Synapses and Plasticity One Flashcards
Describe the basic features of a neuron:
Soma (cell body)
Axon (Only, it carries output AP) (Mostly myelonated 50ms velocity vs 1ms)
Dendrites (many of these- incoming information)
Many synapses on the dendrites
What is unique about a neuron?
Polarised cell.
Where can synapses occur?
On the dendrite (neuron to neuron)
On glia
On muscle (neuromuscular junction)
10 trillion synapses in the brain
What do synapses allow?
Rapid communication
What do synapses allow the formation of?
Neural circuits
How are neural circuits formed?
Synapses allow the transmission of APs by:
Converting an Electrical Information (AP) into Chemical Information (Neurotransmitter release) which crosses the synaptic cleft and activated a receptor (ligand gated ion channel), Post synaptic cleft receptors convert this chemical information back into the Electrical information which travels through dendrites and its processed with all other incoming information (as many dendrites and even more synapses)
What are synapses thought as?
The basic information processing units in the brain
Describe the structure of a synapse.
Presynaptic cleft: Contains vesicles packaging neurotransmitter, which are bound to cytoskeleton by Calcium sensitive vesicular proteins. The base of the presynaptic cleft is a dense zone (Lots of protiens, where neurotransmitter binds)
Synaptic cleft (Extracellular space where neurotransmitter crosses)
Postsynaptic cleft: Contains receptors for neurotransmitter that activate ligand gated ion channels. Followed internally a post synaptic density (protein dense)
On the presynaptic cleft, what is the dense zone also referred to?
The active zone
What is the role of the active zone?
It is the region where vesicles fuse to the presynaptic terminal and release their neurotransmitter. It is an active process because of the Ca dependent proteins that mediate this process.
Why is the role of the post synaptic density?
It is protein rich area and its role is to get the receptors where they need to be to receive neurotransmitter release. Highly coordinated event to allow synaptic transmission to occur.
How does disease influence synapses?
Every disease tends to involve changes in synapses i.e number of location of efficency
What happens to the vesicles once they have fused with the presynaptic terminal?
They are recycled
Describe neurotransmission
Neurotransmitter is synthesised and packaged into vesicles.
AP reaches the presynaptic cleft and activae voltage gated Ca channels.
Ca influxes.
This activates Ca sensitive proteins and causes vesicles to fuse with the presynaptic membrane.
Neurotransmitter is released and crosses the synhaptic cleft and binds to receptors on the post synaptic celft, activating the ligand gated ion channels influxing ions and causing an AP.
How does the vesicles release neurotransmitter?
Snare proteins mediate exocytosis.
Ca dependant snare proteins on the membrane and vesicle wrap around each other, pulling the vesicle close to the membrane, once close enough exocytosis occurs
What are some examples of snare proteins?
On the vesicle:
Synaptobrenin
Synaptotagmin
Membrane:
Syntaxin
SNAP25
What are the main types of synpases?
Excitatory Synapses or Inhibitory Synapses
What is the function of inhibitory synapses?
Allows balance between excitation and inhibition
What does disease do to inhibitory synapses?
It leads to an off balance between excitation and inhibition which presents as symptoms
Whats an example of a group of inhibitory synapses?
5% of interneurons are inhibitory.
What makes interneurons inhibitory?
They are extremely polarised and contain many processes.
Releasing inhibitory neurotransmitter at their synapse.
e.g GABA and Glycine
What are the affects of GABA and Glycine?
They bind to their receptors on excitatory neurons (and inhibitory neurons), these channels allow the influx of Cl ions therefore transiently hyperpolarising the resting membrane potential
The affects of inhibitory neurotransmitter are called?
Inhibitory Post Synaptic Potential
What is the main neurotransmitter for excitatory synapses?
90% of excitatory neurons are glutamanergic.
What are the post synaptic receptors for gultamate?
The post synaptic receptors for glutamate are:
Ion channels:
1) AMPA
2) NMDA
GPCR’s
3) Metabloic glutamate receptors
Why are there multiple receptors?
The different receptors have different properties
Is there a difference between AMPA and NMDA receptors?
Yes their properties are very different.
AMPA receptors activate when glutamte binds and allows the passage of primariily Na and some K ions
NMDA receptors allow the passage of primarily Ca and some Na, K
When it comes to plasticity what kind of glutamate receptor is most important?
NMDA
When it comes to activation what is the difference between NMDA and AMPA?
AMPA receptors are neurotransmitter dependent only.
NMDA receptors require Neurotransmitter and are voltage gated.
How are NMDA receptors voltage gated?
At RMP (-60mV) NMDA receptors have a Mg ion blocking off the channel. (So binding of neurotransmitter can occur but no Ca flux.) When the membrane potential depolarises (i.e AMPA receptors have being activated) the channel undergoes a conformational change causing Mg release and allowing the influx of Ca ions, providing neurotransmitter has bound.
Requires lots of Na influx from AMPA
Why do synapses have two types of receptors?
AS different properties change the strength of the synapse.
What is a requirement for high levels of Ca influx with NMDA receptors?
High levels of Pre and Post synaptic activation will result in high levels of Ca influx.
What is the high levels of pre and post synaptic activation called? in reference to NMDA receptors?
Co-incidence detectors
What is meant by co-incident detectors?
NMDA receptors detect high levels of pre and post synaptic co-activation
What is co-activation important in?
Synaptic plasticity
