Synaptic integration
- Created by: 11APhillips
- Created on: 03-01-20 14:51
Transmitters
1. Synthesis of transmitter substance
2. Storage and release of transmitter
3. Transmitter interacts with the postysnaptic receptor.
4. Transmitter is removed from the synaptic cleft.
- Transmitter - A substance which is released at a synapse by one neuron and affects a postsynaptic target in a specific manner for a short period.
- Formal criteria for a transmitter:
Must be synthesised in a neuron
Must be present in the presynaptic terminal and released, giving a defined postsynaptic respone.
When administered as a drug, it must exactly mimic a transmitter
There must be a mechanism for removing it from the cleft.
Types of neurotransmitter
1. Small molecule neurotransmitters - These are amino acid derivatives that are packaged into small synaptic vesicles, but also some dense core vesicles.
These affect the excitability of neurons
2. Neuroactive peptides - These are large amino acid polymers packed into dense core vesicles.
These affect the gene expression/synaptogenesis/morphology of neurons
Neuroactive peptides
- These are syntehsised at the soma.
- Their exocytosis is not highly regulated, and rapid recycling does not occur.
- Not associated with fast sustained transmission
- Tagging atrial natriuretic factor with GFP shows that the peptide continualy moves up and down the neuron, and is releasd with needed at bouton swirls.
Small molecule neurotransmitters
- There are three groups:
The biogenic amines - E.G serotonin/dopamine
The amino acids E.G. Glutamate/GABA
Miscellaneous E.G. acetylcholine
- Many biogenic amines have a shared synthesis pathway:
L-tyrosine -> L-DOPA -> Dopamine -> noradrenaline -> adrenaline
- Depending on what transmitter they release, neurons have different frequencies of the required synthesis enzymes.
Small molecule neurotransmitters
- There are three groups:
The biogenic amines - E.G serotonin/dopamine
The amino acids E.G. Glutamate/GABA
Miscellaneous E.G. acetylcholine
- Many biogenic amines have a shared synthesis pathway:
L-tyrosine -> L-DOPA -> Dopamine -> noradrenaline -> adrenaline
- Depending on what transmitter they release, neurons have different frequencies of the required synthesis enzymes.
Filling vesicles
- Occurs at the synaptic terminal and requires ATP.
- H+ enters the vesicle against its concentration gradient through a v-ATPase.
- H+ exits the vesicle down its concentration gradient through an antiport transporter, with 2 proteins allowing 1 neurotransmitter molecule to enter.
- Transporters/v-ATPases are targets for amphetamine and extasy (which depletes 5-HT in vesicles and therefore increases levels in the cytoplasm, allowing calcium independant release of 5-HT.
Removing neurotransmitter from the synaptic cleft
- Occurs in three ways:
Diffusion away from the synaptic cleft, called spillover, as the diffused neurotransmitter can activate receptors in neighbouring terminals.
Degradation
Reuptake
Reuptake
- Uses transporters such as Na+ K+ antiport for glutamate (goes in with Na) or Na+ Cl- symport for other neurotransmitters like serotonin or choline (goes in with Na)
- SSRIs like fluoxitine, and also tricyclic antidepressents, block the reuptake of serotonin.
- Cocaine blocks the reuptake of noradrenaline
- Reuptake of acetylcholine works as follows
Acetylcholine --(acetylcholine esterase)--> Choline + acetate
Choline reenters the sell by a choline transporter
Choline + acetylCoA ---(Choline-acetyl transferase)---> acetylcholine
Signalling with gas
- Gases can diffuse direcly and so do not need vesicles.
- An example is NO
- It is synthesised from arginine by nitric oxide synthase
- This enzyme can be activated by the NMDA receptor (activated by glutamate)
- The NO can cross back over the synaptic cleft in retrograde signalling
- Its purpose is to activated soluble guanylyl cyclase, which causes GTP -> cGMP
- It is involved in neuronal plasticity.
Synaptic integration
- The individual input of neurons is not very significant, the important thing is the collected input.
- The information currency of the neuron is the action potential.
- The axon hillock is the integration site - It is called the spike initiating zone as it has a lower threshold than the cell body (+10mV compared to +30mV).
- As it contains the spike initiating zone, there are many voltage gated channels, which is why it is the integration site.
- The integration is through the passive spread of potential from the post synaptic terminal to the trigger zone in the axon hillock.
- It is influenced by the space and time constant (see earlier notes).
Spacial summation
- Two inputs are received at the same site, but only if both are received can an action potential be triggered.
- If the two inputs are received far apart in space, then decay by the space constant means that there won't be an action potential.
Temporal summation
- This is where a single site is activated twice in short succession and so there is no decay due to the time constant. The larger the time constant the more temporal summation can occur.
- Dendrites can encode the temporal sequence of synaptic inputs.
- Labelling and stimulating dendrites shows that the sequence of stimulation influences the amount of depolarisation.
Inhibitory potentials
- Inhibitory neurons work in conjunction with excitatory neurons, reducing passive depolarisation.
- A large time and length constant means that responses from lots of neurons can be integrated.
- A small time and length constant allows few inputs matched closely in time to be integrated.
- The electrical properties of neurons can be influenced by experience.
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