Pre Clinical Medical Science SBAs
Pre Clinical Neuromuscular: (54 questions)

Questions

• 1
  What is the stimulus for release of adrenaline from the adrenal medulla?
  Difficulty: Easy     Topic: Adrenaline release
  a

  Acetylcholine at muscarinic receptors

  b

  Acetylcholine at nicotinic receptors

  c

  Adrenaline at beta-adrenoreceptors

  d

  Noradrenaline at alpha-1-adrenoreceptors

  e

  Noradrenaline at alpha-2-adrenoreceptors
  Explanation: Adrenaline is released by enterochromaffin cells within the adrenal medulla. It is released in response to activation of pre-ganglionic sympathetic neurones that release acetylcholine, which binds nicotinic receptors. Systemic adrenaline release is a small part of the whole sympathetic response.
• 2
  What is the difference between the neuromuscular junction and other electrical synapses?
  Difficulty: Medium     Topic: Neuromuscular junction
  a

  Calcium causes pre-synaptic transmitter release

  b

  End-plate potential depolarisation is larger than other excitatory post-synaptic potentials

  c

  The post-synaptic potential decays

  d

  There is re-uptake of transmitter

  e

  Transmitter diffuses across the cleft
  Explanation: The neuromuscular junction (NMJ) is like a specialised electrical synapse with a motor end-plate on the myofibres. The end-plate generates an end-plate potential (EPP) when acetylcholine (ACh) binds nicotinic receptors. The EPP is a large excitatory post-synaptic potential (EPSP), which has a high chance of stimulating an action potential. The EPP decays, like other EPSP. ACh acts like other transmitters: released by calcium, diffuses across the cleft and is re-uptaken.
• 3
  What is the mechanism of action of lidocaine?
  Difficulty: Easy     Topic: Lidocaine
  a

  Extracellular block of sodium channels

  b

  Intracellular block of calcium channels

  c

  Intracellular block of potassium channels

  d

  Intracellular block of sodium channels

  e

  Synaptic block of nicotinic acetylcholine receptors
  Explanation: All local anaesthetics (e.g. lidocaine) act to cause transient inhibition of peripheral nerve conduction without loss of consciousness. They act by blocking voltage-gated sodium channels from intracellularly, which prevents action potential transmission.
• 4
  How does the action of local anaesthetics change in acidic conditions?
  Difficulty: Hard     Topic: Local anaesthetics 1
  a

  Become less ionised

  b

  Increased entry through sodium channels

  c

  Increase transmembrane passage

  d

  Inhibit sodium channels extracellular

  e

  Reduced use-dependent blockade
  Explanation: Local anaesthetics are weak bases so become more ionised in acidic conditions. This prevents them from moving through neurone membranes to reach the intracellular domain of sodium channels. Instead they move through open channels, which promotes use-dependence because they will enter neurones more easily that are firing action potentials and have open sodium channels.
• 5
  Which sensory modality is a local anaesthetic least likely to block?
  Difficulty: Hard     Topic: Local anaesthetics 2
  a

  Crude touch

  b

  Fine touch

  c

  Pain

  d

  Proprioception

  e

  Temperature
  Explanation: Local anaesthetics preferentially block small fibres therefore block C-fibres and A-delta-fibres first. C-fibres transmit only pain. A-delta-fibres transmit pain, temperature and some fine touch. Crude touch is transmitted by A-beta-fibres but proprioception is transmitter by A-alpha fibres, which are larger still and therefore least likely to be blocked by a local anaesthetic.
• 6
  What form of reflex does a muscle spindle activate?
  Difficulty: Easy     Topic: Muscle spindle reflex
  a

  Contralateral monosynaptic

  b

  Contralateral polysynaptic

  c

  Cross-side polysynaptic

  d

  Ipsilateral monosynaptic

  e

  Ipsilateral polysynaptic
  Explanation: Muscle spindles activate an ipsilateral monosynaptic reflex arc. The afferent neurone activates the lower motor neurone innervating the same muscle, which causes it to contract. The spindle is activated by unexpected stretch, therefore it causes muscle contraction in response to stretch. An example of a cross-side polysynaptic reflex is the withdrawal reflex.
• 7
  How do muscle spindles modulate their output to muscle activity?
  Difficulty: Hard     Topic: Muscle spindles
  a

  Inhibition of A-alpha output

  b

  Interaction with golgi tendon organ

  c

  Recruitment of other muscle spindles

  d

  Variation of extrafusal fibre tone

  e

  Variation of intrafusal fibre tone
  Explanation: Muscle spindles are formed of axons wrapped around myofibres, known as intrafusal fibres. The contraction state (tone) of the intrafusal fibres modulates the output of the muscle spindle; this is controlled by gamma motor neurones. This allows the spindle to have a variable output based upon the overall muscle tone. None of the other statements are correct.
• 8
  What is the role of the golgi tendon organ?
  Difficulty: Medium     Topic: Golgi tendon organ
  a

  Contraction against unexpected stretch

  b

  Control of fine movements

  c

  Increase force of contraction

  d

  Relaxation with unexpected contraction

  e

  Relaxation to prevent muscle injury
  Explanation: Golgi tendon organs (GTO) are activated by high force being transmitted through a muscle's tendon. This passes through a polysynaptic reflex arc to cause inhibition of the lower motor neurone innervating that muscle. It was originally thought to serve a protective function it is more likely to be act for fine-tuning of muscle contraction especially when carrying objects.
• 9
  What enzyme is released into the circulation following muscle breakdown?
  Difficulty: Easy     Topic: Muscle enzymes
  a

  1-alpha-hydroxylase

  b

  Alanine aminotransferase (ALT)

  c

  Alkaline phosphatase (ALP)

  d

  Creative kinase

  e

  Gamma glutamyl-transferase (GGT)
  Explanation: Muscles contain many enzymes but in muscle damage CK (creatine kinase), lactate dehydrogenase (LDH) and aspartate aminotransferase (AST) can be found raised in the blood. ALP and GGT are biliary enzymes. ALT is specific to the liver. 1-alpha-hydroxylase is found most in the kidney and is used in vitamin D metabolism.
• 10
  What is the most common underlying pathology in motor neurone disease?
  Difficulty: Hard     Topic: Motor neurone disease
  a

  Antibody block of the neuromuscular junction

  b

  Antibody-mediated peripheral demyelisation

  c

  Inflammatory damage to proximal muscles

  d

  Lower motor neurone cell body death

  e

  Upper motor neurone demyelination
  Explanation: The most common form of motor neurone disease is amyotrophic lateral sclerosis, also known as Lou Gherig disease or anterior horn cell disease because there is death of lower motor neurone cell bodies. Myasthenia gravis causes antibody block of nicotinic acetylcholine receptors. Guillain-Barré syndrome causes antibody mediated demyelination. Myositis is inflammatory muscular damage. Multiple sclerosis causes central demyelination.
• 11
  What is the theory behind use of neostigmine in myasthenia gravis?
  Difficulty: Hard     Topic: Neostigmine
  a

  Agglutinate pathogenic antibodies

  b

  Block acetylcholine re-uptake

  c

  Direct stimulation of nicotinic receptors

  d

  Inhibit breakdown of acetylcholine in the synaptic cleft

  e

  Kill plasma cells responsible for antibody production
  Explanation: Neostigmine is an acetylcholinesterase inhibitor. It blocks the enzyme that normally acts to breakdown acetylcholine (ACh) in the neuromuscular junction. This means that ACh persists for longer and there is increased stimulation of nicotinic receptors, despite the presence of antibody. Other treatments may be given with an aim of reducing antibody but this is not the action of neostigmine.
• 12
  Where are the cell bodies located for the sympathetic pre-ganglionic neurones that innervate the face?
  Difficulty: Easy     Topic: Sympathetic supply of face
  a

  Anterior horn of C6

  b

  Lateral horn of C5

  c

  Lateral horn of T1

  d

  Nucleus tractus solitarius

  e

  Superior cervical ganglion
  Explanation: The cell bodies for all sympathetic pre-ganglionic neurones are located in the lateral horn of the spinal cord from T1-L2. Those supplying the face are located at T1, then ascend in the sympathetic chain and synapse in the superior cervical ganglion.
• 13
  What route do neurones takes that pass through the white ramus communicans?
  Difficulty: Medium     Topic: White ramus communicans
  a

  Spinal cord to sympathetic chains

  b

  Sympathetic chain to Coeliac ganglion

  c

  Sympathetic chain to peripheries

  d

  Sympathetic chain to spinal cord

  e

  Sympathetic chain to superior cervical ganglion
  Explanation: The rami communicans are structures that allow nerves to pass between the spinal cord and sympathetic chain. The white ramus communicans transmits myelinated pre-ganglionic fibres from the cord to the chain. The grey ramus communicans transmits post-ganglionic sympathetic neurones from the chain back to the mixed spinal root.
• 14
  What ligand-receptor combination mediates sympathetic neurone vasoconstriction of peripheral arterioles?
  Difficulty: Easy     Topic: Sympathetic vasoconstriction
  a

  Acetylcholine - nicotinic receptor

  b

  Adrenaline - alpha-1-adrenoreceptor

  c

  Adrenaline - beta-adrenoreceptor

  d

  Noradrenaline - alpha-1-adrenoreceptor

  e

  Noradrenaline - beta-adrenoreceptor
  Explanation: Post-ganglionic sympathetic neurones release noradrenaline from secretory vesicles. This acts on alpha-1-adrenoreceptors on vascular smooth muscle to increase intracellular calcium. Acetylcholine binds nicotinic receptors at the pre- to post-ganglionic sympathetic neurone synapse. Adrenaline shows preference for beta-adrenoreceptors. Adrenaline acts at beta-adrenoreceptors to cause vasodilatation in the coronary vessels.
• 15
  How is force of contraction neurally coded?
  Difficulty: Easy     Topic: Force of contraction
  a

  Higher frequency of action potentials

  b

  Larger action potentials

  c

  Recruitment of larger neurones

  d

  Use of gamma-motor neurones

  e

  Use of rubrospinal pathway
  Explanation: Force of contraction is initially coded by increasing the frequency of action potentials. This increases acetylcholine release at the neuromuscular junction and the frequency of action potential in muscle fibres. Larger myofibres, not neurones, are they recruited. Action potentials are all or nothing and cannot be large or small. Gamma motor neurones innervate muscle spindle intrafusal fibres. The rubrospinal pathway helps speed movements and give fine control.
• 16
  What is the autonomic innervation of sweat glands?
  Difficulty: Medium     Topic: Sweat glands
  a

  Parasympathetic acetylcholine release

  b

  Parasympathetic adrenaline release

  c

  Sympathetic acetylcholine release

  d

  Sympathetic adrenaline release

  e

  Sympathetic noradrenaline release
  Explanation: Sweat glands, unlike salivary and lacrimal glands, are supplied by sympathetic neurones. The post-ganglionic sympathetic neurones are unique because they release acetylcholine that acts at nicotinic receptors, to increase sweat production.
• 17
  Which of the following cranial nerves do NOT have a parasympathetic component?
  Difficulty: Easy     Topic: P'symp cranial nerves
  a

  III

  b

  VII

  c

  VIII

  d

  IX

  e

  X
  Explanation: There 4 cranial nerves with parasympathetic action. Occulomotor (III) supplies constrictor pupillae. Facial (VII) nerve supplies submandibular and sublingual salivary glands plus the lacrimal glands. Glossopharyngeal (IX) supplies parotid gland. Vagus (X) supplies many internal viscera.
• 18
  What is the cause of referred pain?
  Difficulty: Medium     Topic: Referred pain
  a

  Aberrant dorsal signalling

  b

  Ascent and descent of neurones in the tract of Lissauer

  c

  Inadequate opioid signalling in the spinal cord

  d

  Shared dorsal root between autonomic and somatic afferents

  e

  Shared efferent autonomic and somatic plexi
  Explanation: Referred pain occurs because of sharing of dorsal root between autonomic afferents and somatic afferents. The central nervous system considers them all to have come from the same (somatic) region therefore visceral pain may be felt in somatic regions. The tract of Lissauer allows ascent/descent of spinothalamic neurones but does not cause referred pain.
• 19
  How is most neurotransmitter formed?
  Difficulty: Medium     Topic: Neurotransmitter production
  a

  Re-uptake intact from the synaptic cleft

  b

  Synthesised in terminal boutons

  c

  Synthesised in the cell body and transported by diffusion

  d

  Synthesised in the cell body and transported by microtubules

  e

  Uptake from the blood by endocytosis
  Explanation: Most neurotransmitter is synthesised in the cell body and then is transmitted to synaptic terminals via microtubules. A minority of transmitter is assembled in the boutons from re-uptake of released transmitter. The consequence of this is that in axonal damage there is interruption of transport of transmitter to the synapse.
• 20
  What is neuropraxia?
  Difficulty: Medium     Topic: Neurone damage
  a

  Compression of a neurone

  b

  Lesion of the neurone cell body

  c

  Transection of an axon

  d

  Transection of a nerve with intact perineurium

  e

  Transection of a neurone with intact endoneurium
  Explanation: Neuropraxia is transient compression of an axon that may cause an alteration in transmission but no permanent damage to the neurone. Axonotmesis is damage to a neurone but where the endoneurium remains intact. Neurotmesis is transection of an entire nerve. Neurones don't recover from cell body damage.
• 21
  What is Wallerian degeneration in the repair of damaged neurones?
  Difficulty: Hard     Topic: Wallerian degeneration
  a

  Growth of multiple axonal sprouts from a damaged axon

  b

  Necrosis of Schwann cells

  c

  Phagocytic action of Schwann cells

  d

  Recruitment of lymphocytes

  e

  Release of neurotransmitter following axonal damage
  Explanation: Wallerian degeneration describes part of the response to damage of peripheral nerves. The myelin sheath degenerates and some Schwann cells begin to apoptose, in addition to axon damage. Surrounding Schwann cells, and recruited macrophages, clear the apoptotic cells and damaged tissue by phagocytosis before proliferating to repair the defect.
• 22
  Why does neurone repair not occur within the CNS?
  Difficulty: Hard     Topic: CNS damage
  a

  Absence of growth response

  b

  Haemorrhage prevents growth

  c

  Inhibitory ligands and lack of NTF

  d

  Lack of astrocytes

  e

  Neurites cannot enter adjacent endoneurium
  Explanation: Following CNS damage there is an initial inflammatory response with haemorrhage and oedema. Neurones attempt re-growth despite this, using neurotrophic factor (NTF) from astrocytes. Some sprouting neurites may enter an adjacent endoneurium and re-connect the neurone. However there is then a build up of ligands that inhibit growth and a relative lack of NTF that causes overall growth failure.
• 23
  Where are the vasa nervosum located in a peripheral nerve?
  Difficulty: Medium     Topic: Nerve structure
  a

  Between endoneurium and axons

  b

  Between epineurium and perineurium

  c

  Between perineurium and endoneurium

  d

  Outside the epineurium

  e

  Within the epineurium
  Explanation: Peripheral nerves are surrounded by the epineurium. Within this there is fat, blood vessels (vasa nervosum) and bundles of neurones surrounded by perineurium. Each axon is individually covered in an endoneurium, within which Schwann cells reside.
• 24
  Which cells form the blood-brain barrier?
  Difficulty: Easy     Topic: CNS glia
  a

  Astrocytes

  b

  Ependymal cells

  c

  Microglia

  d

  Oligodendrocytes

  e

  Pericytes
  Explanation: There are 4 main CNS glial cells. Astrocytes are support cells that form the blood-brain barrier with end feet that wrap around CNS capillaries. They are also important for water regulation and glucose transport. Ependymal cells line the ventricles and secrete CSF. Microglial are phagocytic cells. Oligodendrocytes myelinate CNS neurones - each oligodendrocyte may myelinate many neurones (unlike Schwann cells). Pericytes are cells that support capillaries in the peripheries.
• 25
  What roots form the brachial plexus?
  Difficulty: Easy     Topic: Brachial plexus
  a

  C2-C8

  b

  C3-T1

  c

  C4-T2

  d

  C5-T1

  e

  C5-T2
  Explanation: The brachial plexus is formed from C5-T1. It lies in the posterior triangle of the neck, posterior to the subclavian vessels and scalene muscles but anterior to trapezius. The main nerves that branch from it are: long thoracic nerve, axillary, musculocutaneous, median, ulnar and radial.
• 26
  Which nerve supplies the skin overlying the anatomical snuff box?
  Difficulty: Medium     Topic: Hand innervation
  a

  Axillary

  b

  Median

  c

  Musculocutaneous

  d

  Radial

  e

  Ulnar
  Explanation: The dorsal surface of the hand is supplied by the radial nerve laterally (to include the anatomical snuff box) and the ulnar nerve medially. The palmar surface is supplied by the median nerve for the lateral 3 1/2 digits, and the ulnar nerve medially.
• 27
  Which nerve supplies the skin on the posterior of the lower leg?
  Difficulty: Medium     Topic: Leg innervation
  a

  Common peroneal

  b

  Femoral

  c

  Saphenous

  d

  Sural

  e

  Tibial
  Explanation: The lower leg is supplied by: the tibial nerve on the posterior aspect, the common peroneal nerve on the lateral aspect and the saphenous nerve medially. The sural nerve supplies most of the plantar surface of the foot. The femoral nerve supplies the anterior compartment of the thigh, with a cutaneous branch supplying the skin over the medial thigh.
• 28
  What process causes movement of neurotransmitter across the synaptic cleft?
  Difficulty: Easy     Topic: Neurotransmitter movement
  a

  Chemotaxis

  b

  Diffusion

  c

  Electrical gradient

  d

  Enzymatic action

  e

  Osmosis
  Explanation: Neurotransmitter is released into the synaptic cleft when calcium stimulates fusion of vesicles with the presynaptic membrane. It then is free to passively diffuse across the small synaptic cleft. Chemotaxis describes the movement of cells towards a concentration gradient of a chemoattractive factor. Neurotransmitters are not electrically charged. Enzymatic action may terminate neurotransmitter effect but does not influence its movement. Only water moves by osmosis.
• 29
  What maintains intracellular & extracellular ion gradients?
  Difficulty: Easy     Topic: Ion gradients
  a

  Active ion pumps

  b

  Ion leak channels

  c

  Ligand gated ion channels

  d

  Osmosis

  e

  Voltage-gated channels
  Explanation: Active ion transporters, specially the sodium-potassium pump, are used to maintain the ion gradients between compartments. The sodium-potassium pump acts against the ions electrochemical gradients by pumping sodium extracellularly and potassium intracellularly. The overall ion gradients are determined by passive leak channels in cell membranes, but the gradients are maintained by the sodium potassium pump.
• 30
  What is the resting membrane potential of neurones?
  Difficulty: Medium     Topic: Membrane potential 1
  a

  -35mV

  b

  -45mV

  c

  -55mV

  d

  -65mV

  e

  -75mV
  Explanation: The resting potential of a neurone is approximately -65mV. The threshold for activation of an action potential is approximately -50mV. Cardiac ventricular myocytes have a much lower resting potential of nearly -90mV.
• 31
  What is the name of the calculation of a cell’s resting membrane potential?
  Difficulty: Medium     Topic: Membrane potential 2
  a

  Bernoulli principle

  b

  Constant field equation

  c

  Fick's law

  d

  Graham's law

  e

  Nernst equation
  Explanation: The constant field equation uses the electrochemical gradient and permeability of each ion for one cell to calculate its resting membrane potential. The Nernst equation does this process but with respect to one ion; the constant field equation combines many Nernst equations. The Bernoulli principle describes a reduction in pressure when gas travels faster. Fick's law describes the factors involved in diffusion. Graham's law describes the factors influencing diffusion of a gas.
• 32
  What is the role of ATP hydrolysis in the sodium potassium ATPase?
  Difficulty: Medium     Topic: Sodium-potassium ATPase
  a

  Allows release of potassium

  b

  Allows sodium to bind

  c

  Exchanges position of sodium and potassium

  d

  Externalisation of sodium

  e

  Internalisation of potassium
  Explanation: Sodium and ATP bind intracellularly to the channel. ATP hydrolysis causes externalisation of sodium, which is then released. This then allows potassium to bind, whilst only a phosphate group is bound. Loss of the phosphate causes the potassium to become internalised and then both sodium and ATP can bind again.
• 33
  What change occurs when action potential depolarisation threshold is passed?
  Difficulty: Easy     Topic: Action potential
  a

  Closure of voltage-gated calcium channels

  b

  Closure of voltage-gated potassium channels

  c

  Opening of nicotinic acetylcholine receptors

  d

  Opening of voltage-gated calcium channels

  e

  Opening of voltage gated sodium channels
  Explanation: For an action potential to be activated, depolarisation threshold must be passed. Once it is exceeded, voltage-gated channels become activated. On neurones this is sodium and potassium however the sodium channels open much more quickly than potassium channels so sodium permeability rises rapidly. This results in sodium influx and a depolarisation spike of an action potential.
• 34
  What is the consequence of a neurone membrane depolarisation to -60mV?
  Difficulty: Easy     Topic: Membrane potential 3
  a

  Action potential generated

  b

  Depolarisation persists until further stimulus

  c

  Em returns to baseline

  d

  Receptor potential stimulated

  e

  Small action potential generated
  Explanation: The action potential threshold for neurones is approximately -55mV. If the membrane is depolarised to less than this, the transient change in membrane potential will dissipate. This is usually a receptor potential, a small membrane potential change that decays. Action potentials are all-or-nothing events - a 'small' action potential is not possible.
• 35
  How do sodium and potassium permeabilities vary during an action potential?
  Difficulty: Medium     Topic: Ion permeabilities
  a

  Potassium permeability is raised longer than sodium permeability is raised

  b

  Potassium permeability rises as a consequence of sodium permeability increase

  c

  Potassium permeability rises at a greater rate than sodium permeability

  d

  Sodium permeability falls to baseline before potassium permeability rises

  e

  Sodium permeability rises after potassium permeability
  Explanation: Sodium permeability rises much more quickly than potassium. Both sets of voltage-gated channels are activated at threshold but sodium channels are 'fast'; rapidly opening causing a large increase in permeability and then close quickly. Whereas potassium channels open and then close more slowly with a longer duration but a smaller increase in permeability.
• 36
  What is the cause of the absolute refractory period?
  Difficulty: Medium     Topic: Refractory period
  a

  Excessive membrane depolarisation

  b

  Excessive potassium channels open

  c

  Insufficient calcium channels available for activation

  d

  Insufficient sodium channels available for activation

  e

  Membrane hyperpolarisation
  Explanation: The refractory period follows membrane depolarisation during an action potential. First is the absolute refractory period, where the are too few sodium channels available for activation, no matter the depolarisation stimulus. Potassium channels may be open and the membrane may be hyperpolarised but these are not the cause of the refractory period. The relative refractory period describes the state where an action potential requires a larger depolarisation stimulus than normal.
• 37
  What is a node of Ranvier?
  Difficulty: Easy     Topic: Node of Ranvier
  a

  Collection of neurotransmitter

  b

  Collection of Schwann cells

  c

  Gap between myelinated sections on an axon

  d

  Growth from a damaged neurone

  e

  Peripheral sympathetic ganglion
  Explanation: Myelin sheaths are discontinuous and the gaps between are known as nodes of Ranvier. These are areas where there is membrane with normal ion conductance, this causes depolarisation to move between nodes of Ranvier in transmission of an action potential - a process that greatly increases the speed of transmission. Nissl substance is synthesised transmitter in the cell body. Damaged neurones form growth cones of axons that may develop into neuromas.
• 38
  What factors cause an increase in action potential propagation speed?
  Difficulty: Easy     Topic: Conduction velocity
  a

  Greater diameter, myelinated and sensory neurones

  b

  Greater diameter and myelinated neurones

  c

  Greater diameter and un-myelinated neurones

  d

  Smaller diameter and myelinated neurones

  e

  Smaller diameter and un-myelinated neurones
  Explanation: Increased neurone diameter reduces resistance to passage of current, which allows for a higher conduction velocity. Myelination increases speed of transmission by insulating sections of the axon, causing depolarisation to jump between nodes of Ranvier. Being a sensory neurone does not increase transmission velocity.
• 39
  Which sensory fibre type conveys proprioception?
  Difficulty: Medium     Topic: Fibre types
  a

  A-alpha

  b

  A-beta

  c

  A-delta

  d

  A-gamma

  e

  C
  Explanation: A-alpha are the largest, myelinated neurones and are either for proprioception or form motor neurones. A-beta fibres are the 2nd largest neurones and are myelinated, they are involved in perception of innocuous touch and also in innervation of muscles. A-delta are general sensory fibres that can transmit both innocuous and noxious stimuli - they are small and myelinated. A-gamma and small & myelinated, for motor supply to muscle spindles. C-fibres and small and unmyelinated, and convey pain.
• 40
  Which form of synapse is most likely to stimulate an action potential in the post-synaptic neurone?
  Difficulty: Medium     Topic: Synapses
  a

  GABAergic axo-axonic

  b

  GABAergic axo-somatic

  c

  Glutaminergic axo-axonic

  d

  Glutaminergic axo-dendritic

  e

  Glutaminergic axo-somatic
  Explanation: Synaptic terminals can connect onto any part of a neurone: axon, dendrite or cell body (perikaryon). The closer the synapse is to the cell body, the higher the probability that an action potential will be triggered by a depolarising stimulus. Glutamate is an excitatory neurotransmitter, which causes membrane depolarisation, unlike GABA which causes hyperpolarisation.
• 41
  What proteins comprise gap junctions?
  Difficulty: Medium     Topic: Gap junctions
  a

  Actin

  b

  Cadherins

  c

  Connexins

  d

  Fibrillin

  e

  Intermediate filaments
  Explanation: Gap junctions are chemical synapses that facilitate the direct passage of small molecules between two adjacent cell's cytosol. They are comprised of collections of pores called connexons. Each connexon is made of 6 small proteins called connexins. Actin and intermediate filaments are part of the cell cytoskeleton. Cadherins are intercellular adhesion molecules with a role intracellular signalling. Fibrillin is an extracellular structural protein.
• 42
  Which ions have a higher extracellular than intracellular concentration?
  Difficulty: Easy     Topic: Extracellular ions
  a

  Potassium, calcium and chloride

  b

  Potassium, calcium and magnesium

  c

  Sodium, calcium and chloride

  d

  Sodium, potassium and calcium

  e

  Sodium potassium and chloride
  Explanation: The main extracellular ions are sodium (140mmol/L) and chloride (120mmol/L), these have much lower intracellular concentrations. The converse is true for potassium, which has a higher intracellular than extracellular concentration. Magnesium and calcium are also predominantly extracellular but at much lower concentrations than sodium.
• 43
  What change occurs when an action potential arrives at synaptic bouton?
  Difficulty: Easy     Topic: Synaptic transmission
  a

  Activation of phosphodiesterase

  b

  Activation of vesicle docking proteins

  c

  Closure of voltage-gated potassium channels

  d

  Opening of voltage-gated calcium channels

  e

  Opening of voltage-gated potassium channels
  Explanation: The first step in synaptic transmission is arrival of an action potential at the synaptic bouton. This causes activation, and subsequently opening, of voltage-gated calcium channels. Calcium associates with a number of specific proteins that result in fusion of synaptic vesicles with the pre-synaptic membrane.
• 44
  What kind of receptor is GABA-B?
  Difficulty: Hard     Topic: GABA
  a

  Anion ion-channel

  b

  Cation ion-channel

  c

  G-protein coupled

  d

  Non-receptor tyrosine kinase

  e

  Receptor tyrosine kinase
  Explanation: GABA (gamma-aminobutyric acid) binds receptors -A or -B. Both are inhibitory, resulting in a reduction of activity in the post-synaptic neurone. GABA-A are anion ion-channels, such that when activated then causing chloride entry. GABA-B are metabotropic receptors; they are G-protein coupled and have a more complex downstream signalling pathway.
• 45
  What is a sarcomere?
  Difficulty: Medium     Topic: Sarcomeres 1
  a

  Distance between two M-lines on a myofibre

  b

  Distance between two myofilaments

  c

  Distance between two Z-lines on a myofibril

  d

  One A-band on a myofibril

  e

  One I-band on a myofibre
  Explanation: A sarcomere is defined as the distance between two Z-lines on a myofibril. Myofibrils are the contractile structures within skeletal muscle cells (myofibres). Myofilaments are the contractile proteins that comprise myofibrils. Z-lines are where thin (actin) filaments attach.
• 46
  Which sarcomere band shortens during myofibre contraction?
  Difficulty: Medium     Topic: Sarcomeres 2
  a

  A

  b

  H

  c

  I

  d

  M

  e

  Z
  Explanation: The I band represents the area with only thin filaments. During contraction the thick filaments move into this area, overlapping with the thin filaments - shortening the I-band and increasing the A-band (the area with fibres overlapping). The H-zone is the area with only thick filaments, this is relatively unchanged during contraction. The Z-line is where thin filaments (actin) insert and the M-line is where thick filaments (myosin) inserts.
• 47
  What is the role of troponin in skeletal muscle contraction?
  Difficulty: Medium     Topic: Troponin
  a

  Bind ATP

  b

  Bind ATP and link actin to myosin

  c

  Bind calcium and link actin to tropomyosin

  d

  Block ATP binding-sites on myosin

  e

  Block myosin binding-sites on actin
  Explanation: There are three troponin molecules. Troponin C, I and T. Troponin C binds to calcium; it is linked to troponin I, which binds to actin, and troponin T that is bound to tropomyosin. The binding of calcium to Trop C causes movement in troponin I and T, which results in movement of tropomyosin out of the myosin binding-sites on actin.
• 48
  What is the role of T-tubules in skeletal myofibres?
  Difficulty: Medium     Topic: T-tubules
  a

  Attachment of myofilaments

  b

  Bring sarcolemma close to sarcoplasmic reticulum

  c

  Form the neuromuscular junction

  d

  Propagation of action potential to adjacent fibres

  e

  Store calcium for release during contraction
  Explanation: T-tubules are invaginations of the sarcolemma that bring the membrane in close opposition with the sarcoplasmic reticulum. This is necessary to facilitate excitation-contraction coupling; linking myofibre action potential to myofibril contraction. Sarcolemmal depolarisation activates DHP-receptors, which causes opening of ryanodine receptors on the sarcoplasmic reticulum. This releases calcium that goes on to initiate contraction.
• 49
  What protein on the sarcoplasmic reticulum mediates calcium release in response to dihydropyridine activation?
  Difficulty: Medium     Topic: DHP-calcium release
  a

  AMPA-receptor

  b

  NMDA-receptor

  c

  Ryanodine receptor

  d

  SERCA

  e

  Src
  Explanation: The ryanodine receptor forms a physical link with the voltage-gated calcium channel on the sarcolemma, called the dihydropyridine receptor. Membrane depolarisation enough to activate the DHP receptor causes a conformational change in both the DHP and ryanodine receptor. The result is release of calcium from the sarcoplasmic reticulum, which actively stores calcium using the SERCA pump. AMPA- and NMDA- and glutamate receptors. Src is a non-receptor tyrosine kinase.
• 50
  What process allows formation of cross-bridges in skeletal muscle contraction?
  Difficulty: Medium     Topic: Sliding filament hypothesis 1
  a

  ATP hydrolysis on myosin

  b

  Binding of ATP to myosin

  c

  Binding of calcium to myosin heads

  d

  Loss of phosphate on myosin

  e

  Movement of tropomyosin on actin
  Explanation: Cross-bridges form when myosin binding-sites on actin become available. This occurs when tropomyosin moves out of the blocking position, which takes place due to the presence of calcium and its interaction with troponin proteins. ATP hydrolysis causes myosin heads to revert to baseline position. ATP binding causes breakage of cross bridges. Phosphate loss causes the 'power stroke' hinge movement of myosin. Calcium does not bind the myosin head.
• 51
  What is the consequence of phosphate group loss from myosin in skeletal muscle contraction?
  Difficulty: Medium     Topic: Sliding filament hypothesis 2
  a

  Breaking of cross-bridges

  b

  Calcium loss from troponin

  c

  Change of myosin head angle

  d

  Formation of cross-bridges

  e

  Movement of tropomyosin on actin
  Explanation: Cross-bridges form when myosin has ADP + Pi bound and it is the loss of phosphate that causes the change in angle of the myosin hinge, which generates sarcomere shortening. Cross-bridges break when ATP exchanges for ADP. Cross-bridges form when tropomyosin moves on actin, due to the presence of raised calcium.
• 52
  How do type II skeletal myofibres differ from type I fibres?
  Difficulty: Medium     Topic: Skeletal muscle types
  a

  Type I are more resistant to anaerobic metabolism

  b

  Type I have less stored glycogen

  c

  Type II form most postural musculature

  d

  Type II have a higher maximum force of contraction

  e

  Type II have less stored myoglobin
  Explanation: Broadly, there are two types of skeletal muscle fibre: I and II. Type I fibres generate low contraction force, use aerobic metabolism (utilising glycogen), are very fatigue resistant and comprise the postural musculature. Whereas type II fibres are anaerobic, with high contraction force but fatigue quickly; they have myoglobin stored to use when oxygen falls very low.
• 53
  What is a myosatellite cell?
  Difficulty: Medium     Topic: Myosatellite cells
  a

  Macrophage-like cell in muscle

  b

  Muscle spindle cell

  c

  Myofibre progenitor cell

  d

  Peripheral myofibre

  e

  Resident muscle plasma cell
  Explanation: Satellite cells (myosatellites) are progenitor cells that lie toward the edge of muscle fibres. When muscle is damaged they multiply and can become incorporated into myofibres for formation of new tissue.
• 54
  What is the relationship between motor neurones (MN) and myofibres in a motor neurone
  Difficulty: Easy     Topic: Motor unit
  a

  Each MN innervates many myofibres of different types

  b

  Each MN innervates many myofibres of one type

  c

  Each MN innervates one myofibre

  d

  Each MN is innervated by many MN of one type

  e

  Each myofibre is innervated by many MN of different types
  Explanation: A motor unit is defined as one lower motor neurone and all the fibres that it innervates. Each myofibre is innervated by one LMN but each LMN innervates many fibres. Muscle fibre type is determined by the LMN type, for example a type II LMN will cause all the myofibres it innervates to be type II.