STPM BIOLOGY Nervous System
STPM BIOLOGY Nervous System
Resting potential
1. The membrane potential in a resting neuron or muscle cell is its resting potential
(-70mV). The membrane is said to be polarized.
2. The ion channels that establish the membrane potential have selective
permeability, meaning that they allow only certain ions K+ to pass.
3. The diffusion of K+ through open potassium channels is critical for formation of
the resting potential.
4. In resting potential, the ion channels allow K+ to pass in either direction across the
membrane. Because the concentration of K+ is much higher inside, the chemical
concentration gradient favours net outflow of K+.
5. Since the potassium channels allow only K+ to pass, Cl- and other anions inside
cannot accompany K+ across the membrane.
6. The outflow of K+ leads to an excess of negative charge inside the cell. This
buildup of negative charge within the neuron is the source of membrane potential.
7. The excess negative charges inside the cell exert an attractive force that opposes
the flow of additional positively charged K+ out of the cell.
8. The separation of charge thus results in an electrical gradient that counterbalances
the chemical concentration gradient of K+.
Action potential
– Whenever there is a stimulus (light or vibration), the voltage-gated sodium
channels will open resulting flow of Na+ into the neuron.
– The influx of Na+ will in turn trigger some more voltage-gated sodium channels to
open. If the stimulus is strong enough, the depolarization of membrane will reach
a particular point, called threshold (-55mV).
– Action potential is initiated and it has a magnitude that is independent of the
strength of the triggering stimulus. (all-or-none law)
Mechanism of action potential
1. At the resting potential, most voltage-gated potassium and sodium channels are
closed.
2. When stimulus depolarizes the membrane, some gated sodium channels open,
allowing more Na+ to diffuse into the cell. The Na+ inflow causes further
depolarization, which open more gated sodium channels, allowing even more Na+
to diffuse into the cell.
3. Once the threshold is crossed, this positive feedback cycle rapidly brings the
membrane potential close to ENa. This stage is the rising phase.
4. However, two events prevent the membrane potential from actually reaching ENa:
voltage-gated sodium channels inactivate soon after opening, halting Na+ inflow;
and most voltage-gated potassium channels open, causing a rapid outflow of K+.
both events quickly bring the membrane potential back towards EK. This stage is
called the falling phase.
5. In the final phase, called the undershoot, the membrane’s permeability to K+ is
higher than it is at the resting potential. The gated potassium channels eventually
close and the membrane potential returns to the resting potential.
Refractory period
– The sodium channels remain inactivated during the falling phase and the early
part of the undershoot.
– As a result, if a second depolarizing stimulus occurs during this period, it will be
unable to trigger an action potential.
– The downtime following an action potential when a second action potential
cannot be initiated is called the refractory period.
– When axon is in repolarisation state, the axon membrane is in absolute
refractory period. Another action potential cannot be initiated no matter how
great a stimulus is applied.
– When the Na gated channels are reset, neuron enters a relative refractory
period. During this period, the axon can transmit impulse, but the threshold is
higher.
All-or-none law
Conduction speed
Synapse
– The majority of the synapses are chemical synapses, which involve the release of
a chemical neurotransmitter by the presynaptic neuron.
– The cell body and dendrites of one of the postsynaptic neuron may receive inputs
from chemical synapse terminals.
– At each terminal, the presynaptic neuron synthesizes the neurotransmitter and
packages it in multiple membrane-bounded compartments called synaptic
vesicles.
– The action potential depolarizes the plasma membrane of presynaptic terminal,
opening voltage-gated calcium ion channels that allow Ca2+ to diffuse in.
– The resulting rise in Ca2+ concentration in the terminal causes some of the
synaptic vesicles to fuse with the terminal membrane, releasing the
neurotransmitter.
– The neurotransmitter in synaptic cleft bind to binding site of ligand-gated ion
channels and trigger the influx of Na+ and thus initiate action potential.
Postsynaptic potentials
– Two EPSPs occur at a single synapse in such rapid succession that the
postsynaptic neuron’s membrane potential has not returned to the resting potential
before the arrival of the second EPSP. When that happens, the neuron EPSPs add
together, an effect called temporal summation.
– EPSPs produced nearly simultaneously by different synapses on the same
postsynaptic neuron can also add together, an effect called spatial summation.
– Through spatial and temporal summation, several EPSPs can depolarize the
membrane at the axon hillock to the threshold, resulting in initiation of action
potential.
– Summation applies as well to IPSP: two or more IPSPs occurring nearly
simultaneously or in rapid succession have a larger hyperpolarizing effect than a
single IPSP.
– Through summation, an IPSP can also counter the effect of an EPSP.
Neuromuscular junction
– Each striated muscle fiber is a long, cylindrical cell with many nuclei.
– The plasma membrane, known as the sarcolemma in a muscle fiber, has multiple
inward extensions that form a set of T tubules.
– The cytoplasm of a muscle fiber is called sarcoplasm and the endoplasmic
reticulum is called the sarcoplasmic reticulum.
– Myofibrils, which are threadlike structures, run lengthwise through the muscle
fiber. They consist of even smaller structures, the myofilaments or simple
filaments.
– There are two types of myofilaments: myosin and actin filament.
– Myosin filaments are thick, consisting mainly of the protein myosin.
– The thin actin filaments consist mostly of the protein action; they also contain the
protein tropomyosin and the troponin complex that regulate the actin filament’s
interaction with the myosin filaments.
– Sarcomere is the basic units of muscle contraction.
– Sarcomeres are joined at their ends by an interweaving of filaments called the Z
line. M line is the anchorage site for myosin filaments.
– The I band consists of parts of actin filaments of two adjacent sarcomeres. The A
band is wide, dark region that includes overlapping myosin and actin filaments.
– Within the A band is a narrow, light area, the H zone, made up exclusively
myosin filaments.
Mechanism of muscular contraction based on the sliding filament theory
1. Muscle fiber in relaxed state. Note that I band and H zone are relatively wide.
2. Muscle fiber contracting. Actin and myosin filaments slide past one another,
increasing amount of overlap between actin and myosin filaments. Note that I
band and H zone decrease in length. Filaments themselves do not become shorter.
3. Contracted muscle fiber. Actin filaments overlap, eliminating H zone. I band also
disappear as Z line are pulled close to myosin filaments.
1. Sliding filament model was developed by two British biologists, Hugh Huxley
and Andrew Huxley.
2. When a motor neuron transmits a message, it releases the neurotransmitter
acetylcholine into the synaptic cleft.
3. Acetylcholine binds with receptors on each muscle fiber, causing depolarization
which causes generation of action potential.
4. Action potential travels along the sarcolemma and into the system of T tubule
membrane. Depolarization of the T tubule opens calcium channels in the
sarcoplasmic reticulum and stored calcium ions are released into the myofibrils.
5. Calcium ions bind to a protein in the troponin complex on the actin filaments,
which changes the shape of the troponin.
6. This change results in the troponin pushing the myotroponin away from the active
sites on the actiin filaments. These active sites, also called myosin-binding sites,
are now exposed.
7. One end of each myosin molecule is folded into two globular structures called
myosin heads. The rounded heads of the myosin molecules extend away from the
body of the myosin filaments.
8. Each myosin molecules has a long tail that joins other myosin tails to form the
body of the thick filaments.
9. ATP is bound to the myosin when the muscle fiber is at rest.
10. Myosin is an ATPase that converts the chemical energy of ATP into mechanical
energy of sliding filaments.
11. According to the model, ADP and Pi initially remain attached to the myosin head.
The myosin head is in an energized state; it is cocked.
12. The myosin head binds to an exposed active site on the actin filaments, forming a
cross bridge linking the myosin and actin filaments.
13. The inorganic phosphate and ADP is then released, which triggers a
conformational change in the myosin head. The myosin bends about 45 degrees,
in a flexing motion which pulls the actin filament closer to the center of the
sarcomere.
14. A new ATP must be bind to the myosin head before the myosin can detach from
the actin. Energized again, myosin heads contact a second set of active sites on
the actin filaments; this next set is farther down the molecule, closer to the end of
the sarcomere.
15. This series of stepping motions pulls the actin filaments toward the center of the
sarcomere.
1. A motor neuron realeases acetylcholine, which binds with receptors on the muscle
fiber, causing depolarization and an action potential.
2. The action potential spreads through T tubule, triggering Ca2+ release fro, the
sarcoplasmic reticulum.
3. Troponin that has bound Ca2+ undergoes a conformational change that causes
binding sites on the actin filaments to be exposed.
4. ATP (attached to myosin) is split and the energized myosin head is cocked; it
binds to the binding site on the actin filaments, forming cross bridge.
5. The release of Pi form the myosin head triggers the power stroke.
6. The power stoke occurs as the filaments is pulled toward the center of the
sarcomere and ADP is released.
7. The myosin head binds ATP and detaches from the actin. If the concentration of
Ca2+ is high enough, the sequence repeats from step 3.
8. When impulses from the motor neurone cease, Ca2+ is pumped back into
sarcoplasmic reticulum by active transport. The myotroponin once again covers
the myosin-binding site.
9. Muscle relaxation is restored.
Drug abuse
Cocaine
Curare
– Curare mimics the shape of acetylcholine and competes with acetylcholine to bind
to the ligand-gated ion channels on the postsynaptic membrane.
– Thus, no action potentials are initiated in the postsynaptic membrane.
– The muscles are unable to contract and may lead to paralysis and causes lung
failure if curare is present in the synaptic cleft of intercostal muscle.