Review questions for term test

1) Describe cross-bridge cycling?

1) At rest - tropomyosin is held in place by troponin over the myosin-binding
sites of actin. Attached to the myosin head is an ADP and a phosphate (P i) myosin can't bind to actin yet. An action potential creates an increase in
Ca2+ ions and these bind to Troponin C. This causes a change in shape,
which pulls tropomyosin out of the way, exposing the myosin-binding site on
actin allowing myosin to bind.
This binding causes a change in the nucleotide pairing site of ADP and P i. The
Pi "falls off", releasing an extended position to allow myosin to pull. This
causes a change in the nuclear binding site and ADP "falls off" and ATP comes
in and binds.
ATP binds causing actin and myosin to separate. ATP hydrolyzes to ADP and P i
on the myosin head, resetting to the original stretched position. The myosin
then reattaches to a 'new' actin. Cross-bridge cycling will continue until actin
'run out'.
When tropomyosin tries to come in, we need troponin to come in between
actin and myosin - the ATP hydrolyses to ADP and Pi after actin and myosin
separate. The troponin slips in and blocks continued cycling.
When the [Ca2+] of the sarcoplasmic reticulum decreases the Ca2+ falls off
the Troponin C.

2) How come smooth muscle can be stretched up to many times its own
length, but still be able to generate force? How come smooth muscle can
generate an overall force as opposed to skeletal muscle which can only
generate force in the direction of its filaments? What structures within the
smooth muscle allow for this dynamic expansion and contraction?
2) The muscle structure is such that extension doesn't prevent actin and
myosin interactions like in skeletal muscle. Instead of a linear arrangement of
filaments we have actin filaments projecting in various directions within the
smooth muscle, originating from dense bodies. The dense body is an
important structure in smooth muscle, acting as an anchor for actin
filaments, and also anchored to the cell membrane. These thin filaments have
a directionality (one end is "positive" the other "negative" so as to align with
other actin filaments projecting from nearby dense bodies - this is not an
electrical concept, just an orientation one). Thick filaments (of myosin) are
formed when we stimulate the phosphorylation of myosin. Otherwise, dephosphorylated myosin will cause thick filaments to disintegrate into dimers.
So, a smooth muscle cell at rest has no thick filaments, but does have a cloud
of dimers throughout the sarcoplasm. When the MLCK (myosin-light-chain

kinase) phosphorylates them, they straighten out and will come together to
form a thick filament but need two thin filaments close enough together
of opposing direction to act as a scaffold.
The breaking down of thick filaments between contractions allows for
extreme stretching - will still have some dense body thin filaments close
enough together to permit formation of thick filaments.

3) How is contraction in smooth muscle triggered? How is it inhibited?

3) There is no structure covering the binding site for myosin on the actin, but
myosin heads will not bind spontaneously - they need to be phosphorylated
in order to become 'active' on the light chain of myosin. To intiate contraction,
we need to phosphorylate the myosin light chain. An increase in sarcoplasmic
concentration of calcium will trigger contraction in smooth muscle cells, but
the mechanism is much different from that of skeletal muscle.
Calcium will bind to calmodulin (CaM), which changes its shape - now
calmodulin can bind to MLCK (myosin-light-chain kinase) and activate it. The
whole complex of Ca2+-CaM-MLCK will phosphorylate the light chain of
myosin. We then get the active form of myosin and this will bind with actin to
generate contractions.
Contractions in smooth muscle are inhibited as the concentration of calcium
drops. Ca2+ will fall off of CaM, resulting in CaM falling off of MLCK. MLCP
(myosin-light-chain phosphatase), which is always present, will remove P i
from the myosin.

4) What are the roles of glucagon and insulin?

4)
Glucagon: Stimulates the release of glucose to the blood. 1 molecule of
glucagon can trigger the release of about a million glucose molecules. 2
processes:
1) glycogenolysis: breakdown of glycogen into glucose monomers
2) gluconeogenesis: formation of new glucose molecules from organic
precursors.
Insulin: Causes decrease of blood glucose levels. This hormone stimulates the
uptake of glucose by target tissues (most have insulin receptors).
- most tissues will be used in metabolism/storage
- insulin will trigger conversion of glucose to lipids and storage in
adipocytes
- binds to tyrosine kinase receptors.
5) How is frequency and intensity (volume) of sound determined?
5) Frequency of the perceived sound is determind by which part of the
cochlear duct is stimulated. Information about frequency is translated into
information about position on the basilar membrane. Amount of movement

at a given location depends on the amount of force applied by the stapes,

which is a function of the energy of the sound. The louder the sound, the
more the basilar membrane moves.
The intensity of the perceived sound is determind by how many of the hair
cells at that location are stimulated.
6) What is the organ of Corti?
6) The hair cells of the cochlear duct are located in this structure; it sits on
the basilar membrane, which separates the cochlear duct from the
tympanic duct. The hair cells are arranged in a series of longitudinal rows,
they lack kinocilia and their sterocilia are in contact with the overlying
tectorial membrane.
7) Why must the basilar membrane be stiff?
7) Sound waves from the vestibular duct across the thin vestibular
membrane into the cochlear duct will cause the basilar membrane to vibrate
when their frequencies match. All structures with a mechanical stiffness have
a frequency at which they will vibrate; resonance frequency. Different
places along the basilar membrane have different resonance frequencies.

8) How is the pressure in the middle ear kept the same to the external
environment?
8) Eustachian tube (aka: "Auditory tube") connecting to the pharynx
allows equalization of pressure.
9) Why doesn't an action potential propagate along dendrites? How does an
electrical signal travel in dendrites?
9) Because dendrites don't have channels which allow for propagation of
action potentials/electrical signals. Passive diffusion controls passage of
electrical signals: graded potential. There is a distance limitation.
10) Describe post-synaptic events IPSP (inhibitory post-synaptic potential)
and EPSP (excitatory post-synaptic potential)?
10) If the effect of the opening and closing of ion channels is a net movement
of (+) ions out of the cell, or (-) ions into the cell, the cell membrane will be
hyperpolarized. Since this means the resting potential of the post-synaptic
cell will be further from the threshold level required to create an action
potential, this is referred to as inhibitory post-synaptic potential (IPSP).
If the effect of the opening and closing of ion channels is a net movement of
(-) ions out of the cell or (+) ions into the cell, the cell membrane will be

depolarized. Since this means the resting potential of the membrane will be
closer to the threshold level required to create an action potential, this is
referred to as an excitatory post-synaptic potential (EPSP).
11) Compare spatial and temporal summation? What happens if both an
EPSP (excitatory postsynaptic potential) and an IPSP (inhibitory postsynaptic
potential) occur on the same location at the same time?
11)

12) What are proteasomes? What do they require in order to function?

12) Proteasomes are organells that contain an assortment of proteindigesting enzymes/proteases. They remove/break-down abnormal or
damaged proteins. Cytoplasmic enzymes attach chains of ubiquitin, a
molecular tag, to proteins destined for recycling. These tagged proteins are
quickly transported into the proteasome and disassembled into amino acids
and small peptides, which can be released to the cytoplasm. The 20S core
contains the active sites, while the 19S regulator ends regulate entry into the
destruction chamber by recognizing polyubiquitin tags.

13) What are cell junctions? What are the three most common types?
13) Tight junctions, desmosomes and gap junctions.