Neuronal communication Flashcards
What is the somatic nervous system
motor nerves from CNS to skeletal muscles. Voluntary control.
What is the autonomic nervous system
nerves from CNS to internal organs e.g., heart
What is an excitatory synapse
electrical activity in presynaptic neuron to increase the excitability of postsynpatic neuron. (Inhibitory – decreases)
What is a chemical synapse
prevent direct electrical propagation of AP from pre – to post - synaptic neuron
What happens when an action potential reaches a synapse
- Pores in cell membrane open allowing influx of Ca2+ into pre-synaptic terminal
- Neurotransmitter is released into synaptic cleft
- Neurotransmitter diffuses across the synaptic cleft and interacts with receptors on the post-synaptic membrane
- the neurotransmitter causes a pore to open allowing an influx of ions into the post-synaptic terminal which is propagated along the dendrite towards the soma
How long is the synaptic delay
~0.5ms
How long is the sypase
20-30nm
What is removed and uptaken at the synapse
enzymes, reuptake by glial cells
Fusion of vesicle with presynaptic membrane - part 1
- Opening of Ca 2+ channels and actin.
- Fusion protein macromolecules (FPMs) separate to allow fusion.
- Vesicle membrane incorporated into presynaptic membrane.
Fusion of vesicle with pre-synaptic membrane - part 2
- Clathrin molecules assist inward movement of the vesicle membrane. Dynamic assists in FPM pairs and pinching the neck of the emerging vesicle.
- Vesicles are now free for recycling.
How are neurotransmitters removed from the synaptic cleft
- Enzymatic breakdown
- Active reuptake (rapid) - pumped back into pre-synaptic terminal
- Active uptake (rapid) - pumped into glial cells
How does novichok poison you
inhibits acetylcholinesterase
Symptoms of novichok poisoning
Symptoms: Spasm, prevents relaxation of muscles (cardiac and respiratory). Cause of death asphyxiation or cardiac arrest
Features of novichok poisoning
Fast acting. Remain poisonous for a long time period
Features of an excitatory post-synaptic potential (EPSP)
fast rise time, slower decay time - depolarising
What causes EPSP
Usually caused by ligand gated channels once neurotransmitter has binded, Na enters to depolarise. G protein couples receptors can also cause this, (neurotransmitters bind)
What are EPSPs and IPSPs
‘mini action potentials’ which cause transient a small transient change in membrane potential of a cell (either aid or hinder action potential formation. They can summate (an opposed to Aps).
Excitatory neurotransmitters
Glutamic acid (most common) and acetylcholine are excitary neurotransmitters and cause influx of Na (EPSP)
Inhibitory neurotransmitters
Glycine and GABA, produce an increase in negative potential (away from action potential threshold). Chloride entering cell of Potassium leaving the cell cause this.
What is convergence of neuronal communication
integrating information from a number of inputs
What is divergence of neuronal communication
response to be felt from a number of effectors
What happens if Ex1 fires twice with sufficient time between the 2
the post synaptic potential has decayed so there is no summation of inputs and no action potential, firing.
When does temporal summation occur
EX1 fires twice in a short time, so can summate sufficient to cause an action potential.
What happens when EX1 and EX2 are fired at the same time
EPSPS can summate and cause an action potential
What can prveent an action potential firing
An inhibitory presynaptic input
Wat do inhibitory neurotransmitters cause
IPSPs which can prevent action potentials firing
Why are action potentials required
for correction functioning of the brain, heart and skeletal muscles.
What is a nerve fibre
the axon of a single neuron
What is a nerve
a bundle of nerve fibres
What is intracellular recording
recording electrical activity across a membrane of one single cell (one electrode is inside the cell and one (earth) is outside).