Neurobiology Theme 2

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  • Created by: Splodge97
  • Created on: 19-05-17 15:21
Describe the features of dendrites
Primary dendrites branch from the cell body, before dividing into secondary and tertiary dendrites. They grow, branch and prune during development and taper with distance from the stoma.
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What are spines?
Mushroom-shaped appendages of some dendrites, amplify post-synaptic potentials by increasing surface area
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What are neural integrators?
Cells with a large number of dendrites, allows them to fine-tune synaptic inputs. Purkinje cells of cerebellum are prime example; have one primary dentrite with thousands of branches in the same plane (maximising synaptic contacts)
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What are pyramidal cells?
Present in the cerebral cortex and hippocampus (layered structures), have a dendritic tree arranged in layers so they can recieve inputs from all layers of these structures simultaneously
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Why are small axons more likely to be myelinated?
As they have a greater lonitudinal resistance than longer (thicker) axons, so without myelination conductance velocity insufficient
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What are the features of myelin?
Comprised of 70-80% lipids (rest proteins), so has insulating properties as ions can't flow through lipids. Means only Nodes of Ranvier (many Na+ VGC's) need to be depolarised, as AP pushed through myelin by high resistance (saltatory conduction).
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What are terminal arbours?
The many branching fibres of axon terminals (allowing generation of motor units)
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What connections may axons make?
Axosomatic (to a neighbouring cell body), axodendritic (to a dentrite of a neighbouring cell) or axoaxonic (to the axon hillock of a neighbouring axon - these are rarer)
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What are axonal transport mechanisms necessary?
Diffusion of nutrients/waste along the length of the axon would be too slow, so must occur via kinesin/dynein along microtubules threaded through the axoplasm
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What are the features of fast anterograde transport?
Moves chemicals vital to synaptic transmission (neurotransmitters, organelles) rapidly (100-400mm/day) from the cell body to the axon terminal. Uses kinesin.
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What are the features of slow anterograde transport?
Moves substances non-essential to synaptic transmission (soluble substances) from the stoma to the axon terminal more slowly. A fibres transmit cytoskeleton components at 0.2-1mm/day, B fibres transmit smaller proteins at 2-5mm/day. Uses kinesin.
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What are the features of fast retrograde transport?
Transports excess substances (metabolites) from the axon terminal to the stoma using dynein. They travel encased in lysosomes (which hydrolyse their contents in the stoma) at 200-300mm/day. May carry toxins/viruses to stoma.
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What are multipolar neurones?
Interneurones and motorneurones
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What are bipolar neurones?
Connected to the sensory organs, comprising only 0.9% of neurones. Other end of the axon connects with the CNS, and cell bodies are present in dorsal root ganglia.
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Describe the Golgi staining technique
Uses silver to stain only 1% of neurones so they can be studied in isolation with good black/white contrast (though now tagged flourophores - as DNA fragments specific to certain neurones - are used)
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What is the state of the axon's ion channels during resting potential?
70% Na+ VGC's are open at the h gate (closed at the m gate), n gates of K+ VGC's are closed; means Vrest mainly determined by K+ leakage channels (as fewer for Na+)
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What is an ions equilibrium potential (E)?
Stable state of little energy consumption where Vnernst is equal to Vm so there is no net movement of the ion. All ions move to achieve this state.
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When does a change in permeability impact the Goldma equation the most?
In excitable cells with voltage gated channels
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What are the features of passive propagation?
Occurs due to the static (cable) properties of axon membranes which don't change; they would propagate AP's in both directions (if not prevented by the refractory period), but cause an exponential decrease in the AP amplitude over time/distance
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What are the features of active propagation?
The active transmisssion of impulses along axons, takes into account the electrical properties of neurones (triggered by Vm changes in action potentials); they prevent the AP decrementing over long periods/distances
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When are Na+ VGC's triggered to close at the h gate during an AP?
The overshoot which occurs upon reaching the AP peak (+40mV); this occurs 1ms after depolarisation. Close slower than the m gates open (otherwise would be permanently closed).
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When do K+ VGC's open at the n gate during an AP?
1-2ms after the AP peak (allows repolarisation through K+ efflux); later close upon hyperpolarisation
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Why is the refractory period necessary?
To limit the maximum frequency of AP's so the body tissues aren't damaged.
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What occurs in absolute refractory period?
The closure of the h gates of Na+ VGC's at the peak of an action potential. Whilst these h gates are closing no more AP's can be generated as the Na+ VGC's are unavailable to open at the m gate (despite the size of the stimulus)
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What occurs in the relative refractory period?
Caused by the re-opening of the h gates of Na+ VGC's after hyperpolarisation. Some Na+ VGC's can open at the m gate, but a stronger stimulus is required (as fewer available to cause depolarisation and because cell hyperpolarised).
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What are the features of electrical synapses?
Produce no transmission delay, allow bidirectional passage via gap juunctions which link the intracellular fluid of neighbouring cells (only 3.5nm between them). These are large so provide a low impedance pathway for current, making transport fast.
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What are the features of chemical synapses?
Occur throughout the CNS (so more frequent than electrical). Transmission is slow between specific neurones, creates a delay when neurotransmitters travel 20-40nm across the synaptic cleft and are unidirectional as the synapse apparatus is fixed.
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What are the active zones of axon boutons?
Darkened areas of membrane where vesicles fuse; Ca2+ VGC's are arranged here in layers. Exocytotic fusion pores form when vesicles fuse here (disappear after 10ms).
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How are chemical synapse transport vesicles reformed?
At the pre-synaptic membrane by clathrin and dynamin; they accept 40% of neurotransmitters back from the synaptic cleft
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What is the SNARE complex?
Formed by T-SNARE's syntaxin and SNAP-25 as well as V-SNARE synaptobrevin. Is a stable protein complex which generates the free energy for vesicle fusion.
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What is the action of synaptotagmin (V-SNARE)?
Acts as a calcium sensor to aid fusion of vesicles with the pre-synaptic membrane
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What are the features of a neurotransmitter?
Must mimic nomal transmission in isolated tissue, be manufactured in pre-synaptic vesicles, produce the expected effects under the influence of drugs and have a meachanism for removal (uptake/enzymatic hydrolysis)
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What is the action of acetycholine?
Mainly present in the PNS (a little in the CNS), innervates motorneurones to skeletal muscle
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What are the neurotransmitters of the CNS?
GABA (inhibitory neurotransmitter in the brain), glycine (inhibitory neurotransmitter in the spinal cord), glutamate (excitatory neurotransmitter)
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What is the difference between ionotropic and metabotropic neurotransmitter receptors?
Ionotropic are ligand-gated, so conformational shape changes upon binding induces fast transmission; metabotropic are g-protein coupled so cause an intracellular signalling cascade which induces conformational shape change in another channel (slower)
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How are EPSP's achieved?
By activating Na+/K+ antiporters on post-synaptic membrane, passively depolarise by moving one K+ in for every Na+ out. Equal increase in permeability of both, moving Vm to 0 as this is between their two E's. They are slow, graded and decrimental.
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How are IPSP's generated?
K+ or Cl- channels are activated on the post synaptic membrane causing hyperpolarisation by moving Vm towards their E's. They are slow, graded and decrimental; essential to prevent hyper-excitability.
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What is a composite post-synaptic potential?
Generated when all IPSP's and EPSP's are integrated in the axon hillock (determining if threshold is met/AP is propagated). Is influenced by summation, produces little change if EPSP's and IPSP's balanced.
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How does a single motor axon activate antagonistic muscle pairs?
Has one terminal releasing an EPSP to the flexor and another relasing an EPSP to an interneurone (in turn releases an IPSP to the extensor). Must be rapidly alternated.
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What are muscle spindles?
Muscle sensory organs which contribute to fine motor control to conrol limb position by sitting parallel to muscle fibres and sensing stretch (as part of proprioception)
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What are Golgi tendon organs?
Present in muscle tendons, measure muscle tension by maintaining the same tension in the tendon (as part of proprioception)
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What are the features of A-alpha fibres (defined by the letter's system)?
Diameter of 13-22um, conductance veolcity of 70-120m/sec. Funcion as A-motorneurones or originate from muscle spindles and primary nerve endings (as Ia fibres) or Golgi tendon organs (as Ib fibres).
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What are the features of A-beta fibres (defined by the letter's system)?
Diameter of 8-13um, conductance veolcity of 17-40m/sec. Function in touch and pressure reception (from muscle spindles or touch sensory endings as II fibres, or from pain, crude touch, pressure and temperature receptors as III fibres).
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What are the features of A-gamma fibres (defined by the letter's system)?
Diameter of 4-8um, conductance veolcity of 15-40m/sec. Function in motor innervation to muscle spindles via intrafusal fibres.
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What are the features of A-delta fibres (defined by the letter's system)?
Diameter of 1-4um, conductance veolcity of 5-15m/sec. Function in sensing pain, cold and touch.
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What are the features of B fibres (defined by the letter's system)?
Diameter of 1-3um, conductance veolcity of 3-14m/sec. Function as preganglionic parasymapthetic axons.
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What are the features of C fibres (defined by the letter's system)?
Diameter of 0.1-1um, conductance velocity of 0.2-2m/sec. Function as postganglionic parasympathetic axons (or as C fibres which originate from pain, touch, pressure or temperature receptors).
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Describe the dorsal column medial lemniscus pathway
Senses pressure, vibration, fine touch and proprioception. Enters dorsal root and then ascends dorsal coulmn ipsilaterally (via gracile fasciculus/cuneate fasciculus). Synapses and decussates in medulla, goes to ventral post lat nucleus of thalamus.
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Describe the anterolateral system
Senses crude touch, pain and temperature. Enters dorsal root to synapse and decussate upon entering the spinal cord. Ascends spinothalamic tract to ventral posterior lateral nucleus of thalamus.
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Describe the trigeminothalamic system
Senses pressure, vibration, proprioception and fine touch from the face. Enters pons via trigeminal ganglion, synapses in trigeminal brainstem complex, ascends to synapse in ventral posterior medial nucleus of thalamus.
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Describe the pain and temperature system
Senses crude touch, pain and temperature from the face. Enters pons through trigeminal ganglion, descends via spinotrigeminal tract to spinotrigeminal complex of medulla/rostral medulla. Decussates and ascends to ventral posterior medial nucleus.
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What is general sensation?
Sensory modality sub-divided into somatic sensation (tactile, thermal, pain and proprioception awareness) and visceral sensation (awareness of internal organs and chemoreceptors/barorecptors)
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What is special sensation?
Sensory modality responsible for vision, smell, taste, hearing and balance
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How are sensory receptors classified?
By their microscopic features (whether free nerve endings/seperate cells), activating stimuli (whether exteroceptors/interoceptors/proprioceptors) and stimulus detected (mechanoreceptors/osmoreceptors)
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Why may chronic pain remain after healing?
Because the internal brain connections are still present
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Describe the ascending pain pathway
A-delta and C fibres run into the spinal cord through Rexed's lamina (C I or II, A-delta II, IV, V or VI). Fibres synapse (A-delta with 2nd order, C with interneurone) and decussate to run up the spinal cord to join the anterolateral system.
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What is deafferentation?
Interruption/destruction of the afferent nerve pathways through nerve damage/amputation; may change pain pathway's synaptic plasticity (since central elements still operating but peripheral not) causing chronic/phantom limb pain.
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How is phantom limb pain treated?
Via a lesion to the thalamus (relevant nucleus) or deep brain stimulation
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What causes referred pain?
Convergence of sensory input on 2nd order neurones (so you don't know which 1st order activated it) or through innervation of dermatomes by multiple nerves (harder to tell them apart)
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What is the gate theory of pain?
Suggests pain perception can be altered by different modulations (e.g. touch). A-alpha and A-beta touch fibres release collateral branches when decussating that synapse with interneurones; give IPSP's to synapses between 1st and 2nd order pain fibres
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Descide the descending (centifugal) pain pathway
Frontal, sensory and limbic cortices --> periventricular nucleus of hypothalamus (endorphins act) --> periaqueductal grey matter (locus coerulus/raphe nucleus, serotonin and glutamate act) --> spinal cord (serotonin and endorphins act)
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How does the decending system inhibit pain?
The endorhins/serotonin/glutamate it releases activates the raphe signal which branches to interneurones that cause IPSP's in synapses of the ascending pain pathway
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How do opioids (morphine and codiene) and NSAID's operate?
Activate the decending system at the periventicular nucleus of the hypothalamus (by inhibiting the interneurones which supress it by releasing GABA to their sysnapses, generating IPSP's) activating it to inhibit the ascending pathway
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