Q: True or false? There is passive signalling in most dendrites. A: True Q: Name all the different types of afferent nerve fibres in the Lloyd classification system. A: Ia Ib II III IV Q: Where do Lloyd group Ia afferent nerve fibres originate? A: Muscle spindles Q: Where do Lloyd group Ib afferent nerve fibres originate? A: Golgi tendon organs Q: Where do Lloyd group II afferent nerve fibres originate? A: Skin tactile receptors Muscle spindles Q: Where do Lloyd group III afferent nerve fibres originate? A: Skin (cold and nociceptive receptors) Q: Where do Lloyd group IV afferent nerve fibres originate? A: Skin nociceptors Cutaneous warm receptors Muscle nociceptors Q: Which of the four Lloyd groups of afferent fibres is unmyelinated? A: IV Q: Which of the groups (A-alpha, A-beta, A-gamma, A-delta, B, C) have the origin/function: Somatic motor muscle afferents Q: Which of the groups (A-alpha, A-beta, A-gamma, A-delta, B, C) have the origin/function: Motor fibres to muscle spindle A: A-gamma A: A-alpha Q: Which of the groups (A-alpha, A-beta, A-gamma, A-delta, B, C) have the origin/function: Efferent - autonomic pre ganglionic A: B Q: Which of the groups (A-alpha, A-beta, A-gamma, A-delta, B, C) have the origin/function: Afferent - pain and thermal A: A-delta Q: Which of the groups (A-alpha, A-beta, A-gamma, A-delta, B, C) have the origin/function: Tactile afferents muscle afferents A: A-beta Q: Which of the groups (A-alpha, A-beta, A-gamma, A-delta, B, C) have the origin/function: Efferent - autonomic post ganglionic Afferent - pain and thermal A: C Q: What does fast anterograde axoplasmic transport transport? A: Membrane glycoproteins (eg fibronectin and N-cam) Vesicles Q: What does intermediate anterograde axoplasmic transport transport? A: Mitochondrial proteins Q: What does slow anterograde axoplasmic transport transport? A: Tubulin (to make axonal microtubules) Actin (to make axonal microfilaments) Q: What is the speed of retrograde axoplasmic transport? A: 100 mm/day Q: What are the 5 functions of axoplasmic transport? A: 1. Maintenance of internal membrane structure of the axon 2. Supply of transmitter or transmitter-synthesising enzymes from cell soma to terminals 3. Supply of trophic materials for target structures of the neurone; and after uptake and retrograde transport, supply of trophic factors for the neurone from the target tissue 4. Possible pathological role - some virii and toxins may be transported 5. Possible experimental research role - can transport tracer substances to reveal connections between different parts of nervous system. Q: This is missing Paragraph A on page 4 - because I don't understand it. A: Ask a conscie about it. Q: What is the neurotransmitter between motoneurone axons and Renshaw cells? A: Acetylcholine Q: What is probably the major excitatory neurotransmitter of the central nervous system? A: Glutamate Q: What additional cation is the NMDA-receptor permeable to that the kainate receptor is not? A: Ca++ Q: Why is the NMDA-receptor said to be both voltage-gated AND transmitter-gated? A: The NMDA-receptor may be opened by either a combination of activation by N-methyl D aspartate and a small depolarisation caused by non-NMDA-receptors (20-30mV) OR simply by adequate depolarisation of the membrane. Q: Name two Ca++ impermeable, Na+/K+ permeable glutamate receptor channels. A: Kainate receptor Quisqualate (or AMPA) receptor Q: What type of component does the NMDA-receptor add to the EPSP? A: A small and delayed component Q: Name a few of the causes of excitotoxicity caused by excess glutamate. A: Ischaemic brain injury due to cardiac arrest, stroke, brain trauma, seizures or other sources of hypoxia Q: What is the mechanism for excitotoxicity? A: Hypoxia in the brain can trigger membrane depolarisation, excess Ca++ influx and excess glutamate release. This leads to further depolarisation and hyperactivity of the central neurones. Excitotoxicity kills central neurones. Q: What is the major inhibitory neurotransmitter of the central nervous system? A: Gamma-amino-butyric acid (GABA) Q: What inhibitory transmitter (other than GABA) is often found certain spinal cord interneurones? A: Glycine (particularly in Renshaw cells of the ventral horn) Q: Which of the three principal subunits (alpha, beta and gamma) of the GABA(a)-receptor does GABA bind to? A: All three Q: Which of the three principal subunits (alpha, beta and gamma) of the GABA(a)-receptor do the barbiturate class of drugs bind to? A: Alpha and beta. (increasing Cl- conductance) Q: Do activated anion selective channels mediated by GABA and Glycine increase or decrease the conductance to Cl- ions? A: Increase Q: What are the two major receptors GABA acts on? A: GABA(a) and GABA(b) receptors Q: Which of the three principal subunits (alpha, beta and gamma) of the GABA(a)-receptor do the anti-anxiety and muscle relaxant benzodiazepine class of drugs bind to? A: Gamma Q: True or false? The GABA channels but not Glycine channels are both transmitter-gated and voltage-gated. A: False. Both GABA channels and Glycine channels are transmitter-gated and NOT voltage-gated. Q: What receptor is blocked by bicuculline? A: GABA(a) receptor Q: What receptor is blocked by phaclofen? A: GABA(b) receptor Q: How does strychnine work? A: It blocks glycine's actions Q: True or false? GABA(b) receptors involve a G-Protein receptor which causes Cl- channels to open? A: False. GABA(b) receptors involve a G-Protein receptor which causes K+ channels to open Q: What category of neurotransmitters do noradrenaline, dopamine and 5-hydroxytryptamine belong to? A: Monoamines Q: What monoamine is prominent in the raphe nucleus? A: Serotonin (5-HT) Q: What is the main monoamine neurotransmitter in the substantia niagra and ventral tegmental area? A: Dopamine Q: What is the main monoamine neurotransmitter concentrated in the locus coeruleus? A: Nor-adrenalin Q: Which neurotransmitter function appears to be impaired in Parkinson's disease? A: Dopamine Q: What category of neurotransmitters do enkephalins and substance P belong to? A: Peptides Q: Name 3 types of nerve networks common to CNS organisation which participate in the process of selective attention? A: 1. Recurrent or feedback inhibition - limits level and spread of neuronal activity 2. Surround inhibition (also lateral or afferent inhibition) - involves pre- and post- synaptic mechanisms. 3. Corticofugal control through sensory relay nuclei - improves resolution os ascending activity Q: True or false? Tetanus toxin and strychnine cause convulsions by directly stimulating the motoneurones. A: False. Tetanus toxin and strychnine cause convulsions because they block Renshaw cell inhibition (which normally limit the level and spread of neuronal activity). Q: The cable equation indicate that a passively transmitted signal fades (a)linearly, (b) parabolically or (c) exponentially? A: c Q: What are 3 reasons for the small space constant (100 - 200 micrometres) of most dendrites? A: * No myelin sheath * High core resistance (due to small fibre diameter) * Branching (more current leakage) Q: True or false? The rods of the eye have passive signalling, where as the cones have active signalling. A: False. Both the rods and the cones (and the bipolar cells as well) have passive signalling, which is sufficient considering the limited distance over which they must transmit. Q: What is the slow degenerative CNS inflammatory disease in which lesions of the myelin sheath of nerve axons which lead to slowing and failure of conduction of nerve signals? A: Multiple sclerosis. Q: What is Guillian-Barre Syndrome? A: Guillian-Barre Syndrome is an acute inflammatory post infectious polyneuropathy in which peripheral motor and sensory nerves display impaired conduction as a result of myelin sheath dysfunction subsequent to some viral infections or immunisation. Q: True or false? The Lloyd classification of nerve fibres applies to efferent fibres only? A: False. The classification applies to afferent fibres only. Q: What feature of nerve fibres in spinal dorsal roots was the Lloyd classification of nerves based on? A: Diameter. Q: What are the 6 major (generalised) causes of neuropathy? A: * Traumatic - e.g. crushing * Autoimmune - e.g. multiple sclerosis * Inflammatory demyelinating disorders - e.g. Guillain-Barre syndrome * Metabolic/Nutritional impairment - e.g. diabetes * Chemical/Drug induced - e.g. toxicity by vincristine * Hereditary - e.g. Charcot-Marie-Tooth disease (aka peroneal muscular atrophy, a hereditary progressive disease leading to muscle wasting) Q: What is Wallerian degeneration? A: The nucleus of a neuron makes a number of substances that are required for normal metabolism and function throughout the cell including to its farthest extensions. Wallerian degeneration occurs following injury or disease and progresses from the place of injury along the axon away from the cell body while the part between the place of injury and the cell body remains intact. If the basement membrane of the schwann cells survive, it can serve as a scaffold for myelination of the axon. Q: What is the typical space constant for a dendrite? A: 100 - 200 micrometres. Q: What is the typical space constant for an axon of a large neuron? A: 3-4 mm. Q: Which cells of the cerebellum have myelinated dendrites? A: Purkinje cells. Q: What are the 2 reasons muscles undergo atrophy when their nerve supply is damaged? A: * Decreased workload * Loss of trophic factors from neuron Q: Outline the major events in neuromuscular synaptic transmission. A: * A wave of depolarisation reaches the axon terminal * This causes a transient increase in Ca2+ permeability * Ca2+ influx into neuron * This causes synaptic vesicles to fuse with plasma membrane * These release acetylcholine into the synaptic cleft * Acetylcholine binds to receptors on the muscle cell membrane (2 acetylcholine molecules to 1 receptor complex) * This causes an ion channel permeable to both Na+ and K+ to open generating an end plate potential * If the End plate potential is above the muscle cell threshold, an action potential will be generated in the muscle cell * Cholinesterases deactivate the released acetylcholine Q: What is the aetiology of myasthenia gravis? A: Myasthenia gravis is an autoimmune disorder that affects the neuromuscular junction. The patient has developed an immune reaction against their own acetylcholine receptors, which are then progressively destroyed. As the number of activated receptors decreases, End Plate Potential goes below threshold and cannot initiate an action potential. Paralysis results and death may follow if the respiratory muscles are affected. Neostigmine, an anticholinesterase, brings symptomatic relief by prolonging the effect of acetylcholine on existing receptors. However, this is not a cure for it still depends on existing receptors for the drug to work. Once all the receptors are destroyed the muscles cannot be stimulated at all no matter how much acetylcholine is present. Q: How does curare act to cause paralysis? A: Curare, the South American Indian arrow poison, acts by blocking the binding site on the acetylcholine receptor. As the number of activated receptors decreases, EPP goes below threshold and cannot initiate an action potential thus causing paralysis. Q: What are the so called 'positive effects' (incorrect perception of stimuli) in neuropathy? A: * Parathesia - 'pins and needles' associated with large fibre disruption * Dysaesthesia - pain associated with light touch * Hyperalgesia - lowered threshold to painful stimuli * Causalgia - burning sensation in field of injured nerve Q: In a typical neurone, which has a higher thresold potential, the axon or the soma? A: The soma. Q: What are the 5 criteria for establishing a substance's status as a neurotransmitter? A: * Must be synthesised and present in presynaptic neurone * Must be released by presynaptic nerve stimulation * Action on postsynaptic neurone of exogenously applied compound should mimic those of presynaptic nerve stimulation * Should be a specific receptor for the compound on on the post synaptic membrane * Should be a mechanism for removal or inactivation of the compound Q: True or false? In the peripheral nervous system, axons and dendrites can be repaired. A: True but with qualifications. In the peripheral nervous system, axons and dendrites can be repaired *if* the cell body remains intact *and* if the neurolemmocytes (Schwann cells) remain active. Q: True or false? Neurones in the human brain proliferate until about the age of 20-25 years when cell division gradually stops and neurones begin to degenerate. A: False. At birth we have all the neurones we need. We cannot make new neurones late in life but there are regenerative processes. Q: What kind of ion channel does tetroclotoxin block? A: Na+. Q: What kind of ion channel does tetraethylammonium (TEA) block? A: K+. Q: What are some of the symptoms of autonomic dysinflexia? A: * Nasal congestion * Tingling sensation in neck * Profues sweating * Pounding headache * Bright flushing in the face * Restlessness * Pounding in ears * Slow pulse * Goose bumps * Eventual increase in blood pressure -> To dangerous levels Q: What are some of the causes of autonomic dysinflexia? A: * Blocked catheter * Compacted bowel * Ingrown toenail * Haemorrhoids * Sexual activity Q: What are the 3 major types of neural inhibition? A: * Reccurent (feedback) inhibition * Surround (lateral/afferent) inhibition * Corticofugal inhibition Q: What are the features of reccurent (feedback) inhibition? A: * Circuit regulates flow of information to prevent overload. * It acts to limit spread and level of neuronal activity. * Collateral branches of excitatory axons pass to inhibitory interneurones which pass back to the original neurone's cell body. * It is interfered with by tetanus (inhibits glycine release from Renshaw cells) and strychnine (competitive blocker of glycine on motoneurones). Both substances cause convulsive fits. * Recurrent inhibitory circuits are found throughout the CNS * Either glycine or GABA are the inhibitory neurotransmitter used in recurrent inhibitory circuits. Q: What are the features of surround (lateral/afferent) inhibition? A: * It limits spread of activity in a population of neurones. * It involves both pre- and post-synaptic mechanisms. Q: What kind of inhibition does the below diagram and description represent? _/ cortex_/>---_ _/O--_ \_ / \ \ \ \ ,~|~~~~|~~~~, | `-. | sensory relay nucleus `~~~~~~~~~|~' | |sensory input A neurone from the cortex synapses in the sensory relay nucleus with an inhibitory interneurone. A: Corticofugal inhibition (which serves to improve the resoltuion of ascending activity and participates in the process of selective activity). Q: What are the 2 major excitatory neurotransmitters within the central nervous system? A: * Glutamate * Acetylcholine Q: True or false? Kainate and quisqualate receptors lead to opening or 'gating' or a cation channel permeable to Na+ and K+ and are distinguishable on the basis of selective action of glutamate agonists kainate and quisqualate. A: True. Q: At resting potential, the NMDA recptor is partly plugged by what type of ions? A: Mg++ ions. Q: When does the NMDA receptor ion channel contribute notably to membrane potential? A: The NMDA receptor ion channel only contributes notably to membrane potential when depolarisation achieved by non-NMDA receptors is great enough. Q: In an NMDA receptor, what potential is necessary to dislodge Mg2+ ions? A: 20-30mV. Q: Why is the NMDA receptor ion channel called a cation selective channel? A: It lets Ca2+ and Na+ in and lets K+ out.