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BScneurotest 2002 Feedback
BScneurotest 2002 Feedback
1. synaptic potentials T
2. generator potentials T
3. electrotonic potentials T
4. action potentials F These are propogated potentials
5. catelectrotonic potentials T
Question: With regard to nerve fibre types
Questions: Neurotrophins
T
2. the tension developed during contraction is proportional to the number of
cross-linkages between the actin and myosin molecules T
1. the axons of the preganglionic neurons leave the spinal cord with the
ventral roots of T1 to L3-4 T
2. the postganglionic nerves to the head originate, in part, in the superior
cervical ganglion T
3. axons of some of the postganglionic nerves reenter the spinal cord via the
white rami communicantes F
grey rami
4. each preganglionic axon diverges to an average of 8 or 9 postganglionic
neurons T
5. postganglionic neurons to the eye originate from the otic ganglion F
ciliary ganglion
1. tyramine T
2. ephedrine T
3. amphetamine T
4. clonidine F stimulates alpha 2 receptors
5. atenolol F blocks beta receptors
1. yohimbine T
2. propanolol T
3. nicotine F stimulates nicotinic receptors
4. neostigmine F inhibits cholinesterase
5. hexamethonium F blocks autonomic conduction
Essay question on the sodium potassium pump: (one mark per non repeated
correct fact). If more than 20 correct, relevant facts, then 20/20 scored. Serious
errors resulted in marks subtracted (this is, however, rare)
The pump is made up of 2 subunits, alpha and beta. Each subunit is essential
for pump function. Each subunit extends through the cell membrane, and has
intracellular and extracellular domains. The alpha subunit is the unit that binds
substances. The major function of the pump is to extrude three sodium ions form
the cell and take in 2 potassium ions for each mole of ATP that is hydrolysed. It
is thus electrogenic, and contributes to the generation of the resting membrane
potential. As it pumps more osmotically active substances out of the cell than
into the cell, it also regulates cell volume. The alpha subunit has biding sites for
sodium ions, ATP and inorganic phosphate ions on the intracellular surface, and
a binding site for potassium ions and ouabain on the extracellular surface.
Sodium ions bind to their binding site. At the same time, ATP binds and is
hydrolysed to ADP and inorganic phosphate. Binding of an inorganic phosphate
to its binding site changes the configuration of the alpha subunit, and this causes
the sodium ions to be pumped out. Potassium ions then bind extracellularly, and
this causes the configuration to change back to the original configuration, and
pumps in the potassium ions. Pump activity is increased by thyroid hormones,
aldosterone, and insulin. The pump is inhibited by dopamine and by ouabain
(binds to extracelluar site). Insulin thus stimulates the uptake of potassium into
the cell, and can be used for the treatment of hyperkalaemia (too high a
potassium ion concentration in blood). Dopamine causes a reduction in sodium
rebasorption in the kidney, and thus increases loss of sodium and water in the
kidney. Ouabain inhibits the pump. This causes the build up of sodium inside
the cell. This reduces sodium influx in the cell via the Na-Ca exchanger (sodium
in; calcium out pump). As a result, calcium is unable to leave the cell and thus is
available for muscle contraction. This is of particular relevance in cardiac
muscle. Digitalis has the same effect. Aldosterone causes the reabsorption of
sodium and secretion of potassium in the renal tubules.
Essay question on smooth muscle: (same marking process): The question was
on the molecular mechanisms.
Calcium ions are involved in the contraction of smooth muscle. Entry of calcium
ions in smooth muscle occurs mainly through the cell membrane from the
extracellular fluid. Very little come from the sarcoplasmic reticulum as the
sarcoplasmic reticulum is poorly developed. Myosin in smooth muscle must first
be phosphorylated before contraction can occur. Calcium ions bind with a
calcium binding protein called calmodulin. There is no troponin C in smooth
muscle. The calcium-calmodulin complex activates an enzyme called
calmodulin-dependant myosin light chain kinase. This phosphorylates the
myosin. ATPase is then activated, and ATP is split into ADP and energy on the
myosin molecule. Myosin then slides on actin, and contraction occurs
(shortening of muscle fibre length). Myosin is dephosphorylated by myosin
phosphatase. This leads to relaxation of smooth muscle in some cases. In other
cases, relaxation does not occur. A unique smooth muscle mechanism called
the latch-bridge mechanism allows for the sustained binding of actin and myosin
even after the intracellular calcium ion concentration has fallen. This mechanism
is a low energy mechanism that is important in maintaining the tone of smooth
muscle (degree of partial contraction)