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Developmental names of forebrain/midbrain/hindbrain
- Forebrain: prosencephalon (telencephalon - deep nuclei and cerebral cortex and diencephalon - hypothalamus and thalamus)
- Midbrain: mesencephalon
- Hindbrain: rhombencephalon - medulla, pons, cerebellum
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Ventricle formation from CNS divisions
- Lateral: in telencephalon
- 3rd: in diencephalon
- 4th: in rhombencephalon
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Ionic distributions of Na, K, Cl, Ca
- Na: IN 15, OUT 150. Eq.p: +62
- K: IN 150, OUT 5.5. Eq.p: -89
- Cl: IN 9, OUT 125. Eq.p: -71
- Ca: IN 10^-4, OUT 1. Eq.p: +124
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Nernst potential
E = RT/zF . log([out]/[in])
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Donnan product rule
- [K]out x [Cl]out = [K]in x [Cl]in
- If both are passively distributed (as in frog muscle - not nerve)
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Active transport of chlorine
2ry active extrusion: coupled to K efflux (KCC) and HCO3- influx (NDCBE - sodium dependent chlorine bicarbonate exchanger)
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Calcium extrusion
- ATP fuelled Ca pump
- NCX (3 Na in, 1 Ca out)
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Problems with gap junctions
- Need a large presynaptic terminal (to deliver sufficient depolarising current)
- Bidirectional
- Not very flexible (eg different transmitter/receptor systems)
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Describe synaptic release
- Vesicle docked at presynaptic active zone
- Vesicle primed by close association between v-SNARE and t-SNARE
- Synaptotagmin acts as a Ca sensor
- Vesicle fuses with plasma membrane
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3 criteria for neurotransmitters
- Present in presynaptic terminal
- Stimulation causes release
- Exogenously applied transmitter has the same effect
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4 main categories of neurotransmitters
- amino acid: glutamate, GABA, glycine
- bioactive amines: ACh, NA, 5-HT, DA, Histamine
- purines: ATP, Adenosine
- peptide: often co-released, inc opioids, pituitary, secretins, insulins, tachykinins, somatostatins, gastrins
- gaseous: NO, CO, H2S
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Difference between AMPA and NMDA receptors
- AMPA: fast, Ohmic, mainly impermeable to divalent cations
- NMDA: slow, long lasting, non-Ohmic: low current near resting potential where they are blocked by extracellular Mg2+
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Long and Short receptors
- Long: require APs eg cutaneous, cranial, olfaction
- Short: graded -> create graded generator potential in the 2nd order cell which modulates the rate of spike firing. Eg smell, taste, hearing
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Magnitude of an EPSP created by a single Group 1A afferent
~0.5mV
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Glutamate gated channel in spinal cord permeable to? How has this been shown?
Both Na and K: reversal potential is ~0mV
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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
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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
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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
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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
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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
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2 types of spinal reflex (other than stretch)
- flexor withdrawal: cutaneous nociceptors: flexors stimulated to withdraw limb
- crossed extensor: contralateral extensors stimulated (and flexors inhibited) to retain balance
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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
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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.
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Synapses studied in LTP experiments
Schaffer collaterals and commisural fibres to pyramidal cells in area CA1 of hippocampus
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Mechanism of LTP
AMPA channels open -> post-synaptic depolarisation -> NMDA channels open -> Ca influx -> protein kinaseses -> increased AMPA channel production
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