0824 - Principles of Neural Circuitary Flashcards
Explain how EEG traces arise
Whole point - It only tells you where sinks and sources are relative to the surface. It doesn’t actually tell you what’s going on.
EEG tracks electrical activities in synapse populations near the electrode. If you are looking close to the surface, a depolarising (inward/excitatory) current means that charge is flowing away from the electrode and into the cell, using the cell as a sink , and more distal tissue as a source, giving negative EEG polarisation.
Local hyperpolarising (outward/inhibitory) current flows from the cell to the surrounding area, giving positive EEG polarisation.
These reverse when you’re deep enough to be sourcing current from a more superficial source to the synapse.
Synapses are bigger current events than APs, so you mostly see synapses. You only start seeing AP’s when there’s a huge amount of synchronisation between cells (e.g. epilepsy), where you’ll get the net effect of spike/wave pattern.
How do EPSPs and IPSPs affect the EEG?
A deep EPSP (layer IV), or a superficial IPSP (layer II, III) will cause a positive (downward) deflection of the EEG.
A superficial EPSP, or a deep IPSP will cause a negative (upward) deflection of the EEG.
Think of it - EPSP makes extracellular space negative at synapse, IPSP makes it positive at synapse, and vice-versa away from the synapse. Then the electrode is just recording what is happening near it.
How does epilepsy manifest on an EEG?
“Spike and wave” patterns.
What are the different wave forms on the EEG?
Adjust for level of alertness/thinking.
Alpha waves - 10Hz - relaxed and eyes closed
Beta - 20 Hz - eyes open/concentrating (in parietal and occipital particularly)
Gamma - 30+Hz - Perception.
Theta - 5Hz - Drowsiness.
Delta - 2Hz - Slow wave sleep.
The more you are thinking the steeper and closer together/faster your waves are.
Discuss the concept of cortical column and microcircuit
A microcircuit is a series of connections between neurons that allows the cortex to perform different functions despite having an (effectively) uniform structure throughout. Basically, the cortex will process whatever comes in due to its uniform structure, it is the inputs and circuits that allow specialisation. As JD puts it ‘a bunch of neurons organised in a circuit that will receive inputs from a specific region’.
A column is the arrangement of interconnected neurons (possibly one microcircuit) spanning the depth of the cortex.
Illustrate how excitation is routed through microcircuit
Enters layer 4, relayed to ⅔, and then goes to L5 which allows for projection outside the cortex.
Feedback loop from L6 projects to thalamus.
Outline how inhibition endows microcircuit with richness
36 different cell types, which are very specific in type, location, and target.
Basket Cell - Can completely inhibit action potentials (perisomatic inhibition)
Bipolar Cell - Target basal dendrites of pyramids, don’t really know what they do.
Excitatory cells just run a very simple circuit between each other and out to other areas. Excitation leads to excitation due to the recurrent amplifier effect. Inhibitory cells can inhibit basically any particular part of the neurons up to the axon hillock and in doing so provide a very localised and specialised layer of inhibition to direct signals etc. They can tweak, tune, and channel the excitatory neurons.
Identify how connectivity shapes processing of input signals
Neurons diverge and then converge, allowing amplification of what would otherwise be a small signal - you’ll definately get a signal of some sort in 3rd order neuron, but wont be able to tell exactly which first order neuron fired it. Flip cost is that you lose localisation. But when you add in inhibitory interneurons, it allows you to see the strongest path, giving localisation.
Recognise how excitation and inhibition can drive network patterns
If you have a bilateral system, with inhibitory neurons running between, then one side can inhibit the other, allowing excitation on one side, with reciprocal inhibition. As the excitation drops off, the reciprocal inhibition drops off, allowing the other side to become more excitable and flipping the circuit.
But you need self-limiting AP’s (funky refractory period) and input of some sort on both sides. This is where spinal injury comes in - if you can replace the input originally from the brain, then you can trigger the CPG.
Illustrate how electrical stimulation can evoke locomotor activity in spinal patients.
Key of proof of concept of CPG
Basically, the input from the brain that is required to ‘trigger’ the CPG is missing. If you can replace that, you can fire up the CPG again.
