TABARAK PRIVATE SCHOOL

BIOLOGY NOTE (G12)

CONTROL AND COORDINATION

The nervous system

The nervous system is built from specialized nerve cells called neurons.
Neurons are grouped to form

There are three types of neurons:

1. Sensory neurons: have a single long dendron, which brings impulses

towards the cell body, and a single axon which carries impulses away
from the cell body. Sensory neurons transmit impulses from receptors
to the spinal cord or brain.

1
2. Intermediate neurons (also known as relay or interneurons): have
numerous, short fibres. They connect sensory neurons and motor
neurons
3. Motor neurons: have a cell body that lies within the brain or spinal
cord. Many highly-branched cell processes (dendrites) extend from the
cell body. Dendrites receive impulses from other neurons and conduct
them towards the cell body. A single long axon transmits impulses
away from the cell body. The function of a motor neuron is to transmit
impulses from the CNS to effector organs, such as muscles or glands.

2
Sensory receptors and the conversion of energy into impulses: The
sense cells (receptors) are specialized to detect stimuli and to respond by
producing an impulse (an action potential). Different types of sensory
receptors exist in the body. The property of a sense cell is to transfer the
energy of a particular type of stimulus into the electrochemical energy of an
impulse, which is then conducted to other parts of the nervous system. The
stimulus that the sense cell responds to is some form of energy, mechanical,
chemical, thermal, or light (photic).

3
 Chemoreceptors: responding to chemical stimulation

Chemoreceptors are specialized sensory receptors in our sense organs

that recognize chemical stimuli. The senses of taste and smell are the most
common examples of chemoreception in humans. Humans have
approximately 100,000 chemoreceptor cells in taste buds, located on the
upper surface of the tongue, soft palate, upper esophagus, and epiglottis.

Dissolved chemicals from food enter the taste bud through the taste pore
and bind to the receptor cells, causing a change in the shape of the
chemoreceptor protein on the cell surface. This change in shape causes
chemical-gated sodium channels in the cells to open, resulting in an influx of
sodium ions into the cells. This causes the cell membrane to depolarise. This
depolarization is transmitted to the taste neurons, resulting in an action
potential. The action potential is ultimately transmitted to the medulla
oblongata in the brain, where it is recognized as a specific taste.

4
 Transmission of an impulse

Impulses are transmitted along nerve fibers (neurons). These impulses travel
very rapidly along the cell surface membrane from one end of the cell to the
other.

Resting potential: The difference in electrical potential that is maintained

across the cell surface membrane of a neuron when it is not transmitting an
action potential. It is normally about –70 mV inside and is partly maintained
by sodium–potassium pumps

In a resting neuron, it is found that the inside of the axon always has a slightly
negative electrical potential compared with the outside. The difference
between these potentials, called the potential difference, is often between
−60 mV and −70 mV.

5
The resting potential is produced and maintained by the sodium–potassium
pumps in the cell surface membrane (active transport). These constantly
move sodium ions, Na⁺, out of the axon, and potassium ions, K⁺, into the
axon.

There is also facilitated diffusion of potassium ions out and sodium ions
back in. The membrane is far more permeable to potassium ions flowing out
than to sodium ions returning. As a result, the inside becomes more and
more negatively charged compared with the outside; the resting neuron is
said to be polarised.

Action potential: A brief change in the potential difference from –70 mV to

+30 mV across the cell surface membranes of neurones and muscle cells
caused by the inward movement of sodium ions.

An impulse (action potential) is triggered by a stimulus received at a receptor

cell or sensitive nerve ending. In the action potential, the energy transferred
by this stimulus causes a temporary and local reversal of the resting
potential. The result is that the membrane is briefly depolarised at this point.

6
 Ion movements during the action potential

1. During the resting potential, the ion channels for Na⁺ ions and K⁺ ions
are both closed.
2. Na⁺ channels open and Na⁺ ions rush in (by diffusion).
3. The interior of the axon becomes increasingly more positively charged
to the outside.
4. Equally suddenly, Na⁺ channels close at the same moment as K⁺
channels open, and K⁺ ions rush out (by diffusion).
5. The interior of the axon now starts to become less positive again.
6. Na⁺/K⁺ pump starts working, together with facilitated diffusion, so that
the resting potential is re-established

Action potentials are only generated if the potential difference reaches a

value between –60 mV and –50 mV. This value is the threshold potential.
If this value is not reached, an action potential does not occur.

The action potential travels along the whole length of the neuron fiber. At any
one point, it exists for only two 2 milliseconds before the membrane starts to
re-establish the resting potential.

7
Refractory period: A period of time during which a neuron is recovering from
an action potential, and during which another action potential cannot be
generated.

In the body, action potentials begin at one end of an axon, such as the
junction between the axon and the cell body. ‘New’ action potentials are
generated ahead and not behind. This is because the region behind is
recovering from the action potential that has just occurred, so the sodium ion
voltage-gated channels are closed. These channels are so tightly closed that
they cannot open. This period of recovery, when the axon is unresponsive,
is called the refractory period. This means:

• Action potentials are discrete events; they do not merge into one another

• There is a minimum time between action potentials occurring at any one

place on a neuron

• The length of the refractory period determines the maximum frequency at

which impulses are transmitted along neurones; for many neurones, this is
between 200 and 300 impulses per second

• The impulse can only travel in one direction along the neuron.

Speed of conduction of the action potential: In unmyelinated neurons,

the speed of conduction is slow, being as low as 0.5 m s−1 in some cases.
In a myelinated human neuron, action potentials travel at speeds of up to
100 m s−1. Myelin speeds up the rate at which action potentials travel by
insulating the axon membrane. Sodium and potassium ions cannot flow
through the myelin sheath, so depolarization or action potentials can't occur
in parts of the axon that are surrounded by the myelin sheath.

8
Action potentials can only occur at the nodes of Ranvier, where all the
channel proteins and pump proteins are concentrated. Consequently, the
action potentials are forced to jump from node to node. This is called
saltatory conduction. This is an advantage, as it greatly speeds up the rate
of transmission.

Synapses – the junctions between neurons: Where two neurons meet,

they do not touch. A tiny gap, called a synapse, is the link point between
neurons. Synapses consist of the swollen tip (synaptic knob) of the axon of
one neuron (the presynaptic neuron) and the dendrite or cell body of
another neuron (the postsynaptic neuron). Between these is the synaptic
cleft, a gap of about 20nm.

The practical effect of the synaptic cleft is that an action potential cannot
cross it. Transmission occurs through particular chemicals, known as
transmitter substances. These substances are all relatively small, diffusible
molecules. Acetylcholine (ACh) is a commonly occurring transmitter
substance released by cholinergic neurons.

9
10
 Steps to synapse transmission

1. The arrival of an action potential at the synaptic knob opens calcium

ion (Ca²⁺) channels in the presynaptic membrane. Calcium ions flow in
from the synaptic cleft.
2. The calcium ions cause vesicles of the transmitter substance to fuse
with the presynaptic membrane, and they release a transmitter
substance into the synaptic cleft.
3. The transmitter substance diffuses across the synaptic cleft and binds
with a receptor protein.
4. The transmitter substance on the receptors is quickly inactivated. This
reaction causes the ion channel of the receptor protein to close,
allowing the resting potential in the postsynaptic neuron to be re-
established.
5. The inactivated products of the transmitter re-enter the presynaptic
knob, are resynthesized into transmitter substance, and packaged for
reuse.

The structures of striated muscle

Skeletal muscle fibers appear striped under the light microscope, so the
skeletal muscle is also known as striated muscle. Striated muscle consists
of bundles of muscle fibers. The muscle fiber can shorten to half or even a
third of its relaxed or resting length. Each fiber is composed of a mass of
myofibrils, but only an electron microscope can reveal this important detail.

The striped appearance of skeletal muscle is due to an interlocking

arrangement of two types of protein filaments, known respectively as thick

11
(myosin) and thin (actin) filaments. These protein filaments are aligned,
giving the appearance of stripes (alternating light and dark bands).

How a motor nerve ending makes a connection with a muscle fiber

Striated muscle fibers are innervated by a motor neuron nerve ending at a

motor end plate or neuromuscular junction. Upon arrival of an action potential
at the neuromuscular junction, acetylcholine vesicles are released, and
the transmitter molecules bind to receptors on the sarcoplasm. This triggers
the release of calcium ions from the sarcoplasmic reticulum into the
cytoplasm around the myofibrils, via the T-tubule system.

Calcium ions then remove the blocking molecules on the binding sites of the
actin filaments, which then kickstart the contraction process. When action
potentials stop arriving at the muscle fibers, calcium ions return to the
sarcoplasmic reticulum, and the binding sites are again covered by blocking
molecules.

12
 Skeletal muscle contracts by sliding the filaments

When skeletal muscle contracts, the actin and myosin filaments slide past
each other in response to nervous stimulation. This causes the shortening of
the sarcomeres. A great deal of ATP is used in the contraction process.
Shortening is possible because the thick filaments are composed of many
myosin molecules, each with a bulbous head that protrudes from the length
of the filament. Along the actin filament are a complementary series of
binding sites to which the bulbous heads fit. However, in muscle fibers at
rest, the binding sites carry blocking molecules (a protein called
tropomyosin), so binding and contraction are not possible. Calcium ions
play a critical part in the muscle fiber contract mechanism, together with the
proteins tropomyosin and troponin.

The contraction of a sarcomere is described in the following four steps.

1. The myofibril is stimulated to contract by the arrival of an action

potential. This triggers the release of calcium ions from the
sarcoplasmic reticulum, which surrounds the actin molecules. Calcium
ions now react with an additional protein present (troponin) which,
when so activated, triggers the removal of the blocking molecule,
called tropomyosin. The binding sites are now exposed.
2. Each bulbous head to which ADP and Pi are attached (called a charged
bulbous head) reacts with a binding site on the actin molecule beside
it. The phosphate group (Pi) is shed at this moment.
3. The ADP molecule is then released from the bulbous head, and this is
the trigger for the rowing movement of the head, which tilts at an angle
of about 45°, pushing the actin filament along. At this step, the power
stroke, the myofibril has been shortened (contraction).
13
4. Finally, a fresh molecule of ATP binds to the bulbous head. The protein
of the bulbous heads includes the enzyme ATPase, which catalyzes
the hydrolysis of ATP. When this reaction occurs, the ADP and
inorganic phosphate (Pi) formed remain attached, and the bulbous
head is now ‘charged’ again. The charged head detaches from the
binding site and straightens.

14
 Control and coordination in plants

Plants’ sensitivity and responses are less dramatic than those of animals.
Plant responses are mostly growth movements. An example of this is the
growth of young stems towards light. Another is the growth of the main root
down into the soil in response to gravity. Chemicals known as plant
hormones or plant growth regulators are responsible for most
communication within plants. Unlike animal hormones, plant growth
regulators are not produced in specialized cells within glands, but in various
tissues. They move in the plant either directly from cell to cell (by diffusion or
active transport) or are carried in the phloem sap or xylem sap.

Auxins and elongation growth

Plants make several chemicals known as auxins, the principal one being
IAA (indole-3-acetic acid). Auxin is synthesized in the growing tips
(meristems) of shoots and roots, where the cells divide. It is transported back
down the shoot, or up the root, by active transport from cell to cell, and also
to a lesser extent in phloem sap. Growth in plants occurs at meristems, such
as those at shoot tips and root tips. Growth occurs in three stages: cell
division by mitosis, cell elongation by absorption of water, and cell
differentiation. Auxin is involved in controlling growth by elongation.

15
Auxin stimulates cells to pump hydrogen ions (protons) into the cell wall. This
acidifies the cell walls, which leads to a loosening of the bonds between
cellulose microfibrils and the matrix that surrounds them. The cells absorb
water by osmosis, and the pressure potential causes the wall to stretch so
that these cells become longer, or elongate. Molecules of auxin bind to a
receptor protein on the cell surface membrane. The binding of auxin
stimulates ATPase proton pumps to move hydrogen ions across the cell
surface membrane from the cytoplasm into the cell wall. In the cell walls are
proteins known as expansins that are activated by the decrease in pH. The
expansins disrupt the non-covalent interactions between the cellulose
microfibrils and surrounding substances, such as hemicelluloses, in the cell
wall. This disruption occurs briefly so that microfibrils can move past each
other, allowing the cell to expand without losing much of the overall strength
of the wall.

16