Neurones / ST / Summation Flashcards
What is divergence in terms on neuronal pathways
When 1 presynaptic neurone branches into large number of postsynaptic neurones
(Collaterals)
What is convergence
When large numbers of presynaptic neurones converge to affect 1 or less postsynaptic neurones (summation)
What is spatial summation (convergence)
When EPSPs originate at different locations on a neurone due to 2+ excitatory neurones
Why do more neurones come together in summation to allow epsps
Because separately , the excitatory post synaptic potential would be sub threshold
Together they can be suprathreshold
Can fire an ap in post synaptic neurone axon hillock
Why can summation sometimes be postsynaptic inhibition?
If one of the neurones converging graded potentials are hyperpolarising (iPsp)
Eg through Cl- entering cell or k+ out = ipsp
This would mean the summed potential is sub threshold
No AP fired
What is temporal summation
Graded potential (epsp) from the same presynaptic neurone happen close together
The EPSP then join into a an EPSP which is suprathreshold
What is post synaptic modulation?
When the neurone in summation receives modulation signals that decide the strength of the signal
If modulation signal in neurone is above threshold
Neurone decides an AP
Why can synaptic modulation have big effect eg if the signal is below threshold
Due to divergence meaning 1 neurone decides whether many target cells (collaterals) respond/are stimulated
What is pre synaptic modulation
Modulation pre synapse of a cell which is either inhibitory or excitatory. You can purposefully use pre synaptic modulation to stop or stimulate a cell
How could presynaptic modulation be used to inhibit 1 cell
An inhibitory neurone firing an ipsp to a cell is added pre synapse (damping the action potential) This causes no NTS to be released and the cell therefore doesn’t respond
Name the 2 different receptors and the channels they are on on the synapse
Ionotropic receptors - on ligand gated ion channels
Metabotropic receptors - on G protein coupled receptors
What happens in an EPSP graded potential and an IPSP graded potential via the ionotropic receptors on ligand channels
If EPSP- Na will move in when a conformational change has occurred depolarisation occurs
If IPSP - Cl can move in through the ligand channel or K+ can move out. Hyperpolarising the cell
When a molecule binds to the metabotropic receptor what happens
This activates a secondary messenger pathway
When a secondary messenger pathway on the G protein coupled receptor is activated, what 3 things does this do
Modifies proteins/ regulates synthesis of new proteins
Eg new ligand channels
Or causes ion ligand channels to close (with the K+ channel in EPSP) or Na channel in IPSP
Or causes ion ligand channels to open
(If Na channel causes EPSP)
If Cl or K channel = IPSP
Name the 6 types of NTs that are in the normal synapse
AcH
Amines - eg dopamine , adrenaline
Purines - ATP , AMP
Some polypeptides
Amino acids - GABA , glycine , glutamate
Gases - NO
What is the main excitatory neurotransmitter in the brain (because it uses ionotropic receptors on ca,k and Na Ligand channels)
Glutamate
What are the 2 main inhibitory NTs due to them binding to ionotropic receptors on Cl- channels?
GABA and glycine
Name some NTs that bind to mono tropic receptors
Adrenaline
AcH
ATP
Histamine
What is the ionotropic and metabotropic receptors called that bind to AcH
Ionotropic = nicotinic
Metabotropic = muscarinic receptor
What is synaptic plasticity
Once synapses form they aren’t fixed
Synaptic transmission can change depending on sensory input eg Past events
Responsible for things like memory
What is an example of synaptic plasticity and where was it found
Long term potentiation
Found in hippocampus (how memory works)
Explain the process of long term potentiation with glutamate involvement
When glutamate is released into the synapse, it binds to the ionotropic receptors on a NA ligand gated channel.
This triggers an EPSP
Repeated stimulation of this with glutamate causes depolarisation
Depolarisation causes mg2+ on the nmda receptor to eject causing calcium to move into the cell
The cell then becomes more sensitive to glutamate and can even release more
How does long term potentiation work?
Repetitive stimulation through binding of glutamate - synaptic efficacy
What is AcH effect on the metabotropic receptor on heart muscle
G protein activates secondary messenger
Camp produced
Causes k+ channels to open and k+ leaves the cell = hyperpolarisation
