Neuroglia Functions: Pathogens Neurons

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A). The diaphysis is the main or midsection (shaft) of a long bone.

It is made up of cortical
bone and usually contains bone marrow and adipose tissue (fat).
It is a middle tubular part composed of compact bone which surrounds a central marrow cavity which
contains red or yellow marrow. In diaphysis, primary ossification occurs.

B).Neuroglia Functions

 It offers essential nutrients. It includes oxygen to neurons.


 Next, it also helps create the myelin sheath. The sheath is
important in the functioning of the nervous system. It promotes
and speeds up the electrical impulse conduction. It does so by
wrapping around the axons.
 Further, it also helps to maintain homeostasis within the
neurons. Homeostasis is how a cell maintains a stable internal
environment despite disturbances.
 It destroys pathogens. It helps protect the neurons.
 Finally, it also provides structural stability. It forms a support
structure that the neurons can inhabit.
C).

The bone remodeling process is controlled by various local and systemic factors, and their expression
and release, in a well organized manner. Calcitonin (CT), parathyroid hormone (PTH), vitamin D3
[1,25(OH)2 vitamin D3] and estrogen are the major hormonal regulators of osteoclastic bone resorption.
Secretion of the first three is driven by the requirement to control the physiological serum calcium level.
In addition to systemic hormonal regulation, it has become more and more apparent that growth factors
such as IGFs, TGF-β, FGFs, EGF, WNTs, and BMPs play significant roles in regulation of physiological bone

D).

The axon hillock is a specialized part of the cell body (or soma) of a neuron that connects to
the axon. It can be identified using light microscopy from its appearance and location in a neuron
and from its sparse distribution of Nissl substance.[1]
The axon hillock is the last site in the soma where membrane potentials propagated from synaptic
inputs are summated before being transmitted to the axon
E).

After orgasm, both men and women experience a resolution stage. At this time, their
bodies “recover” from sexual excitement and return to their normal states. For men, the
penis becomes flaccid again and he goes through a refractory period.
During the refractory period, a man doesn’t think about sex or get aroused. His body does
not respond to sexual stimulation and he is unable to reach orgasm again until the period
is over. The length of the refractory period is different for every man. It may take a half
hour or more for his body to perform sexually again.

Younger men may need only a few minutes of recovery time, but older men usually have a
longer refractory period, sometimes between 12 to 24 hours. For some men, the refractory
period can last a few days.

F)*********** Neurons are highly polarized cells that consist of three main structural and
functional domains: a cell body or soma, an axon, and dendrites. These domains contain smaller
compartments with essential roles for proper neuronal function, such as the axonal presynaptic
boutons and the dendritic postsynaptic spines

G)

Reflexes are functionally defined by an efferent (motor) output system leading


to a distinct effector response when activated and by the population of afferent
neurons stimulated. They are fragments of more complex somatomotor
behaviors and are used in the laboratory as tools to study experimentally the
central organization of neural regulation of movement. In this isolated context
they are experimental artifacts or fictions [1]. The same applies to autonomic
reflexeswhen seen in this restricted experimental context. Systematic
experimental studies of autonomic reflexes using measurements of effector
responses, recording from functionally identified autonomic neurons,
pharmacological interventions, histological techniques, tracer methods etc. have
given and will continue to give invaluable insight into the central and peripheral
neural mechanisms underlying regulations in which the autonomic nervous
system is involved.

h).

What is hypogonadism?
Hypogonadism occurs when your sex glands produce little or no sex
hormones. The sex glands, also called gonads, are primarily the testes in men
and the ovaries in women. Sex hormones help control secondary sex
characteristics, such as breast development in women, testicular development
in men, and pubic hair growth. Sex hormones also play a role in the menstrual
cycle and sperm production.
Hypogonadism may also be known as gonad deficiency. It may be called low
serum testosterone or andropause when it happens in males.

I).

What Is a Vasectomy?

A vasectomy is a small operation to prevent pregnancy. It


blocks sperm from getting to your semen when you ejaculate. With no
sperm leaving your body, you can’t get someone pregnant. You can still
have an orgasm and ejaculate./
Vasectomy is minor surgery to block sperm from reaching the semen that is
ejaculated from the penis. Semen still exists, but it has no sperm in it. After a
vasectomy the testes still make sperm, but they are soaked up by the body.
J).

What is corticotrophin-releasing hormone?

Corticotrophin-releasing hormone is secreted by the paraventricular nucleus of


the hypothalamus which, among other functions, releases
hormones. Corticotrophin-releasing hormone has several important actions. Its
main role in the body is as the central driver of the stress hormone system,
known as the hypothalamic–pituitary–adrenal axis. Corticotrophin-releasing
hormone is given this name because it causes release of adrenocorticotropic
hormone from the pituitary gland. Adrenocorticotropic hormone in turn travels
in the bloodstream to the adrenal glands, where it causes the secretion of the
stress hormone cortisol.

3.
Key points:
 A resting (non-signaling) neuron has a voltage across its membrane
called the resting membrane potential, or simply the resting
potential.
 The resting potential is determined by concentration gradients of ions
across the membrane and by membrane permeability to each type of
ion.
 In a resting neuron, there are concentration gradients across the
membrane for \text {Na}^+Na+start text, N, a, end text, start
superscript, plus, end superscript and \text K^+K+start text, K, end text,
start superscript, plus, end superscript. Ions move down their gradients
via channels, leading to a separation of charge that creates the resting
potential.
 The membrane is much more permeable to \text K^+K+start text, K, end
text, start superscript, plus, end superscript than to \text {Na}^+Na+start
text, N, a, end text, start superscript, plus, end superscript, so the resting
potential is close to the equilibrium potential of \text K^+K+start text,
K, end text, start superscript, plus, end superscript (the potential that
would be generated by \text K^+K+start text, K, end text, start
superscript, plus, end superscript if it were the only ion in the system).

Introduction
Suppose you have a dead frog. (Yes, that's kind of gross, but let's just
imagine it for a second.) What would happen if you applied an electrical
stimulus to the nerve that feeds the frog's leg? Creepily enough, the dead leg
would kick!
The Italian scientist Luigi Galvani discovered this fun fact back in the 1700s,
somewhat by accident during a frog dissection. Today, we know that the
frog's leg kicks because neurons (nerve cells) carry information via electrical
signals.

How do neurons in a living organism produce electrical signals? At a basic


level, neurons generate electrical signals through brief, controlled changes in
the permeability of their cell membrane to particular ions (such as \
text{Na}^+Na+start text, N, a, end text, start superscript, plus, end
superscript and \text K^+K+start text, K, end text, start superscript, plus, end
superscript). Before we look in detail at how these signals are generated, we
first need to understand how membrane permeability works in a resting
neuron (one that is not sending or receiving electrical signals).
[What is permeability?]

In this article, we'll see how a neuron establishes and maintains a stable
voltage across its membrane – that is, a resting membrane potential.

The resting membrane potential


Imagine taking two electrodes and placing one on the outside and the other
on the inside of the plasma membrane of a living cell. If you did this, you
would measure an electrical potential difference, or voltage, between the
electrodes. This electrical potential difference is called the membrane
potential.
[Is this the same as a voltage in a wire?]
Diagram of a voltmeter measuring the membrane potential. One electrode is
outside the cell. The other electrode is in the interior of the cell. The
voltmeter shows a -70 mV voltage across the membrane.
_Image modified from "How neurons communicate: Figure 2," by OpenStax College, Biology (CC BY 4.0)._

Like distance, potential difference is measured relative to a reference point.


In the case of distance, the reference point might be a city. For instance, we
can say that Boston is 190190190 \text{miles}milesstart text, m, i, l, e, s, end
text northeast, but only if we know that our reference point is New York City.

For a cell’s membrane potential, the reference point is the outside of the cell.
In most resting neurons, the potential difference across the membrane is
about 303030 to 909090 \text{mV}mVstart text, m, V, end text (a \
text{mV}mVstart text, m, V, end text is 1/10001/10001, slash, 1000 of a
volt), with the inside of the cell more negative than the outside. That is,
neurons have a resting membrane potential (or simply, resting potential)
of about -30−30minus, 30 \text{mV}mVstart text, m, V, end text to -
90−90minus, 90 \text{mV}mVstart text, m, V, end text.

Because there is a potential difference across the cell membrane, the


membrane is said to be polarized.

 If the membrane potential becomes more positive than it is at the


resting potential, the membrane is said to be depolarized.
 If the membrane potential becomes more negative than it is at the
resting potential, the membrane is said to be hyperpolarized.

Diagrams of voltmeters with one electrode inside the cell and one in the fluid
outside of the cell. The first voltmeter shows hyperpolarization: it reads -80
mV. The second voltmeter shows the resting potential: it reads -70 mV. The
third voltmeter shows depolarization: it reads +40 mV.
_Image modified from "How neurons communicate: Figure 2," by OpenStax College, Biology (CC BY 4.0)._

All of the electrical signals that neurons use to communicate are either
depolarizations or hyperpolarizations from the resting membrane potential.
Where does the resting membrane potential come
from?
The resting membrane potential is determined by the uneven distribution
of ions (charged particles) between the inside and the outside of the cell, and
by the different permeability of the membrane to different types of ions.

Types of ions found in neurons


In neurons and their surrounding fluid, the most abundant ions are:

 Positively charged (cations): Sodium (\text{Na}^+Na+start text, N, a,


end text, start superscript, plus, end superscript) and potassium (\
text{K}^+K+start text, K, end text, start superscript, plus, end
superscript)
 Negatively charged (anions): Chloride (\text{Cl}^-Cl−start text, C, l,
end text, start superscript, minus, end superscript) and organic anions
In most neurons, \text{K}^+K+start text, K, end text, start superscript, plus,
end superscript and organic anions (such as those found in proteins and
amino acids) are present at higher concentrations inside the cell than outside.
In contrast, \text{Na}^+Na+start text, N, a, end text, start superscript, plus,
end superscript and \text{Cl}^-Cl−start text, C, l, end text, start superscript,
minus, end superscript are usually present at higher concentrations outside
the cell. This means there are stable concentration gradients across the
membrane for all of the most abundant ion types.
This diagram represents the relative concentrations of various ion types inside
and outside of a neuron.

 K+ is more concentrated inside than outside the cell.


 Organic anions are more concentrated inside than outside the cell.
 Cl- is more concentrated outside than inside the cell.

 Na+ is more concentrated outside than inside the cell.

How ions cross the membrane


Because they are charged, ions can't pass directly through the hydrophobic
("water-fearing") lipid regions of the membrane. Instead, they have to use
specialized channel proteins that provide a hydrophilic ("water-loving")
tunnel across the membrane. Some channels, known as leak channels, are
open in resting neurons. Others are closed in resting neurons and only open in
response to a signal.
Ion channels. The channels extend from one side of the plasma membrane to
the other and have a tunnel through the middle. The tunnel allows ions to
cross. One of the channels shown allows Na+ ions to cross and is a sodium
channel. The other channel allows K+ ions to cross and is a potassium
channel. The channels simply give a path for the ions across the membrane,
allowing them to move down any electrochemical gradients that may exist.
The channels do not actively move ions from one side to the other of the
membrane.

Some ion channels are highly selective for one type of ion, but others let
various kinds of ions pass through. Ion channels that mainly allow \
text{K}^+K+start text, K, end text, start superscript, plus, end superscript to
pass are called potassium channels, and ion channels that mainly allow \
text{Na}^+Na+start text, N, a, end text, start superscript, plus, end
superscript to pass are called sodium channels.
[What about Cl- and organic anions?]

In neurons, the resting membrane potential depends mainly on movement of \


text {K}^+K+start text, K, end text, start superscript, plus, end
superscript through potassium leak channels. Let's see how this works.
What happens if only \text K^+K+start text, K,
end text, start superscript, plus, end superscript can
cross the membrane?
The membrane potential of a resting neuron is primarily determined by the
movement of \text K^+K+start text, K, end text, start superscript, plus, end
superscript ions across the membrane. So, let's get a feeling for how the
membrane potential works by seeing what would happen in a case
where only \text K^+K+start text, K, end text, start superscript, plus, end
superscript can cross the membrane.

We'll start out with \text{K}^+K+start text, K, end text, start superscript, plus,
end superscript at a higher concentration inside the cell than in the
surrounding fluid, just as for a regular neuron. (Other ions are also present,
including anions that counterbalance the positive charge on \text K^+K+start
text, K, end text, start superscript, plus, end superscript, but they will not be
able to cross the membrane in our example.)
Starting state:

Zero voltage across the membrane, as measured by a voltmeter with one


electrode inside and one electrode outside the cell. The inside of the cell and
the outside of the cell are separated by a membrane with potassium channels,
which are initially closed. There is a higher concentration of potassium ions
on the inside of the cell than on the outside. Each potassium ion (on either
side of the membrane) is balanced by an anion, so the system as a whole is
electrically neutral.
[Where are the Na+ and Cl- ions?]

If potassium channels in the membrane open, \text K^+K+start text, K, end


text, start superscript, plus, end superscript will begin to move down its
concentration gradient and out of the cell. Every time a \text{K}^+K+start text,
K, end text, start superscript, plus, end superscript ion leaves the cell, the
cell's interior loses a positive charge. Because of this, a slight excess of
positive charge builds up on the outside of the cell membrane, and a slight
excess of negative charge builds up on the inside. That is, the inside of the
cell becomes negative relative to the outside, setting up a difference in
electrical potential across the membrane.
System moving towards equilibrium:

If K+ can cross via channels, it will begin to move down its concentration
gradient and out of the cell. (Channels are shown opening, potassium is
shown moving from the interior to the exterior of the cell through channels.)

The movement of K+ ions down their concentration gradient creates a charge


imbalance across the membrane. (The potassium ions that have crossed from
the interior to the exterior of the cell are not partnered with anions on the
outside of the cell. They line up along the membrane on the outside, and the
unpartnered anions they left behind on the inside line up along the membrane
on its inside face. The voltmeter now registers a slight negative voltage.)

The charge imbalance opposes the flow of K+ down the concentration


gradient.

For ions (as for magnets), like charges repel each other and unlike charges
attract. So, the establishment of the electrical potential difference across the
membrane makes it harder for the remaining \text K^+K+start text, K, end
text, start superscript, plus, end superscript ions to leave the cell. Positively
charged \text K^+K+start text, K, end text, start superscript, plus, end
superscript ions will be attracted to the free negative charges on the inside of
the cell membrane and repelled by the positive charges on the outside,
opposing their movement down the concentration gradient. The electrical and
diffusional forces that influence movement of \text K^+K+start text, K, end
text, start superscript, plus, end superscript across the membrane jointly form
its electrochemical gradient (the gradient of potential energy that
determines in which direction \text K^+K+start text, K, end text, start
superscript, plus, end superscript will flow spontaneously).

Eventually, the electrical potential difference across the cell membrane builds
up to a high enough level that the electrical force driving \text{K}^+K+start
text, K, end text, start superscript, plus, end superscript back into the cell is
equal to the chemical force driving \text{K}^+K+start text, K, end text, start
superscript, plus, end superscript out of the cell. When the potential
difference across the cell membrane reaches this point, there is no net
movement of \text{K}^+K+start text, K, end text, start superscript, plus, end
superscript in either direction, and the system is considered to be in
equilibrium. Every time one \text{K}^+K+start text, K, end text, start
superscript, plus, end superscript leaves the cell, another \text{K}^+K+start
text, K, end text, start superscript, plus, end superscript will enter it.
At equilibrium:

At equilibrium, the concentration gradient of K+ is exactly balanced by the


electrical potential difference across the membrane. Although K+ ions still
cross the membrane via channels, there is no net movement of K+ from one
side to the other. The voltmeter registers a negative membrane potential that
is equal to the K+ equilibrium potential (for the K+ concentrations present in
the cell and in the surrounding fluid).

The equilibrium potential


The electrical potential difference across the cell membrane that exactly
balances the concentration gradient for an ion is known as the equilibrium
potential. Because the system is in equilibrium, the membrane potential will
tend to stay at the equilibrium potential. For a cell where there is only
one permeant ionic species (only one type of ion that can cross the
membrane), the resting membrane potential will equal the equilibrium
potential for that ion.
The steeper the concentration gradient is, the larger the electrical potential
that balances it has to be. You can get an intuitive feeling for this by
imagining the ion concentrations on either side of the membrane as hills of
different sizes and thinking of the equilibrium potential as the force you'd
need to exert to keep a boulder from rolling down the slopes between them.

Left panel: Two compartments separated by a semi-permeable membrane,


labeled A and B. There is a voltmeter between A and B. The ion of interest is
much more concentrated in A than in B, and the voltmeter with electrodes in
A and B registers a large negative voltage. The voltage is analogous to the
force we would have to exert to keep a boulder from rolling from a very high
place down a hill to a very low place.

Right panel: Same setup, but with A and B having a much slighter difference
in concentration of the ion of interest (B slightly less concentrated than A). In
this case, the voltage is only slightly negative. This is analogous to the case
where we have a very high place and a slightly lower place and are exerting a
force to keep a boulder from rolling down this not-very-steep hill.

If you know the \text{K}^+K+start text, K, end text, start superscript, plus, end
superscript concentration on both sides of the cell membrane, then you can
predict the size of the potassium equilibrium potential.

Does membrane potential equal \text


K^+K+start text, K, end text, start superscript,
plus, end superscript equilibrium potential?
In glial cells, which are the support cells of the nervous system, the resting
membrane potential is equal to the \text K^+K+start text, K, end text, start
superscript, plus, end superscript equilibrium potential.

In neurons, however, the resting membrane potential is close but not identical
to the \text K^+K+start text, K, end text, start superscript, plus, end
superscript equilibrium potential. Instead, under physiological conditions
(conditions like those in the body), neuron resting membrane potentials are
slightly less negative than the \text K^+K+start text, K, end text, start
superscript, plus, end superscript equilibrium potential.

What does that mean? In a neuron, other types of ions besides \text
K^+K+start text, K, end text, start superscript, plus, end superscript must
contribute significantly to the resting membrane potential.
[What experiment would you do to figure this out?]
Both \text K^+K+start text, K, end text, start
superscript, plus, end superscript and \text
{Na}^+Na+start text, N, a, end text, start
superscript, plus, end superscript contribute to
resting potential in neurons
As it turns out, most resting neurons are permeable to \text {Na}^+Na+start
text, N, a, end text, start superscript, plus, end superscript and \text{Cl}^-
Cl−start text, C, l, end text, start superscript, minus, end superscript as well
as \text K^+K+start text, K, end text, start superscript, plus, end superscript.
Permeability to \text{Na}^+Na+start text, N, a, end text, start superscript,
plus, end superscript, in particular, is the main reason why the resting
membrane potential is different from the potassium equilibrium potential.

Let’s go back to our model of a cell permeable to just one type of ion and
imagine that \text{Na}^+Na+start text, N, a, end text, start superscript, plus,
end superscript (rather than \text K^+K+start text, K, end text, start
superscript, plus, end superscript) is the only ion that can cross the
membrane. \text{Na}^+Na+start text, N, a, end text, start superscript, plus,
end superscript is usually present at a much higher concentration outside of a
cell than inside, so it will move down its concentration gradient into the cell,
making the interior of the cell positive relative to the outside.

Because of this, the sodium equilibrium potential—the electrical potential


difference across the cell membrane that exactly balances the \
text{Na}^+Na+start text, N, a, end text, start superscript, plus, end
superscript concentration gradient—will be positive. So, in a system where \
text{Na}^+Na+start text, N, a, end text, start superscript, plus, end
superscript is the only permeant ion, the membrane potential will be positive.

Starting state:

Zero voltage across the membrane, as measured by a voltmeter with one


electrode inside and one electrode outside the cell. The inside of the cell has a
low concentration of sodium ions, and the outside of the cell has a higher
concentration of sodium ions. Each sodium ion is counterbalanced by an
anion that is found on the same side of the membrane as the sodium ion.
There are sodium channels in the membrane, but they are initially closed.

The channels open and Na+ can move through them.

At equilibrium:

The voltmeter now registers a positive voltage equal to the sodium


equilibrium potential for this particular pair of sodium concentrations.. The
Na+ ions have moved down their concentration gradient until their further
movement is opposed by a countervailing electrical potential difference
across the membrane. There are extra positive charges on the inside of the
cell in the form of Na+ ions, and these Na+ ions line up along the membrane.
On the opposite side of the membrane, there are extra anions (the former
partners of the Na+ ions, which are unable to cross), which also line up at the
membrane.

In a resting neuron, both \text{Na}^+Na+start text, N, a, end text, start


superscript, plus, end superscript and \text{K}^+K+start text, K, end text, start
superscript, plus, end superscript are permeant, or able to cross the
membrane.

 \text{Na}^+Na+start text, N, a, end text, start superscript, plus, end


superscript will try to drag the membrane potential toward its (positive)
equilibrium potential.
 \text{K}^+K+start text, K, end text, start superscript, plus, end
superscript will try to drag the membrane potential toward its
(negative) equilibrium potential.
You can think of this as being like a tug-of-war. The real membrane potential
will be in between the \text{Na}^+Na+start text, N, a, end text, start
superscript, plus, end superscript equilibrium potential and the \
text{K}^+K+start text, K, end text, start superscript, plus, end
superscript equilibrium potential. However, it will be closer to the
equilibrium potential of the ion type with higher permeability (the one that
can more readily cross the membrane).
[I would like a more technical explanation of this concept]
Opening and closing ion channels alters the
membrane potential
In a neuron, the resting membrane potential is closer to the potassium
equilibrium potential than it is to the sodium equilibrium potential. That's
because the resting membrane is much more permeable to \text K^+K+start
text, K, end text, start superscript, plus, end superscript than to \text
{Na}^+Na+start text, N, a, end text, start superscript, plus, end superscript.

 If more potassium channels were to open up—making it even easier


for \text{K}^+K+start text, K, end text, start superscript, plus, end
superscript to cross the cell membrane—the membrane would
hyperpolarize, getting even closer to the potassium equilibrium
potential.
 If, on the other hand, additional sodium channels were to open up—
making it easier for \text{Na}^+Na+start text, N, a, end text, start
superscript, plus, end superscript to cross the membrane—the cell
membrane would depolarize toward the sodium equilibrium potential.
Changing the number of open ion channels provides a way to control the
cell’s membrane potential and a great way to produce electrical signals. (We
will see the opening and closing of channels again when we discuss action
potentials.)
The \text{Na}^+Na+start text, N, a, end text,
start superscript, plus, end superscript-\text
K^+K+start text, K, end text, start superscript,
plus, end superscriptpump maintains \
text{Na}^+Na+start text, N, a, end text, start
superscript, plus, end superscript and \
text{K}^+K+start text, K, end text, start
superscript, plus, end superscript gradients
The \text{Na}^+Na+start text, N, a, end text, start superscript, plus, end
superscript and \text{K}^+K+start text, K, end text, start superscript, plus, end
superscript concentration gradients across the membrane of the cell (and thus,
the resting membrane potential) are maintained by the activity of a protein
called the \text{Na}^+Na+start text, N, a, end text, start superscript, plus,
end superscript-\text K^+K+start text, K, end text, start superscript, plus,
end superscript ATPase, often referred to as the sodium-potassium pump. If
the \text{Na}^+Na+start text, N, a, end text, start superscript, plus, end
superscript-\text K^+K+start text, K, end text, start superscript, plus, end
superscriptpump is shut down, the \text{Na}^+Na+start text, N, a, end text,
start superscript, plus, end superscript and \text K^+K+start text, K, end text,
start superscript, plus, end superscript concentration gradients will dissipate,
and so will the membrane potential.
[Why is a pump needed to maintain the concentration gradients?]
Like the ion channels that allow \text{Na}^+Na+start text, N, a, end text, start
superscript, plus, end superscript and \text K^+K+start text, K, end text, start
superscript, plus, end superscript to cross the cell membrane, the \
text{Na}^+Na+start text, N, a, end text, start superscript, plus, end
superscript-\text K^+K+start text, K, end text, start superscript, plus, end
superscript pump is a membrane-spanning protein. Unlike potassium
channels and sodium channels, however, the \text{Na}^+Na+start text, N, a,
end text, start superscript, plus, end superscript-\text K^+K+start text, K, end
text, start superscript, plus, end superscript pump doesn’t just give \text
{Na}^+Na+start text, N, a, end text, start superscript, plus, end
superscript and \text K^+K+start text, K, end text, start superscript, plus, end
superscript a way to move down their electrochemical gradients. Instead,
it actively transports \text{Na}^+Na+start text, N, a, end text, start superscript,
plus, end superscript and \text{K}^+K+start text, K, end text, start superscript,
plus, end superscript against their electrochemical gradients.

The energy for this "uphill" movement comes from ATP hydrolysis (the
splitting of ATP into ADP and inorganic phosphate). For every molecule of
ATP that's broke down, 333 \text{Na}^+Na+start text, N, a, end text, start
superscript, plus, end superscript ions are moved from the inside to the
outside of the cell, and 222 \text K^+K+start text, K, end text, start
superscript, plus, end superscript ions are moved from the outside to the
inside.
1. Three sodium ions bind to the sodium-potassium pump, which is open
to the interior of the cell.
2. The pump hydrolyzes ATP, phosphorylating itself (attaching a
phosphate group to itself) and releasing ATP. This phosphorylation
event causes a shape change in the pump, in which it closes off on the
inside of the cell and opens up to the exterior of the cell. The three
sodium ions are released, and two potassium ions bind to the interior of
the pump.
3. The binding of the potassium ions triggers another shape change in the
pump, which loses its phosphate group and returns to its inward-facing
shape. The potassium ions are released into the interior of the cell, and
the pump cycle can begin again.
_Image modified from "The sodium-potassium exchange pump," by Blausen staff (CC BY 3.0)._

[See the details of how the pump transports ions]


Because 333 \text{Na}^+Na+start text, N, a, end text, start superscript, plus,
end superscript are exported for every 222 \text K^+K+start text, K, end text,
start superscript, plus, end superscript brought into the cell, the pump makes a
small direct contribution to the resting membrane potential (making it slightly
more negative than it would otherwise be). The pump's big contribution to the
membrane potential, however, is indirect: It maintains steady \text
{Na}^+Na+start text, N, a, end text, start superscript, plus, end
superscript and \text K^+K+start text, K, end text, start superscript, plus, end
superscript gradients, which give rise to the membrane potential as \text
{Na}^+Na+start text, N, a, end text, start superscript, plus, end
superscript and \text K^+K+start text, K, end text, start superscript, plus, end
superscript move down their respective concentration gradients through leak
channels.
4.
Molecular Mechanism of Muscle Contraction

INTRODUCTION

An animal performs most of its behavior through the contraction


and relaxation of muscles. Skeletal muscles have an organization in
which bundles of protein filaments make up muscle cells, and
bundles of muscle cells make up muscles. Muscle cells are the
products of the fusion of many different cells, so each muscle cell
contains many nuclei. The subcellular organization of a muscle cell
also includes the previously mentioned bundles of protein filaments,
called myofibrils. Lying end-to-end within these myofibrils are the
actual contractile units, the sarcomeres. When the sarcomeres
within a muscle cell contract, the muscle itself contracts and
shortens. In the accompanying animation, we examine the
mechanism by which a sarcomere shortens during contraction.

1. A muscle's contractile units lie within individual muscle cells,


which are also called muscle fibers. Each muscle fiber contains
numerous bundles of protein filaments. These bundles, called
myofibrils, are organized into repeating contractile units called
sarcomeres.
2. A sarcomere contains two types of protein filaments: actin
filaments and myosin filaments. Each actin filament is attached
to a Z line, which is found at either end of a sarcomere. The
thick myosin filaments lie between the Z lines, but are not
attached to them directly. Instead, they are held in position by
a protein called titin.
3. A proposed mechanism for the relaxation and contraction of a
sarcomere is called the sliding filament theory. During a
contraction, sarcomeres shorten. However, the actin and
myosin filaments remain the same size—they simply slide past
each other, changing their relative positions as the muscle
contracts and relaxes.
4. Contraction is triggered when an action potential in a somatic
motor neuron reaches the neuromuscular junction—the
junction between the neuron and the skeletal muscle.
Depolarization of the axon terminal causes the release of the
neurotransmitter acetylcholine into the synaptic cleft between
the neuron and muscle.
5. The neurotransmitters trigger the muscle fiber to fire an action
potential of its own. This electrical signal propagates along the
muscle fiber's plasma membrane. It also propagates into the
plasma membrane's tubular invaginations, called T tubules.
6. The T tubules lie adjacent to the sarcoplasmic reticulum (SR),
an organelle that consists of a membranous network of
compartments. The SR stores calcium ions, sequestering them
from the rest of the cytoplasm. When the action potential
passes through the T tubules, the SR releases calcium into the
cytosol.
7. The calcium ions diffuse throughout the cytoplasm of the
sarcomeres. Within the sarcomeres, the actin filaments look
like two strings of pearls twisted around each other. The
myosin filaments are thicker and have knoblike heads at their
ends.
8. Actin filaments are decorated with two types of proteins. One
protein, troponin, lies at regular intervals along the actin
filaments. Another protein, called tropomyosin, runs the length
of each actin strand. The myosin heads at this point are bound
to molecules of ADP and inorganic phosphate (Pi).
9. After the sarcoplasmic reticulum has released calcium, the
calcium ions bind to molecules of troponin. Upon binding,
troponin shifts position and pulls the tropomyosin molecule
aside. When tropomyosin moves, it exposes a myosin-binding
site on each of the actin subunits of the actin filament.
10. The neighboring myosin heads can now bind to the actin
filament. When a myosin head binds to actin, it forms what is
referred to as a cross-bridge.
11. After myosin binds to the actin filaments, Pi is released.
The release triggers the myosin heads to pivot, forcing the
actin and myosin filaments to slide past each other, and ADP is
released. This movement represents the "power stroke" of
muscle contraction.
12. Before the myosin heads can release and perform
additional power strokes, they must first bind to ATP. When
ATP binds to the myosin heads, the heads release the actin
filament. ATP is quickly hydrolyzed into ADP and P i. The energy
released by hydrolysis cocks the myosin heads, preparing
them for another cycle.
13. Soon after the action potential ceases, the sarcoplasmic
reticulum pumps the calcium that it had released back into its
interior. After calcium leaves the troponin molecules, the
tropomyosin molecules again hide the myosin-binding sites.
Actin and myosin filaments then slide back to their original
positions, relaxing and lengthening the sarcomere.
14. The sarcomeres of a muscle fiber contract and relax again
with each signal from a motor neuron.

CONCLUSION

A muscle contraction can be explained by the cycle of molecular


events that take place between actin and myosin filaments. In a
single cycle, a myosin head binds to an actin filament, performs a
power stroke, and then releases. Note that for the two filaments to
disconnect, the myosin head must bind to a fresh molecule of ATP.
After myosin releases actin, it hydrolyzes its ATP and initiates
another cycle of actin/myosin interactions.
Although we focused on a single myosin head, in fact a myosin
filament has many myosin heads. Each myosin filament is also
surrounded by six actin filaments to which the different myosin
heads can bind. Therefore, when a myosin head breaks its contact
with actin, other myosin heads still connect to actin filaments and
thus prevent the sarcomere from sliding back to its relaxed position.

The relaxation of the sarcomere occurs after calcium returns to the


sarcoplasmic reticulum. Whereas the release of calcium from the
sarcoplasmic reticulum is by a passive event in which calcium
moves through ion channels, the return of calcium is an active
event that requires energy. The control of muscle contraction
happens at the level of free calcium in the cytoplasm—all other
components involved in muscle contraction are always present and
essentially await calcium ions to begin the action.

5.

Key Points

 The ovarian cycle refers to the series of changes in the ovary during which the
follicle matures, the ovum is shed, and the corpus luteum develops.
 The follicular phase describes the development of the follicle in response to follicle
stimulation hormone ( FSH ). As luteinizing hormone ( LH ) and FSH levels
increase they stimulate ovulation, or the release of a mature oocyte into the
fallopian tubes.
 In the luteal phase, the corpus luteum forms on the ovary and secretes many
hormones, most significantly progesterone, which makes the endometrium of the
uterus ready for implantation of an embryo.
 If implantation does not occur, the corpus luteum will be degraded, resulting in
menstruation.
 If implantation occurs the corpus luteum is maintained.

Key Terms

 ischemic phase: The final part of the secretory phase. The endometrium
becomes
pale and arteries constrict due to lower hormone release by the disintegrating
corpus
luteum.
 granulosa cells: These cells produce
hormones and growth factors that interact with the oocyte during its
development.
 menstrual cycle: The recurring cycle of physiological changes in the females of
some animal species that is associated with reproductive fertility.
 luteal phase: The latter part of the menstrual cycle that occurs after ovulation, in
which the corpus luteum secretes progesterone to prepare the endometrium for
the implantation of an embryo.
 follicular phase: The phase of the estrous cycle that involves follicular maturation
within the ovary and, controlled by the hormone estradiol.

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