Alpha & Gamma
Motor Neuron Functions
By
Dr. Khaled Ibrahim
The Efferent Neurons
 The efferent neurons of the spinal cord include:
(i) Somatic efferents, which join the somatic nerves to innervate skeletal
muscles.
(ii) Visceral efferents, which join the autonomic
innervation of visceral organs and blood vessels.
nerves
for
 In each segment of the spinal cord, several thousand somatic efferent
motor neurons are located in the anterior horns of the cord gray matter .
These neurons are of two types ; “alpha” motor neurons and “gamma’
motor neurons .
Alpha Motor Neurons
 The -motor neurons are large neurons that give rise to type A-alpha
nerve fibers (about 14 m in diameter), which innervate the large skeletal
muscle fibers (extrafusal fibers).
 The  - motor neurons, are called the “final common motor
pathway”, because all the motor commands originating anywhere in the
nervous system have to pass through it before reaching skeletal muscles.
Regulation of - Motor Neuron discharge
 The firing rate of an - motor neuron is determined by “the magnitude
of the membrane potential at the initial segment of its axon”.
 Such potential is ever- changing , and at any given time it is determined
by the net summation of all the excitatory and inhibitory inputs to the motor neuron at that time.
 Alpha motor neurons receive excitatory presynaptic input from many
sources in the nervous system to be activated and discharge efferent motor
signals.
 The sources of this presynaptic excitation include :
(i) spinal cord interneurons,
(ii) sensory afferents from muscle spindles, and
(iii) descending pathways from the higher motor centers in the brain and
brain stem.
 Whereas, inhibition of -MNs originates from inhibitory interneurons,
that can be activated by:
(i) afferent signals from peripheral receptors such as the Golgi tendon
organs , and
(ii) by signals from the inhibitory descending motor tracts.
 The  - motor neurons, are called the “final common motor
pathway”, because all the motor commands originating anywhere in the
nervous system have to pass through it before reaching skeletal muscles.
Gamma Motor Neurons
 Gamma motor neurons (-motor neurons) are located in the ventral
horns of the spinal gray matter, intermingled with the -motor neurons.
 The -motor neurons are smaller in size than the -motor neurons and
transmit their discharge along “A-gamma axons”, that innervate the
“intrafusal fibers” of muscle spindles to regulate their function
Muscle Spindles
Central part
- Non-contractile
- Contains the nuclei of the fibers &
Peripheral part
- Contractile
- Striated (contains myofilaments).
sensory endings arise form it.
So, its stretch initiates stretch reflex.
So, when contracted ------> stretch of the
central part -----> stretch reflex.
Efferent (Motor) Innervation of muscle spindle
- Supplies the peripheral contractile parts on the intrafusal muscle fibers.
- Their cell bodies are located in gamma motor neurons (-MNs) which are the small AHCs
(30% of AHCs).
- Their axons are thin (diameter 3-6 µm).
- According to their functions, Gamma motor neurons (-MNs) are of 2 types:
a) Static  - MNs which innervate the nuclear chain fibers
b) Dynamic - MNs which innervate the nuclear-bag fibers.
Stimulation of -MNs
afferent impulses along -afferent fibers
contraction of the peripheral contractile parts of the intrafusal muscle
fibers stretch of the central (receptor) part
depolarization of the central part
action potential & impulse discharge along 1ry & 2ry endings
stimulation of α-MNs innervating the stretched muscle
impulses along the α- efferent fibers
muscle contraction (stretch reflex).
N.B.: contraction of
the peripheral
contractile part
causes stretch of
the central part as:
a) the intrafusal
muscle fiber is not
too strong to
shorten the muscle.
b) the ends of the
intrafusal muscle
fiber is fixed to the
membranes of the
extrafusal muscle
fibers.
- Control of  - MNs discharge:
I- Supraspinal
control
(mainly).
II- Reflex
control.
I- Supraspinal control (mainly):
- Presynaptic impulses from higher centers in the brain & brainstem reach the  - MNs
through the descending motor pathways.
- These impulses may:
- Stimulate (facilitate)  - MNs ----> - Inhibit  - MNs ----> ↓ discharge along 
↑discharge along  efferents ------> ↑the efferents ------> ↓ the magnitude of the
magnitude of the existing stretch reflex.
existing stretch reflex.
- The centers which send these impulses - The centers which send these impulses
are called "Facilitatory centers" & they are called
"inhibitory centers" & they
include:
include:
1) 1ry motor area (area 4).
1) Premotor area (area 6).
2) Neocerebellum.
2) Paleocerebellum.
3) Facilitatory reticular formation.
3) Inhibitory reticular formation.
4) Vestibular nuclei.
4) Red nucleus.
II- Reflex Control:
By impulses along a presynaptic terminals arising from peripheral receptors such as:
 Golgi tendon organ of the same muscle ------> inhibition of -MNs (this is called inverse
stretch reflex).
 1ry sensory endings of the antagonistic muscles -------> inhibition of -MNs (this is
called reciprocal innervation).
 Other nearby contracted muscles ------> facilitation of -MNs (this is called Jendrassik
maneuver).
 Cutaneous receptors (especially pain receptors) ------> facilitation of -MNs of the
flexor muscles & inhibition of -MNs of the antagonistic muscles.
- Significance (Importance) of  - MNs innervation:
Stimulation of  - MNs ------> stimulation of the muscle spindle -----> ↑
magnitude of the already existing stretch reflex & vice versa.
1) Adjust muscle spindle sensitivity:
The sensitivity of the muscle spindle is controlled by the level of activity of the  MNs as follows:
↑ activity of  - MNs (↑the level of motor
↓ activity of  - MNs (↓ the level of motor
impulses discharge along - efferents)
impulses discharge along - efferents)
more contraction of the intrafusal muscle
less contraction of the intrafusal muscle
fibers -------> slight stretch of the whole
fibers -------> greater stretch of the whole
muscle is needed to stretch the spindle to
muscle is needed to stretch the spindle to
the adequate level needed for sensory
the adequate level needed for sensory
discharge -----> production of the required
discharge & production of the required
level of the stretch reflex.
level of the stretch reflex.
i.e., the spindle becomes more sensitive.
i.e., the spindle becomes less sensitive.
So, continuous discharge along the  efferent fibers keeps the muscle spindle
sensitive to the slightest change in the muscle length.
2) Adjusting Muscle Length:
- The higher centers determine the proper length of the muscle needed to achieve
certain posture.
- This is done through adjustment of the magnitude of the discharge of -MNs by
impulses from the higher centers as follow:
If the actual length of the muscle > the
If the actual length of the muscle < the
desired length (i.e., the contraction of the
desired length (i.e., the contraction of the
muscle is not enough)
muscle is not much)
Facilitatory higher centers ----->
inhibitory higher centers ----> ↓ discharge
↑discharge along -MNs ----> ↑stretch
along -MNs ----> ↓ stretch of the muscle
of the muscle spindles ---> ↑magnitude of
spindles ---> ↓ magnitude of the stretch
the stretch reflex -----> more contraction --- reflex -----> less contraction ---->
-> shortening of the muscle to the desired
lengthening of the muscle to the desired
length.
length.
3) Co- activation of  and -MNs:
- When the higher motor centers in the brain direct a particular muscle to contract,
there is almost always an associated ↑ of -MNs along with the delivered -MNs
discharge that initiate the movement.
-This is called co-activation of -and -MNs.
- This co –activation of -MNs helps to:
a) Prevent laxation of muscle spindles during active muscle contraction. This maintains
the spindle continuously sensitive & maintains continuous information of the higher
centers especially the cerebellum about the changes in the muscle length & body posture
during contraction.
b) maintain adequate excitatory impulses to α-MNs needed to perform the desired
motor performance (see before).
Lower Motor Neuron Lesions
Injury or damage of the lower motor neurons in the spinal ventral horns
(or the corresponding neurons in the motor nuclei of cranial nerves)
innervating a given muscle impairs the ability of the muscle to contract and
thereby results in its paralysis.
Effects of LMN Lesions
1) Flaccid Paralysis
 The denervated muscle is completely paralyzed , since there is loss of
all types of movements, including voluntary movements , postural
movements, and reflex movements
 The paralyzed muscle is also hypotonic (flaccid) due to interruption of
the motor component of the stretch reflex pathway, and as a result there is
loss of the tendon jerks in the affected muscle.
 The extent of paralysis is often limited in LMN lesions , because the
lower motor neurons are widely spread in the brain stem and spinal cord,
and their axons proceed to innervate skeletal muscles via a large number of
peripheral somatic nerves. Thus, it is not common to have a lesion which
would cause damage of a large proportion of these neurons simultaneously .
2) Fasiculations and Fibrillations
 These are abnormal contractions that occur in the denervated muscle.
Fasiculations
These begin to appear few days after muscle denervation.
 As a part of the axon degenerates, injury potentials produced by
depolarization at the sites of injury of the neuronal membrane cause
spontaneous action potentials to travel along the intact distal portions of
the axon and stimulate all the muscle fibers innervated by the injured axon
(a complete motor unit).
 This elicits synchronous contractions of all the muscle fibers of the unit,
which are thus visible to the observer. These contractions are called
“fasiculations” and persist as long the distal segment of the axon is still
intact.
Fibrillations
 As the axon degenerates further, its terminal branches become isolated
from each other, but the injury potentials are still generated in these
branches and still cause muscular contractions. Since the muscle fibers of
the affected motor unit are no longer joined by a functioning main axon,
the different muscle fibers no longer contract simultaneously as a unit.
 The resulting contractions are very small and are not visible on the body
surface. These contractions are called “fibrillations”, and can be detected
electrically by means of an electromyogram.
 Fibrillations start few weeks after the occurrence of motor neuron injury
and persist untill the motor nerve terminals degenerate completely, or until
the regenerating proximal segment of the axon successfully re-innervates
the muscle fibers.
3) Denervation Supersensitivity
 When the motor innervation to a skeletal muscle is damaged, we find
that, instead of being restricted only to the region of the motor end plate,
progressively more and more of the muscle cell’s surface becomes sensitive
to acetylcholine; a phenomenon called “denervation supersensitivity”
 Denervation supersensitivity is due to spread out of acetylcholine
receptors which ultimately cover the entire surface of the muscle cell’s
membrane
4) Abnormal Response to Electrical Stimulation : Reaction of Degeneration
Response of the Normal Muscle
(i) Faradic currents:
These currents produce clonic or tetanic contraction, depending on the
frequency of the alternating cycles of the current
(ii) Galvanic currents:
 Galvanic currents produce contraction only at: (1) the beginning of
current flow (closing the electric circuit) giving rise to closing contraction,
and (2) at the termination of the current flow (opening of the circuit) giving
rise to opening contraction. No contraction is produced when the galvanic
current is flowing in the muscle at a steady level.
Also, the muscle responds to the galvanic current at these two instances
whether the stimulating electrode is the “cathode” of the electric circuit
producing a cathodal contraction, or is the “anode” producing an anodal
contraction.
 When we start stimulation of the muscle by the least effective galvanic
current then gradually increase its strength, we will notice that the first
contraction to appear is the cathodal closing contraction (CCC). A stronger
current is needed to evoke the anodal closing contraction (ACC), then the
anodal opening contraction (AOC) comes next, while the cathodal opening
contraction (COC) is the last one to appear. These responses can be
expressed by the following shortened formula : CCC > ACC > AOC >
COC.
Response of the Denervated Muscles
(i) Failure of response to faradic currents, because of decreased excitability
of the denervated muscle, therefore, the duration of any faradic current
cycle becomes too short to be effective.
(ii) The muscle still responds to galvanic current (because of its longer
duration), but the contractions produced are weak and slow, and the anodal
closing current becomes more effective than the cathodal closing current,
thus the “ACC” becomes greater than the “CCC”;
ACC > CCC.
 These characteristic changes in the response of the denervated muscle to
electric stimulation are known as the “reaction of degeneration” . This
reaction can be elicited from the muscle only during the period that passes
between loss of excitability of the nerve and loss of excitability of the
muscle. But, it disappears if re-innervation fails with consequent complete
degeneration of the muscle, or when the muscle is successfully reinnervated by the regrowing motor neuron axons .