Short: graded -> create graded generator potential in the 2nd order cell which modulates the rate of spike firing. Eg smell, taste, hearing
Magnitude of an EPSP created by a single Group 1A afferent
Glutamate gated channel in spinal cord permeable to? How has this been shown?
Both Na and K: reversal potential is ~0mV
Glycine gated channels in alpha-motor neurons permeable to? How has this been shown?
Cl-: reversal at -80mV; made less negative by injecting Cl ions from recording electrode
Evidence for axon hillock having lowest threshold?
Experiments involving stimulating a pyramidal cell in a cortical slice at afferents/soma/dendrites and looking at where AP is initiated: always at axon hillock
Interaction of excitatory and inhibitory synaptic inputs
Addition: 2 exc on neighbouring dendrites
Subtraction: 1 exc, 1 inh on neighbouring dendrites
Division: 'shunting inhibition': 1 inh closer to soma on same dendrite as 1 exc
Pre-synaptic inhibition at axo-axonic synapses
Opening K or Cl channels: causes hyperpolarisation
Opening Cl channels still works even if the Nernst potential for Cl is more positive than the resting potential, because Cl would flow to make the potential less negative. This would be depolarising the cell ('primary afferent depolarisation') which would partially inactivate Na channels.
Both ways (as well as any 2nd messenger systems) cause reduced opening of VGCC
2 types of inhibition of spinal reflexes
Feedback: inhibitory interneurons via recurrent axon collaterals (to itself and synergists) eg Renshaw cells stabilise firing rate
Feedforward: antagonistic pathway inhibited
2 types of spinal reflex (other than stretch)
flexor withdrawal: cutaneous nociceptors: flexors stimulated to withdraw limb
Synaptic facilitation vs synaptic depression... and after effects?
Facilitation: build up of Ca in pre-synaptic terminal
Depression (after ~50ms): Vesicle depletion
Post-tetanic potentiation: for several minutes, due to effect of Ca on stimulation
My understanding of LTP!
High frequency tetanic stimulation causes a long lasting increase in EPSP amplitude following stimulation. Both presynaptic stimulation and postsynaptic depolarisation are required. It is probably due to AMPA channels opening, depolarising the cell and allowing NMDA channels to open. Ca influx acts via protein kinases to increase AMPA receptor density, meaning AMPA responses are greater later on. There may also be effects from retrograde messengers eg NO and arachidonic acid that modulate presynaptic transmitter release. This response is Hebbian, because it obeys 'an input is strengthened when it plays a role in firing the target cell'.
Associative LTP: if there is a weak presynaptic input and a strong one, each individually will cause its own LTP. If they are stimulated at the same time, both EPSPs persistently increase.
Synapses studied in LTP experiments
Schaffer collaterals and commisural fibres to pyramidal cells in area CA1 of hippocampus
Mechanism of LTP
AMPA channels open -> post-synaptic depolarisation -> NMDA channels open -> Ca influx -> protein kinaseses -> increased AMPA channel production