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Figrev: Reflex, Hematopoiesis

FIGURE 9-3 (Berne and Levy)

Y Motor Neurons adjust the sensitivity of the Spindle

Efferent innervation to muscle spindles y motor neuron

A: steady stretch

B: alpha stimulated; muscle shortens

o extrafusal contracts
o muscle spindle is unloaded by resultant shortening of muscles
o muscle spindle afferent may stop discharging
o insensitive to further changes in muscle length
o afferent fires again during relaxation

C: alpha and gamma stimulated together

o Can counteract unloading of spindle
o Intrafusal to shorten along the extrafusal
o Polar regions contract (equatorial doesnt contract because no
contractile protein)
o Equatorial lengthens and regains sensitivity
o Relaxation: decrease in gamma motor neuron
Intrafusal relaxes
Prevent tension on central portion of intrafusal from
reaching a level at which firing of afferents is saturated
o Gamma motor neurons allow muscle spindle to operate over a wide
range of muscle lengths while retaining high sensitivity
o No unloading of spindle: afferent continues

Figrev: Reflex, Hematopoiesis
FIGURE 55-9 (Guyton)
Neuronal Mechanism of the Flexor Reflex. The lefthand portion of Figure 55-9 shows the
neuronal pathways for the flexor reflex. In this instance, a painful stimulus is applied to the
hand; as a result, the flexor muscles of the upper arm become excited, thus withdrawing
the hand from the painful stimulus.
The pathways for eliciting the flexor reflex do not pass directly to the anterior motor
neurons but instead pass first into the spinal cord interneuron pool of neurons and only
secondarily to the motor neurons. The shortest possible circuit is a three- or four-neuron
pathway; however, most of the signals of the reflex traverse many more neurons and
involve the following basic types of circuits: (1) diverging circuits to spread the reflex to the
necessary muscles for withdrawal; (2) circuits to inhibit the antagonist muscles, called
reciprocal inhibition circuits; and (3) circuits to cause afterdischarge that lasts many
fractions of a second after the stimulus is over.
Neuronal Mechanism of the Crossed Extensor Reflex.
The right-hand portion of Figure 55-9 shows the neuronal circuit responsible for the
crossed extensor reflex, demonstrating that signals from sensory nerves cross to the
opposite side of the cord to excite extensor muscles.
Because the crossed extensor reflex usually does not begin until 200 to 500 milliseconds
after onset of the initial pain stimulus, it is certain that many interneurons are involved in
the circuit between the incoming sensory neuron and the motor neurons of the opposite
side of the cord responsible for the crossed extension. After the painful stimulus is
removed, the crossed extensor reflex has an even longer period of afterdischarge than
does the flexor reflex. Again, it is presumed that this prolonged afterdischarge results from
reverberating circuits among the interneuronal cells.

Figrev: Reflex, Hematopoiesis
FIGURE 12-68 (Widmaier)

Element to which oxygen binds on a hemo molecule within an RBC

Small amounts are lost through urine, feces, sweat, cell sloughed from skin,
menstrual blood
For iron homeostasis: must be replaced by ingestion of iron-containing food:
meat, liver, shellfish, egg yolk, beans, nuts, cereals
IRON DEFICIENCY: Negative balance (inadequate hemo production)
HEMOCHROMATOSIS: Positive balance (with serious toxic effects)
Homeostatic control
Primarily in intestinal epithelium (absorbs iron from ingested food)
Negative feedback balance: More iron? Less ingested iron is absorbed
Storage of iron in liver (bound up in ferritin)
o Ferritin is buffer against iron deficiency
Around 50% of total body iron is in hemo
25% in other heme-containing proteins (cytochromes)
25% in liver ferritin
Senescent RBCs are destroyed in spleen (and liver)
Iron is released into plasma and bound to iron-transport plasma protein called
Delivered to the bone marrow to be incorporated into new RBCs
Non-RBCs release irons from their cytochromes into the plasma and take up iron
from it, transferring serving as a carrier

Figrev: Reflex, Hematopoiesis
FIGURE 33-2 (Guyton)
The blood cells begin their lives in the bone marrow from
a single type of cell called the pluripotential
hematopoietic stem cell, from which all the cells of the
circulating blood are eventually derived. Figure 33-2
shows the successive divisions of the pluripotential cells
to form the different circulating blood cells. As these cells
reproduce, a small portion of them remains exactly like
the original pluripotential cells and is retained in the bone
marrow to main- tain a supply of these, although their
numbers diminish with age. Most of the reproduced cells,
however, differentiate to form the other cell types shown
to the right in Figure 33-2. The intermediate-stage cells
are very much like the pluripotential stem cells, even
though they have already become committed to a
particular line of cells and are called committed stem
The different committed stem cells, when grown in
culture, will produce colonies of specific types of blood
cells. A committed stem cell that produces erythrocytes
is called a colony-forming uniterythrocyte, and the
abbreviation CFU-E is used to designate this type of
stem cell. Likewise, colony-forming units that form
granulocytes and monocytes have the designation CFUGM and so forth.
Growth and reproduction of the different stem cells are controlled by multiple proteins called growth inducers. At least four major growth inducers
have been described, each having different characteristics. One of these, interleukin-3, promotes growth and reproduction of virtually all the
different types of committed stem cells, whereas the others induce growth of only specific types of cells.
The growth inducers promote growth but not differentiation of the cells, which is the function of another set of proteins called differentiation inducers.
Each of these differentiation inducers causes one type of committed stem cell to differentiate one or more steps toward a final adult blood cell.
Formation of the growth inducers and differentiation inducers is controlled by factors outside the bone marrow. For instance, in the case of RBCs,
exposure of the blood to low oxygen for a long time causes growth induction, differentiation, and production of greatly increased numbers of RBCs,
as discussed later in the chapter. In the case of some of the white blood cells, infectious diseases cause growth, differentiation, and eventual
formation of specific types of white blood cells that are needed to combat each infection.