurotransmitters.
Reuptake.
Blockers
eg Novichok
Blocks enzyme to breakdown the neurotransmitter so it stays in synapse continuing to have effect
(could cause excessive activation of muscles leading to convulsions –> paralysis, failure of heart muscle, respiration, eye, muscles, GI tract)
Parts of Synaptic Transmission that can be blocked (targets of drugs)
Manufacture (intracellular biochemical processes)
Storage (vesicles)
Release (action potential)
Post-synaptic receptors
Inactivation (break down or reuptake)
Common Fast neurotransmitters (short lasting effects)
Acetylcholine
Glutamate
Gamma-aminobutyric acid (GABA)
Common Slower acting neurotransmitters
Dopamine (DA)
Noradrenalin (NA)
Serotonin (5HT)
How do local anaesthetics work?
Na+ channels blockers
Blocks progress of action potential
Substances affecting ACh
Nictotine, curare, black widow spider toxins, nerve gas)
Substances affecting NA (noradrenaline)
Antidepressant drugs (imipramine blocks re-uptake, MAO inhibitors block break-down)
Stimulants (amphetamine - increases release and blocks re-uptake)
Substances affecting Dopamine
Antipsychotic drugs, stimulants, anti-Parkinson drugs
Substances affecting Serotonin
Anti-depressant drugs, Hallucinogens (eg mushrooms, LSD, ketamine), ecstasy
Substances affecting GABA
Anti-anxiety drug,
Anticonvulsant drugs,
Anaesthetics
