164 SECTION IV CNS/Neural Physiology

Gustatory cortex
(anterior insula-
frontal operculum)

Ventral posterior
medial nucleus of
thalamus

Geniculate
Chorda ganglion
tympani

N. VII

Tongue Nucleus of
N. IX
Petrosal solitary tract
Glossopharyngeal ganglion
N. X Gustatory
area

Nodose
ganglion

Pharynx

FIGURE 17–7 Diagram of taste pathways. Signals from the taste buds travel via different nerves to gustatory areas of the nucleus of
the tractus solitarius that relays information to the thalamus; the thalamus projects to the gustatory cortex N. VII, N. IX, and N. X are the 7th, 9th,
and 10th cranial nerves, respectively. (Modified with permission from Kandel ER, Schwartz JH, Jessell TM [editors]: Principles of Neural Science, 4th ed. McGraw-Hill, 2000.)

Salty Sour Predicted sweet Bitter Umami

receptor (L-glutamate)
α γ
N

N N N N
C C C C C C C
ENaC, others ENaC, HCN, others T1R3 (sac locus) T2R family, others Taste mGluR4

FIGURE 17–8 Signal transduction in taste receptors. Salt-sensitive taste is mediated by a Na -selective channel (ENaC); sour taste is
+

mediated by H+ ions permeable to ENaCs; umami taste is mediated by glutamate acting on a metabotropic receptor, mGluR4; bitter taste is
mediated by the T2R family of G protein–coupled receptors; sweet taste may be dependent on the T1R3 family of G protein–coupled receptors
that couple to the G protein gustducin. (Adapted with permission from Lindemann B. Receptors and transduction in taste. Nature. 2001;413:219.)

CLINICAL CORRELATION
A 10-year-old boy was riding in the front passenger seat of
an automobile being driven by his father. He dropped his
MP3 player and released his seat belt to retrieve it. At that
moment, the car was hit from the rear by a speeding motor-
ist. He received a sharp blow to his nose when he struck
the dashboard. He was taken to the emergency room of a
nearby hospital. An x-ray showed that he had broken his
ethmoid bone that separates the nasal cavity from the
brain. Following this accident, he lost the sense of smell
(anosmia), and his sense of taste was also diminished.
The olfactory nerve runs through the ethmoid bone.
The nerve can be damaged when the bone is broken,
resulting in the loss of the ability to smell. Because of the
close relationship between taste and smell, anosmia is
associated with a reduction in taste sensitivity (hypogeusia).
Major causes of anosmia include upper respiratory tract
infection, nasal polyps, head trauma, tumors of the frontal
lobe, toxins, and prolonged use of nasal decongestants.
Anosmia is generally permanent in cases in which the
olfactory nerve or other neural elements in the olfactory
neural pathway are damaged. In addition to not being able
to experience the enjoyment of pleasant aromas and full
spectrum of tastes, individuals with anosmia are at risk
because they are not being able to detect the odor from
such dangers as gas leaks, fire, and spoiled food
CHAPTER SUMMARY
■ Olfactory sensory neurons, supporting (sustentacular) cells,
and basal stem cells are located in the olfactory epithelium
within the upper portion of the nasal cavity.
■ The cilia located on the dendritic knob of the olfactory sensory
neuron contain odorant receptors that are coupled to heterotri-
meric G proteins.
■ Axons of olfactory sensory neurons contact the dendrites of
mitral and tufted cells in the olfactory bulbs to form olfactory
glomeruli.
■ Information from the olfactory bulb travels via the lateral
olfactory stria directly to the olfactory cortex, including the
anterior olfactory nucleus, olfactory tubercle, piriform cortex,
amygdala, and entorhinal cortex.
■ Taste buds are the specialized sense organs for taste and are
composed of basal stem cells and Type I, II, and III taste cells
that may represent various stages of differentiation of develop-
ing taste cells. They are located in the mucosa of the epiglottis,
palate, and pharynx and in the walls of papillae of the tongue.
■ There are taste receptors for sweet, sour, bitter, salt, and umami
tastes. Signal transduction mechanisms include passage
through ion channels, binding to and blocking ion channels,
and second messenger systems.
■ The afferents from taste buds in the tongue travel via the 7th,
9th, and 10th cranial nerves to synapse in the NTS. From there,
axons ascend via the ipsilateral medial lemniscus to the ventral
CHAPTER 17 Special Senses III: Smell and Taste 165
posteromedial nucleus of the thalamus, and on to the anterior
insula and frontal operculum in the ipsilateral cerebral cortex.
STUDY QUESTIONS
1. Odorant receptors are
A) located in the olfactory bulb.
B) located on dendrites of mitral and tufted cells.
C) located on neurons that project directly to the olfactory cortex.
D) located on neurons in the olfactory epithelium that project to
mitral cells and from there directly to the olfactory cortex.
E) located on sustentacular cells that project to the olfactory bulb.
2. Taste receptors
A) for sweet, sour, bitter, salt, and umami tastes are spatially
separated on the surface of the tongue.
B) are synonymous with taste buds.
C) are a type of chemoreceptor.
D) are innervated by afferents in the facial, trigeminal,
and glossopharyngeal nerves.
E) All of the above are correct.
3. Which of the following does not increase the ability to
discriminate many different odors?
A) many different receptors
B) pattern of olfactory receptors activated by a given odorant
C) projection of different mitral cell axons to different parts
of the brain
D) neural processing in the amygdala
E) lateral inhibition
4. Which of the following are incorrectly paired?
A) ENaC:sour
B) α-gustducin:bitter taste
C) nucleus tractus solitarius:taste
D) fungiform papillae:smell
E) Ebner glands:taste acuity
5. Which of the following is true about olfactory transmission?
A) An olfactory sensory neuron expresses a wide range of
odorant receptors.
B) Lateral inhibition within the olfactory glomeruli reduces
the ability to distinguish between different types of odorant
receptors.
C) Conscious discrimination of odors is dependent on the
pathway to the orbitofrontal cortex.
D) Olfaction is closely related to gustation because odorant
and gustatory receptors use the same central pathways.
E) All of the above are correct.
6. Which of the following is not true about gustatory sensation?
A) The sensory nerve fibers from the taste buds on the anterior
two thirds of the tongue travel in the chorda tympani
branch of the facial nerve.
B) The sensory nerve fibers from the taste buds on the
posterior third of the tongue travel in the petrosal branch
of the glossopharyngeal nerve.
C) The pathway from taste buds on the left side of the tongue
is transmitted ipsilaterally to the cerebral cortex.
D) Sustentacular cells in the taste buds serve as stem cells to
permit growth of new taste buds.
E) The pathway from taste receptors includes synapses in the
nucleus of the tractus solitarius in the brain stem and
ventral posterior medial nucleus in the thalamus.
This page intentionally left blank

Control of Posture
and Movement
Susan M. Barman
O B J E C T I V E S
■ Describe how skilled movements are planned and carried out.
■ Describe the posture-regulating parts of the central nervous system.
■ Describe decerebrate and decorticate rigidity.
■ Describe the function of the basal ganglia in control of movement.
■ Describe the symptoms of Parkinson’s disease.
■ Discuss the functions of the cerebellum and the neurological abnormalities
produced by diseases of this part of the brain.
INTRODUCTION
Somatic motor activity ultimately depends on the pattern and
rate of discharge of the spinal motor neurons and homologous
neurons in the motor nuclei of the cranial nerves. These neu-
rons, the final common pathway to skeletal muscle, receive in-
put from an array of descending pathways, other spinal neurons,
and peripheral afferents. The integration of these multiple in-
puts regulates the posture of the body and makes coordinated
movement possible. The inputs bring about voluntary activity,
adjust body posture to provide a stable background for move-
ment, and coordinate the action of the various muscles to make
movements smooth and precise. As shown by the scheme in
Figure 18–1, voluntary movement is planned in the cortex,
basal ganglia, and lateral cerebellum. The basal ganglia and
cerebellum funnel information to the premotor and motor cor-
tex via the thalamus. Posture is continually adjusted both before
and during movement by descending brain stem pathways and
peripheral afferents. Movement is smoothed and coordinated
by the connections of medial and intermediate portions of the
cerebellum. The basal ganglia and lateral cerebellum are part of
a feedback circuit to the premotor and motor cortex that is con-
cerned with planning and organizing voluntary movement.
18
C H A P T E R
CONTROL OF AXIAL
AND DISTAL MUSCLES
Within the brain stem and spinal cord, pathways and neu-
rons that control skeletal muscles of the trunk and proximal
portions of the limbs are located medially or ventrally. Path-
ways and neurons that are concerned with the control of
skeletal muscles in the distal portions of the limbs are lo-
cated laterally. The axial muscles are concerned with pos-
tural adjustments and gross movements; the distal limb
muscles mediate fine, skilled movements. For example, neu-
rons in the medial portion of the ventral horn innervate
proximal limb muscles, particularly the flexors, and lateral
ventral horn neurons innervate distal limb muscles. Simi-
larly, the ventral corticospinal tract and medial descending
brain stem pathways (rubrospinal, reticulospinal, tectospi-
nal, and vestibulospinal tracts) are concerned with adjust-
ments of proximal muscles and posture, and the lateral
corticospinal and rubrospinal tracts are concerned with
distal limb muscles and, particularly in the case of the corti-
cospinal tract, with skilled voluntary movements.
167
168 SECTION IV CNS/Neural Physiology

Plan Execute

Basal ganglia

Cortical
Idea association Premotor and Movement
areas motor cortex

Lateral
cerebellum Intermediate
cerebellum

FIGURE 18–1 Control of voluntary movement. Commands for voluntary movement originate in cortical association areas. The cortex,
basal ganglia, and cerebellum work cooperatively to plan movements. Movement executed by the cortex is relayed via the corticospinal tracts
and corticobulbar tracts to motor neurons. The cerebellum provides feedback to adjust and smooth movement. (Reproduced with permission from
Barrett KE, Barman SM, Boitano S, Brooks H: Ganong’s Review of Medical Physiology, 23rd ed. McGraw-Hill Medical, 2009.)

CORTICOSPINAL AND Precentral

CORTICOBULBAR TRACTS gyrus
(area 4,
The axons of neurons from the motor cortex that project to etc)
spinal motor neurons form the corticospinal tracts, a large
bundle of about 1 million fibers. About 80% of these fibers
cross the midline in the medullary pyramids to form the lat-
eral corticospinal tract (Figure 18–2). The other 20% form the
ventral corticospinal tract, which does not cross the midline
Corticospinal tract
until it reaches the level of the spinal cord at which it termi-
nates. Lateral corticospinal tract neurons make monosynaptic
connections to motor neurons, especially those concerned Internal capsule
with skilled movements, and on spinal interneurons. The tra-
jectory from the cortex to the spinal cord passes through the Decussation of
corona radiata to the posterior limb of the internal capsule. the pyramids
Within the midbrain corticospinal tract fibers traverse the ce- Pyramids
rebral peduncle and the basilar pons until they reach the med-
ullary pyramids on their way to the spinal cord. Lateral cortico-
The corticobulbar tract is composed of the fibers that pass spinal tract
from the motor cortex to motor neurons in the trigeminal, Ventral cortico- (80% of fibers)
spinal tract
facial, and hypoglossal nuclei. Corticobulbar neurons end ei- (20% of fibers) Anterior
ther directly on the cranial nerve nuclei or on their antecedent horn cell
interneurons within the brain stem. Their axons traverse
through the genu of the internal capsule, the cerebral peduncle Interneuron
Spinal nerve
(medial to corticospinal tract neurons), to descend with corti-
cospinal tract fibers in the pons and medulla.
The motor system can be divided into lower and upper mo-
Distal
tor neurons. Lower motor neurons refer to the spinal and cra- muscle
nial motor neurons that directly innervate skeletal muscles.
Proximal
Upper motor neurons are those in the cortex and brain stem muscle
that activate the lower motor neurons. The pathophysiologic
responses to damage to lower and upper motor neurons are FIGURE 18–2 Corticospinal tracts. This tract originates in the
precentral gyrus and passes through the internal capsule. Most fibers
very distinctive.
decussate in the pyramids and descend in the lateral white matter of
Damage to lower motor neurons is associated with flaccid the spinal cord to form the lateral division of the tract that can make
paralysis, muscular atrophy, fasciculations (visible muscle monosynaptic connections with spinal motor neurons. The ventral
twitches that appear as flickers under the skin), hypotonia division of the tract remains uncrossed until reaching the spinal cord
(decreased muscle tone), and hyporeflexia or areflexia. where axons terminate on spinal interneurons antecedent to motor
Damage to upper motor neurons initially causes muscles to neurons. (Reproduced with permission from Barrett KE, Barman SM, Boitano S,
become weak and flaccid but eventually leads to spasticity, Brooks H: Ganong’s Review of Medical Physiology, 23rd ed. McGraw-Hill Medical, 2009.)
 CHAPTER 18 Control of Posture and Movement 169

hypertonia (increased resistance to passive movement),

hyperactive stretch reflexes, and abnormal plantar extensor
reflex (Babinski sign). The Babinski sign is dorsiflexion of the

Shoulder
Elbow
Wrist
great toe and fanning of the other toes when the lateral aspect

Trunk
Hip
Kne Ank

d
Han
of the sole of the foot is scratched. In adults, the normal

e le

Ri ttle
id g
To
response to this stimulation is plantar flexion in all the toes.

Li
n
e
e

dl
s x
de b

M
It is of value in the localization of disease processes, but its In um k
Th Nec w
o
physiologic significance is unknown. Br all
b
d eye
n e
lida Fac
Eye

VOCALIZATION
Lips

MOTOR CORTEX AND

Ja
VOLUNTARY MOVEMENT Ton w

N
Sw gue

TIO
allo
win

LIVA
N
g

IO
AT
Corticospinal and corticobulbar tract neurons are pyramidal

shaped and located in layer V of the cerebral cortex (see
Chapter 12). Figure 18–3 shows the major cortical regions in-
volved in motor control. About 31% of the corticospinal tract
neurons are from the primary motor cortex (M1; Brodmann’s
area 4) in the precentral gyrus of the frontal lobe, extending into
the central sulcus. The premotor cortex and supplementary
motor cortex (Brodmann’s area 6) account for 29% of the cor-
ticospinal tract neurons. The premotor area is anterior to the
precentral gyrus, on the lateral and medial cortical surface, and
the supplementary motor area is on and above the superior bank
of the cingulate sulcus on the medial side of the hemisphere. The
other 40% of corticospinal tract neurons originate in the pari-
etal lobe (Brodmann’s area 5, 7) and primary somatosensory
area (Brodmann’s area 3, 1, 2) in the postcentral gyrus.
The various parts of the body are represented in M1, with the
feet at the top of the gyrus and the face at the bottom (Figure 18–4).
The facial area is represented bilaterally, but the rest of the repre-
sentation is unilateral, with the cortical motor area controlling
Motor cortex
Supplementary
Primary somatic
motor area
Premotor sensory cortex
cortex Posterior
parietal
cortex
6 4
3,1,2 5 sequences, while M1 executes the movements. When human
7 7
Prefrontal
cortex
FIGURE 18–3 A view of the human cerebral cortex, showing
the motor cortex (Brodmann’s area 4) and other areas concerned
with control of voluntary movement, along with the numbers
assigned to the regions by Brodmann. (Reproduced with permission
from Kandel ER, Schwartz JH, Jessell TM [editors]: Principles of Neural Science, 4th ed.
McGraw-Hill, 2000.)
SA
IC
ST
MA
FIGURE 18–4 Motor homunculus. The figure represents, on a
coronal section of the precentral gyrus, the location of the cortical
representation of the various parts. The size of the various parts is
proportionate to the cortical area devoted to them. Compare with
Figure 13–6. (Reproduced with permission from Penfield W, Rasmussen G:
The Cerebral Cortex of Man. Macmillan, 1950.)
the musculature on the opposite side of the body. The size of the
cortical representation of each body part is proportional to the
number of corticospinal neurons supplying the musculature of
that region of the body and its role in fine, voluntary movement.
Thus, the areas involved in speech and hand movements are es-
pecially large. A somatotopic organization continues through-
out the corticospinal and corticobulbar pathways. The cells in
the cortical motor areas are arranged in columns. Neurons in
several cortical columns project to the same muscle; also, the
cells in each column receive extensive sensory input from
the peripheral area in which they produce movement, providing
the basis for feedback control of movement.
The supplementary motor area (Figure 18–3), which proj-
ects to M1, also contains a map of the body, but it is less precise
than in M1. It is involved in organizing or planning motor
subjects count to themselves without speaking, the motor cor-
tex is quiescent, but when they speak the numbers aloud,
blood flow increases in M1 and the supplementary motor area.
Thus, both M1 and the supplementary motor area are involved
in voluntary movement when the movements being performed
are complex and involve planning.
The premotor cortex (Figure 18–3), which also contains a
somatotopic map, receives input from sensory regions of the
parietal cortex and projects to M1, the spinal cord, and the
brain stem reticular formation. This region is concerned with
setting posture at the start of a planned movement and with
getting the individual prepared to move. It is most involved in
control of proximal limb muscles needed to orient the body
for movement.
170 SECTION IV CNS/Neural Physiology

In addition to providing fibers that run in the corticospinal
and corticobulbar tracts, the somatic sensory area and por-
tions of the posterior parietal lobe project to the premotor
area. Some of the neurons in area 5 (Figure 18–3) are con-
cerned with aiming the hands toward an object and manipu-
lating it, whereas some of the neurons in area 7 are concerned
with hand–eye coordination.
MEDIAL AND LATERAL
BRAIN STEM PATHWAYS:
POSTURE AND VOLUNTARY
MOVEMENT
As mentioned above, spinal motor neurons are organized such
that those innervating the most proximal muscles are located
most medially and those innervating the more distal muscles
are located more laterally. This organization is also reflected in
descending brain stem pathways (Figure 18–5).
The medial brain stem pathways, which work in concert
with the ventral corticospinal tract, are the pontine and med-
ullary reticulospinal, vestibulospinal, and tectospinal tracts.
These pathways descend in the ipsilateral ventral columns of
the spinal cord and terminate predominantly on interneurons
in the ventromedial part of the ventral horn to control axial
and proximal muscles. A few medial pathway neurons synapse
directly on motor neurons controlling axial muscles.
The medial and lateral vestibulospinal tracts were briefly
described in Chapter 16. The medial tract originates in the
medial and inferior vestibular nuclei and projects bilaterally to
cervical spinal motor neurons that control neck musculature.
The lateral tract originates in the lateral vestibular nuclei and
projects ipsilaterally to neurons at all spinal levels. It activates
motor neurons to antigravity muscles (e.g., proximal limb ex-
tensors) to control posture and balance.
The pontine and medullary reticulospinal tracts project to
all spinal levels. They are involved in the maintenance of pos-
ture and in modulating muscle tone, especially via an input to
γ-motor neurons. Pontine reticulospinal neurons are primar-
ily excitatory and medullary reticulospinal neurons are
primarily inhibitory. The tectospinal tract originates in the su-
perior colliculus of the midbrain. It projects to the contralat-
eral cervical spinal cord to control head and eye movements.

A Medial brain stem pathways B Lateral brain stem pathways

Tectum Red nucleus

(magnocellular part)

Medial
reticular
formation

Tectospinal
tract
Lateral and medial
vestibular nuclei
Reticulospinal
tract

Vestibulospinal
tracts

Rubrospinal
tract

FIGURE 18–5 Medial and lateral descending brain stem pathways involved in motor control. A) Medial pathways (reticulospinal,
vestibulospinal, and tectospinal) terminate in ventromedial area of spinal gray matter and control axial and proximal muscles. B) Lateral pathway
(rubrospinal) terminates in dorsolateral area of spinal gray matter and controls distal muscles. (Reproduced with permission from Kandel ER, Schwartz JH,
Jessell TM [editors]: Principles of Neural Science, 4th ed. McGraw-Hill, 2000.)

The main control of distal muscles is from the lateral corti-
cospinal tract, but neurons within the red nucleus of the mid-
brain cross the midline and project to interneurons in the
dorsolateral part of the spinal ventral horn to also influence
motor neurons that control distal limb muscles. This rubrospi-
nal tract excites flexor motor neurons and inhibits extensor
motor neurons.
DECEREBRATION AND
DECORTICATION
A complete transection of the brain stem between the supe-
rior and inferior colliculi permits the brain stem pathways
to function independent of their input from higher brain
structures. This is called a midcollicular decerebration and
is diagramed in Figure 18–6 by the dashed line labeled A.
This lesion interrupts all input from the cortex and red nu-
cleus to distal muscles of the extremities. The excitatory and
inhibitory reticulospinal pathways (primarily to postural
extensor muscles) remain intact. The dominance of drive
from ascending sensory pathways to the excitatory reticu-
lospinal pathway leads to decerebrate rigidity, which is
characterized by hyperactivity in extensor muscles in all
four extremities. This resembles what ensues after uncal
herniation resulting from a supratentorial lesion as seen in
patients with large tumors or a hemorrhage in the cerebral
hemisphere.
After decerebration, section of dorsal roots to a limb (dashed
line labeled B in Figure 18–6) eliminates the hyperactivity of
extensor muscles, suggesting that decerebrate rigidity is spas-
ticity due to facilitation of the myotatic stretch reflex. The ex-
citatory input from the reticulospinal pathway activates
γ-motor neurons that indirectly activate α-motor neurons
(via Ia spindle afferent activity; see Chapter 14). This is called
the gamma loop.
Decerebrate rigidity may also lead to direct activation of
α-motor neurons. If the anterior lobe of the cerebellum is re-
moved in a decerebrate animal (dashed line labeled C in
Figure 18–6), extensor muscle hyperactivity is exaggerated
(decerebellate rigidity). This cut eliminates cortical inhibition
of the cerebellar fastigial nucleus and secondarily increases ex-
citation to vestibular nuclei. This rigidity is not reversed by
cutting the dorsal roots.
Removal of the cerebral cortex (decortication; dashed line
labeled D in Figure 18–6) produces decorticate rigidity that is
characterized by flexion of the upper extremities at the elbow
and extensor hyperactivity in the lower extremities. The flex-
ion can be explained by rubrospinal excitation of flexor mus-
cles in the upper extremities; the hyperextension of lower
extremities is due to the same changes that occur after midcol-
licular decerebration. Decorticate rigidity is seen on the hemi-
plegic side in humans after hemorrhages or thromboses in the
internal capsule. Sixty percent of intracerebral hemorrhages
occur in the internal capsule, and 10% each in the cerebral
cortex, pons, thalamus, and cerebellum.
CHAPTER 18 Control of Posture and Movement 171
BASAL GANGLIA
The basal ganglia are comprised of the caudate nucleus,
putamen, globus pallidus, and the functionally related sub-
thalamic nucleus and substantia nigra (Figure 18–7). The
globus pallidus is divided into external and internal segments
(GPe and GPi). The substantia nigra is divided into pars com-
pacta and pars reticulata. The caudate nucleus and putamen
are collectively called the striatum; the putamen and globus
pallidus form the lenticular nucleus.
The main inputs to the basal ganglia terminate in the stri-
atum (Figure 18–8). They include the excitatory corticostri-
ate pathway from M1 and premotor cortex. There is also a
projection from intralaminar nuclei of the thalamus to the
striatum (thalamostriatal pathway). The connections be-
tween the parts of the basal ganglia include a dopaminergic
nigrostriatal projection from the substantia nigra pars com-
pacta to the striatum and a corresponding GABAergic
projection from the striatum to substantia nigra pars reticu-
lata. The striatum projects to both GPe and GPi. GPe proj-
ects to the subthalamic nucleus, which in turn projects to
both GPe and GPi.
The principal output from the basal ganglia is from GPi via
the thalamic fasciculus to the ventral lateral, ventral anterior,
and centromedian nuclei of the thalamus. From the thalamic
nuclei, fibers project to the prefrontal and premotor cortex.
The substantia nigra also projects to the thalamus.
The main feature of the connections of the basal ganglia is
that the cerebral cortex projects to the striatum, the striatum
to GPi, GPi to the thalamus, and the thalamus back to the cor-
tex, completing a loop. The output from GPi to the thalamus is
inhibitory, whereas the output from the thalamus to the cere-
bral cortex is excitatory.
FUNCTION
The basal ganglia are involved in the planning and program-
ming of voluntary movement (Figure 18–1). They influence
the motor cortex via the thalamus. Also, GPi projects to brain
stem nuclei and from there to motor neurons in the brain stem
and spinal cord.
Three biochemical pathways in the basal ganglia normally
operate in a balanced fashion (Figure 18–8): (1) the nigrostri-
atal dopaminergic system, (2) the intrastriatal cholinergic
system, and (3) the GABAergic system, which projects from
the striatum to the globus pallidus and substantia nigra. When
one or more of these pathways become dysfunctional, charac-
teristic motor abnormalities occur. Diseases of the basal gan-
glia lead to two general types of disorders: hyperkinetic and
hypokinetic. The hyperkinetic conditions are those in which
movement is excessive and abnormal, including tremor,
chorea, athetosis, and ballism. Hypokinetic abnormalities
include akinesia and bradykinesia.
Chorea is characterized by rapid, involuntary “dancing”
movements. Athetosis is characterized by continuous, slow
172 SECTION IV CNS/Neural Physiology

FIGURE 18–6 A circuit drawing representing lesions produced in experimental animals to replicate decerebrate and decorticate
deficits seen in humans. Bilateral transections are indicated by dashed lines A–D. Decerebration is at a midcollicular level (A), decortication is
rostral to the superior colliculus, dorsal roots sectioned for one extremity (B), and removal of anterior lobe of cerebellum (C). The objective was
to identify anatomic substrates responsible for decerebrate or decorticate rigidity/posturing seen in humans with lesions that either isolate the
forebrain from the brain stem or separate rostral from caudal brain stem and spinal cord. (Reproduced with permission from Haines DE [editor]: Fundamental
Neuroscience for Basic and Clinical Applications, 3rd ed. Elsevier, 2006.)

writhing movements. Choreiform and athetotic movements PARKINSON’S DISEASE

have been likened to the start of voluntary movements occur-
ring in an involuntary, disorganized way. In ballism, involun-
tary flailing, intense, and violent movements occur. Akinesia
is difficulty in initiating movement and decreased spontane-
ous movement. Bradykinesia is slowness of movement.
Parkinson’s disease has both hypokinetic and hyperkinetic
features. It was the first disease identified as being due to a de-
ficiency in a specific neurotransmitter; it is due to the degen-
eration of dopaminergic neurons in the substantia nigra pars
 CHAPTER 18 Control of Posture and Movement 173

Caudate nucleus
Thalamus
Thalamus
Internal
capsule

Lateral ventricle

Amygdaloid
nucleus Caudate nucleus
Putamen and
globus pallidus Putamen

Lateral view Globus pallidus:

External segment
Caudate nucleus Thalamus Internal segment

Inte Subthalamic
rna Substantia nucleus
l ca
psu nigra
le
Amygdala
Globus
pallidus Tail of Frontal section
Putamen caudate nucleus

Horizontal section
FIGURE 18–7 Basal ganglia. The basal ganglia are composed of the caudate nucleus, putamen, and globus pallidus and the functionally
related subthalamic nucleus and substantia nigra. The frontal (coronal) section shows the location of the basal ganglia in relation to surrounding
structures. (Reproduced with permission from Barrett KE, Barman SM, Boitano S, Brooks H: Ganong’s Review of Medical Physiology, 23rd ed. McGraw-Hill Medical, 2009.)

compacta. It is one of the most common neurodegenerative cogwheel rigidity and tremor at rest. The absence of motor
diseases; it is estimated to occur in 1–2% of individuals over activity and the difficulty in initiating voluntary movements
age 65. Symptoms appear when 60–80% of the nigrostriatal are striking. Normal, unconscious movements such as swing-
dopaminergic neurons degenerate. ing of the arms during walking, facial expressions, and fidg-
The hypokinetic features of Parkinson’s disease are akine- eting are absent in Parkinson’s disease. The rigidity is different
sia and bradykinesia, and the hyperkinetic features are from spasticity because motor neuron discharge increases to
both the agonist and antagonist muscles. Passive motion of
an extremity meets with a plastic, dead-feeling resistance
Cerebral that has been likened to bending a lead pipe and is therefore
cortex
called lead pipe rigidity. Sometimes a series of “catches”
Glu takes place during passive motion (cogwheel rigidity), but
Globus GABA Striatum the sudden loss of resistance seen in a spastic extremity is
pallidus, ES (acetylcholine) absent. The tremor, which is present at rest and disappears
with activity, is due to regular, alternating contractions of an-
GABA Glu GABA GABA DA
tagonistic muscles.
Subthalamic Glu Globus A common treatment for Parkinson’s disease is the adminis-
SNPR SNPC
nucleus pallidus, IS
tration of l-DOPA (levodopa). Unlike dopamine, this dop-
Brain stem GABA GABA GABA amine precursor crosses the blood–brain barrier and helps
and PPN Thalamus repair the dopamine deficiency. However, the degeneration of
spinal cord
these neurons continues and in 5–7 years, the beneficial effects
FIGURE 18–8 Diagrammatic representation of the principal of l-DOPA usually disappear.
connections of the basal ganglia. Solid lines indicate excitatory
pathways, dashed lines inhibitory pathways. The transmitters are
indicated in the pathways, where they are known. Glu, glutamate; DA,
dopamine. Acetylcholine is the transmitter produced by interneurons CEREBELLUM
in the striatum. SNPR, substantia nigra pars reticulata; SNPC,
substantia nigra pars compacta; ES, external segment; IS, internal
The cerebellum sits astride the main sensory and motor sys-
segment; PPN, pedunculopontine nuclei. The subthalamic nucleus tems in the brain stem and is connected to the brain stem by
also projects to the pars compacta of the substantia nigra; this the superior, middle, and inferior peduncles. From a func-
pathway has been omitted for clarity. (Reproduced with permission from tional point of view, the cerebellum is divided into three
Barrett KE, Barman SM, Boitano S, Brooks H: Ganong’s Review of Medical Physiology, parts (Figure 18–9). The vestibulocerebellum has vestibular
23rd ed. McGraw-Hill Medical, 2009.) connections and is concerned with equilibrium and eye
174 SECTION IV CNS/Neural Physiology

Spinocerebellum ning and programming movements. The medial portion of

To medial
descending the cerebellum is called the vermis and it projects to the
systems Motor brain stem area concerned with control of axial and proximal
To lateral execution limb muscles (medial brain stem pathways). The area just
descending lateral to the vermis projects to the brain stem areas con-
systems
cerned with control of distal limb muscles (lateral brain stem
pathways).
To motor
and Motor
premotor planning
CELLULAR ORGANIZATION
cortices OF THE CEREBELLUM
Cerebrocerebellum To Balance
vestibular and eye The cerebellar cortex contains five types of neurons: Purkinje,
nuclei movements
granule, basket, stellate, and Golgi cells (Figure 18–10). The
Vestibulocerebellum Purkinje cells are among the biggest neurons in the CNS, with
FIGURE 18–9 Functional divisions of the cerebellum. extensive dendritic arbors. They are the only output neurons
(Modified with permission from Kandel ER, Schwartz JH, Jessell TM [editors]: of the cerebellar cortex, and their synaptic actions are inhibi-
Principles of Neural Science, 4th ed. McGraw-Hill, 2000.) tory via GABA release. The granule cells innervate the
Purkinje cells; their axons bifurcate to form a T. The branches
of the T are straight and run long distances; thus, they are
movements. The spinocerebellum receives proprioceptive called parallel fibers. The parallel fibers make synaptic con-
input from the body as well as a copy of the “motor plan” tact with the dendrites of many Purkinje cells and release glu-
from the motor cortex. It functions to smooth out and coor- tamate (an excitatory neurotransmitter).
dinate ongoing movements. The cerebrocerebellum in the The other three types of neurons in the cerebellar cortex are
lateral hemisphere interacts with the motor cortex in plan- inhibitory interneurons that release GABA. Basket cells

5 Stellate
cell Parallel fibers:
Axons of granule
cells
Axon
1 Purkinje
cell

Molecular
layer 2
1
Purkinje
layer
5
Axon Granular 4
layer 3 2 Golgi
cell
4 Granule
3 Basket
cell
cell
Axons

FIGURE 18–10 Location and structure of five neuronal types in the cerebellar cortex. Drawings are based on Golgi-stained
preparations. Purkinje cells (1) have processes aligned in one plane; their axons are the only output from the cerebellum. Axons of granule cells
(4) traverse and make connections with Purkinje cell processes in molecular layer. Golgi (2), basket (3), and stellate (5) cells have characteristic
positions, shapes, branching patterns, and synaptic connections. (Reproduced with permission from Kuffler SW, Nicholls JG, Martin AR: From Neuron to Brain,
2nd ed. Sinauer, 1984.)

Parallel fiber
+ + + bellar nuclei to the brain stem and thalamus.
Cerebellar
+
cortex
BC
PC
GC
− GR
−
Climbing + marked ataxia is characterized as incoordination due to errors in
fiber
− tients, but also in defects of the skilled movements involved in
Deep
nuclei NC + Mossy fiber
+ +
Other
inputs
+ an overshoot to one side or the other. This dysmetria promptly
FIGURE 18–11 Diagram of neural connections in the
cerebellum. Plus (+) and minus (–) signs indicate whether endings
are excitatory or inhibitory. BC, basket cell; GC, Golgi cell; GR, granule
cell; NC, cell in deep nucleus; PC, Purkinje cell. Note that PCs and BCs
are inhibitory. The connections of the stellate cells, which are not
shown, are similar to those of the basket cells, except that they end
for the most part on Purkinje cell dendrites. (Reproduced with permission
from Barrett KE, Barman SM, Boitano S, Brooks H: Ganong’s Review of Medical
Physiology, 23rd ed. McGraw-Hill Medical, 2009.)
receive input from the parallel fibers, and each projects to
many Purkinje cells (Figure 18–10). Their axons form a basket
around the cell body and axon hillock of each Purkinje cell
they innervate. Stellate cells are similar to the basket cells but
more superficial in location. The dendrites of Golgi cells re-
ceive input from the parallel fibers. Their cell bodies receive
input from the mossy fibers, and their axons project to the
dendrites of the granule cells.
The primary afferent inputs to the cerebellum are the mossy
and climbing fibers, both of which are excitatory
(Figure 18–11). The climbing fibers relay proprioceptive in-
put from a single source, the inferior olivary nuclei. The
mossy fibers provide proprioceptive input as well as input
from the cerebral cortex via the pontine nuclei.
The fundamental circuits of the cerebellar cortex are rela-
tively simple (Figure 18–11). Climbing fiber inputs exert a
strong excitatory effect on a single Purkinje cell, and mossy
fiber inputs exert a weak excitatory effect on many Purkinje
cells via the granule cells. The basket and stellate cells are also
excited by granule cells via the parallel fibers, and their output
inhibits Purkinje cell discharge (feed-forward inhibition).
Golgi cells are excited by the mossy fiber collaterals, Purkinje
cell collaterals, and parallel fibers, and they inhibit transmis-
sion from mossy fibers to granule cells.
The output of Purkinje cells is inhibitory to the deep cere-
bellar nuclei. These nuclei also receive excitatory inputs via
collaterals from the mossy and climbing fibers. Thus, almost
all the cerebellar circuitry seems to be concerned solely with
CHAPTER 18 Control of Posture and Movement 175
modulating or timing the excitatory output of the deep cere-
CEREBELLAR DISEASE
Damage to the cerebellum leads to several characteristic
abnormalities, including hypotonia, ataxia, and intention trem-
+
or. Most abnormalities are apparent during movement. The
the rate, range, force, and direction of movement. Ataxia is man-
ifest not only in the wide-based, unsteady, “drunken” gait of pa-
the production of speech. The individual pauses between words
and syllables, a phenomenon referred to as scanning speech.
Voluntary movements are also highly abnormal. As an
example, if one attempts to touch an object with a finger, there is
initiates a gross corrective action, but the correction overshoots
to the other side. Consequently, the finger oscillates back and
forth. This oscillation is the intention tremor of cerebellar dis-
ease. Another characteristic of cerebellar disease is the inability
to stop movement promptly. Normally, for example, flexion of
the forearm against resistance is quickly checked when the re-
sistance force is suddenly broken off. The patient with cerebel-
lar disease cannot stop the movement of the limb, and the
forearm flies backward in a wide arc (rebound phenomenon).
This is one of the reasons these patients show dysdiadochoki-
nesia, the inability to perform rapidly alternating opposite
movements such as repeated pronation and supination of the
hands. Finally, patients with cerebellar disease have difficulty
performing actions that involve simultaneous motion at more
than one joint. They dissect such movements and carry them
out one joint at a time (decomposition of movement).
Motor abnormalities associated with cerebellar damage vary
depending on the region involved. The major dysfunctions
seen after damage to the vestibulocerebellum are ataxia, dyse-
quilibrium, and nystagmus. Damage to the vermis and fastigial
nucleus (part of the spinocerebellum) leads to disturbances in
control of axial and trunk muscles during attempted antigravity
postures and scanning speech. Degeneration of this portion of
the cerebellum can result from thiamine deficiency in alcohol-
ics or malnourished individuals. The major dysfunctions seen
after damage to the cerebrocerebellum are delays in initiating
movements and decomposition of movement.
CLINICAL CORRELATION
About 2 years ago at the age of 34, a man developed pro-
gressive weakness in his right leg and eventually his
whole right side weakened. He was unable to continue
his work as an electrician. He experienced cramps in his
right calf muscle and muscle twitches in his arm and leg.
A neurological examination revealed muscular atrophy,
176 SECTION IV CNS/Neural Physiology
fasciculations (muscle twitches that appear as flickers
under the skin), and hypotonia of muscles in the arm
and leg. He also had marked hyporeflexia. Sensory and
cognitive function tests were normal. All signs were in-
dicative of a lower motor neuron disease affecting mul-
tiple spinal cord levels. He was eventually diagnosed with
amyotrophic lateral sclerosis (ALS). Over the course of
the next year, the disease progressed to the point where
he had difficulty swallowing (dysphagia), so he had to be
fed via a gastric tube. About 6 months ago, he developed
difficulty breathing and was placed on a ventilator. One
week ago, he died of pneumonia.
ALS is a selective, progressive degeneration of α-motor
neurons. “Amyotrophic” means “no muscle nourishment”
and describes the atrophy that muscles undergo because
of disuse. “Sclerosis” refers to the hardness felt when a pa-
thologist examines the spinal cord on autopsy; the hard-
ness is due to proliferation of astrocytes and scarring of
the lateral columns of the spinal cord. This fatal disease is
also known as Lou Gehrig’s disease in recognition of a fa-
mous American baseball player who died of it. The world-
wide annual incidence of ALS is estimated to be 0.5–3
cases per 100,000 people. Most cases are sporadic, but
5–10% of the cases are familial. Forty percent of the famil-
ial cases have a mutation in the gene for Cu/Zn superox-
ide dismutase (SOD-1) on chromosome 21. SOD is a free
radical scavenger that reduces oxidative stress. A defec-
tive SOD-1 gene permits free radicals to accumulate and
kill neurons. The disease has no racial, socioeconomic, or
ethnic boundaries. The life expectancy of ALS patients is
usually 3–5 years after diagnosis. ALS is most commonly
diagnosed in middle age and affects men more often than
women. The causes of ALS are unclear, but may include
viruses, neurotoxins, heavy metals, DNA defects (espe-
cially in familial ALS), immune system abnormalities, and
enzyme abnormalities. There is no cure for ALS; treat-
ments (e.g., physical and occupational therapy) focus on
relieving symptoms and maintaining the quality of life.
CHAPTER SUMMARY
■ The ventral corticospinal tract and medial descending brain
stem pathways (tectospinal, reticulospinal, and vestibulospinal
tracts) regulate proximal muscles and posture. The lateral
corticospinal and rubrospinal tracts control distal limb muscles
and skilled voluntary movements.
■ Decerebrate rigidity leads to hyperactivity in extensor
muscles in all four extremities; it is actually spasticity due
to facilitation of the myotatic stretch reflex. Decorticate
posturing or decorticate rigidity is flexion of the upper
extremities at the elbow and extensor hyperactivity in the
lower extremities.
■ The basal ganglia include the caudate nucleus, putamen, globus
pallidus, subthalamic nucleus, and substantia nigra. The
connections between the parts of the basal ganglia include a
dopaminergic nigrostriatal projection from the substantia nigra
to the striatum and a GABAergic projection from the striatum
to substantia nigra.
■ Parkinson’s disease is due to degeneration of the nigrostriatal
dopaminergic neurons and is characterized by akinesia,
bradykinesia, cogwheel rigidity, and tremor at rest.
■ The cerebellar cortex contains five types of neurons: Purkinje,
granule, basket, stellate, and Golgi cells. The two main inputs
to the cerebellar cortex are climbing fibers and mossy fibers.
Purkinje cells are the only output from the cerebellar cortex
and they generally project to the deep nuclei.
■ Damage to the cerebellum leads to several characteristic
abnormalities, including hypotonia, ataxia, and intention tremor.
STUDY QUESTIONS
1. A primary function of the basal ganglia is
A) sensory integration.
B) short-term memory.
C) planning voluntary movement.
D) neuroendocrine control.
E) slow-wave sleep.
2. The therapeutic effect of l-DOPA in patients with Parkinson’s
disease eventually wears off because
A) antibodies to dopamine receptors develop.
B) inhibitory pathways grow into the basal ganglia from
the frontal lobe.
C) cholinergic neurons in the striatum degenerate.
D) the normal action of nerve growth factor (NGF) is
disrupted.
E) the dopaminergic neurons in the substantia nigra continue
to degenerate.
3. Increased neural activity before a skilled voluntary movement
is first seen in the
A) spinal motor neurons.
B) precentral motor cortex.
C) midbrain.
D) cerebellum.
E) cortical association areas.
4. After falling down a flight of stairs, a young woman is found to
have partial loss of voluntary movement on the right side of her
body and loss of pain and temperature sensation on the left side
below the midthoracic region. It is probable that she has a lesion
A) transecting the left half of the spinal cord in the
lumbar region.
B) transecting the left half of the spinal cord in the upper
thoracic region.
C) transecting sensory and motor pathways on the right
side of the pons.
D) transecting the right half of the spinal cord in the
upper thoracic region.
E) transecting the dorsal half of the spinal cord in the
upper thoracic region.
5. Which of the following are not correctly paired?
A) medial brain stem pathways:axial and proximal
muscle control
B) lateral brain stem pathway:rubrospinal tract
C) upper motor neuron disease:hypotonia
D) cerebellar disease:intention tremor
E) decerebrate rigidity:hyperactivity of extensor muscles

Autonomic Nervous
System
Susan M. Barman
O B J E C T I V E S
■ Describe the location of the cell bodies and axonal trajectories
of preganglionic sympathetic and parasympathetic neurons.
■ Describe the location and trajectories of postganglionic sympathetic
and parasympathetic neurons.
■ Name the neurotransmitters that are released by preganglionic and
postganglionic autonomic neurons.
■ List the major functions of the autonomic nervous system.
■ Identify some of the neural inputs to sympathetic and parasympathetic neurons.
INTRODUCTION
The autonomic nervous system (ANS) is one of the control sys-
tems responsible for homeostasis and is the source of innerva-
tion of organs other than skeletal muscle. Nerve terminals are
located in smooth muscle (e.g., blood vessels, gut wall, urinary
bladder), cardiac muscle, and glands (e.g., sweat glands, salivary
glands). Although survival is possible without an ANS, the abil-
ity to adapt to environmental stressors and other challenges is
severely compromised in diseases that affect this component of
the nervous system. The ANS has two major divisions: sympa-
thetic and parasympathetic nervous systems. It is classically
defined by the preganglionic and postganglionic neurons within
the sympathetic and parasympathetic divisions. A more mod-
ern definition of the ANS takes into account the descending
pathways from several forebrain and brain stem regions as well
as visceral afferent pathways that set the level of activity in sym-
pathetic and parasympathetic nerves.
ANATOMIC ORGANIZATION
OF AUTONOMIC OUTFLOW
Figure 19–1 compares some fundamental characteristics of the
innervation of skeletal muscle and innervation of smooth mus-
cle, cardiac muscle, and glands. As described in Chapter 14,
19
C H A P T E R
α-motor neurons serve as the final common pathway linking
the central nervous system (CNS) to skeletal muscles. Simi-
larly, sympathetic and parasympathetic neurons serve as the
final common pathway from the CNS to visceral targets. How-
ever, the peripheral portion of the ANS is composed of two
neurons: preganglionic and postganglionic neurons. The cell
bodies of the preganglionic neurons are located in the inter-
mediolateral column (IML) of the spinal cord and in motor
nuclei of some cranial nerves. In contrast to the large-diameter
and rapidly conducting α-motor neurons, preganglionic axons
are small-diameter and relatively slowly conducting B fibers.
A preganglionic axon diverges to an average of about nine
postganglionic neurons, making autonomic output diffuse.
The axons of the postganglionic neurons are mostly unmyeli-
nated C fibers and terminate on the visceral effectors.
SYMPATHETIC DIVISION
In contrast to α-motor neurons that are located at all spinal
segments, sympathetic preganglionic neurons are located in
the IML of only the first thoracic to the third or fourth lum-
bar segments. This is why the sympathetic nervous system is
sometimes called the thoracolumbar division of the ANS.
The axons of sympathetic preganglionic neurons leave the
spinal cord at the level at which their cell bodies are located
and exit via the ventral root along with axons of α- and
177
178 SECTION IV CNS/Neural Physiology

CNS Somatic nervous system

Effector
organ
ACh

Autonomic nervous system:

CNS Parasympathetic division

Effector
organ

Ganglion ACh

Autonomic nervous system:

CNS Sympathetic division
Effector
organ

ACh Ganglion ACh NE

Effector
(via bloodstream) organ

Adrenal Epi (also NE, DA, peptides)

medulla
FIGURE 19–1 Comparison of peripheral organization and transmitters released by somatomotor and autonomic nervous systems
(NS). ACh, acetylcholine; DA, dopamine; NE, norepinephrine; Epi, epinephrine. (Reproduced with permission from Widmaier EP, Raff H, Strang KT: Vander’s
Human Physiology. McGraw-Hill, 2008.)

γ-motor neurons (Figure 19–2). They then separate from
the ventral root via the white rami communicans and proj-
ect to the adjacent sympathetic paravertebral ganglion,
where some of them end on the cell bodies of postganglionic
neurons. Paravertebral ganglia are located adjacent to each
thoracic and upper lumbar segment; in addition, there are a
few ganglia adjacent to the cervical and sacral spinal seg-
ments. Paravertebral ganglia form the sympathetic chain
(or sympathetic trunk) bilaterally. The ganglia are connected
to each other via the axons of preganglionic neurons that
travel rostrally or caudally to terminate on postganglionic
neurons located at some distance. This arrangement is
shown in Figures 19–2 and 19–3.
Some preganglionic neurons pass through the sympathetic
chain and end on postganglionic neurons located in preverte-
bral (or collateral) ganglia close to the viscera, including the
celiac, superior mesenteric, and inferior mesenteric ganglia
(Figure 19–3). There are also preganglionic neurons whose
axons terminate directly on an effector organ, the medulla of
the adrenal gland.
The axons of some of the postganglionic neurons leave the
chain ganglia and reenter the spinal nerves via the gray rami
communicans and are distributed to autonomic effectors in
the areas supplied by these spinal nerves (Figure 19–2). These
postganglionic sympathetic nerves terminate on smooth mus-
cle of blood vessels and hair follicles and on sweat glands in the
limbs. Other postganglionic fibers leave the chain ganglia to
enter the thoracic cavity to terminate in visceral organs. Post-
ganglionic fibers from prevertebral ganglia also terminate in
visceral targets.
PARASYMPATHETIC DIVISION
The parasympathetic nervous system is sometimes called the
craniosacral division of the ANS because of the location of its
preganglionic neurons (Figure 19–3). The parasympathetic
nerves supply the visceral structures in the head via the oculo-
motor, facial, and glossopharyngeal nerves, and those in the
thorax and upper abdomen via the vagus nerves. The sacral
outflow supplies the pelvic viscera via branches of the second
to fourth sacral spinal nerves. Parasympathetic preganglionic
fibers synapse on ganglia cells clustered within the walls of vis-
ceral organs; thus, these parasympathetic postganglionic fibers
are very short.
CHEMICAL TRANSMISSION AT
AUTONOMIC JUNCTIONS
ACETYLCHOLINE AND
NOREPINEPHRINE
The principal transmitter agents released by autonomic
nerves are acetylcholine and norepinephrine (Figure 19–1).
The neurons that are cholinergic (i.e., release acetylcholine)
include (1) all preganglionic neurons, (2) all parasympa-
thetic postganglionic neurons, (3) sympathetic postgangli-
onic neurons that innervate sweat glands, and (4) sympathetic
postganglionic neurons that end on blood vessels in some
skeletal muscles and produce vasodilation when stimulated
 CHAPTER 19 Autonomic Nervous System 179

FIGURE 19–2 Projection of sympathetic preganglionic and postganglionic fibers. The drawing shows the thoracic spinal cord,
paravertebral, and prevertebral ganglia. Preganglionic neurons are shown in red, postganglionic neurons in dark blue, afferent sensory pathways
in blue, and interneurons in black. (Reproduced with permission from Boron WF, Boulpaep EL: Medical Physiology. Elsevier, 2005.)

(sympathetic vasodilator nerves). The remaining sympa-
thetic postganglionic neurons are noradrenergic (i.e., release
norepinephrine). The adrenal medulla is essentially a sym-
pathetic ganglion in which the postganglionic cells have lost
their axons and secrete norepinephrine and epinephrine
directly into the bloodstream.
Transmission in autonomic ganglia is mediated primarily
by N2 nicotinic cholinergic receptors that are blocked by
hexamethonium, whereas transmission at the neuromuscu-
lar junction is via N1 nicotinic cholinergic receptors that are
blocked by D-tubocurare. The release of acetylcholine from
postganglionic fibers acts on muscarinic receptors, which
are blocked by atropine. The release of norepinephrine from
sympathetic postganglionic fibers acts on α1-, α2-, β1-, or
β2-adrenoreceptors, depending on the target organ.
Table 19–1 shows the types of receptors at various junctions
within the ANS.
In addition to these “classical” neurotransmitters, some
autonomic fibers also release neuropeptides. The small granu-
lated vesicles in postganglionic noradrenergic neurons contain
ATP and norepinephrine, and the large granulated vesicles
contain neuropeptide Y. Low-frequency stimulation may pro-
mote release of ATP, whereas high-frequency stimulation may
cause release of neuropeptide Y. The viscera contain puriner-
gic receptors, and ATP may be a mediator in the ANS along
with norepinephrine.
RESPONSES OF EFFECTOR
ORGANS TO AUTONOMIC NERVE
IMPULSES
The effects of stimulation of the noradrenergic and cholin-
ergic postganglionic nerve fibers are indicated in Figure
19–3 and Table 19–1. Release of acetylcholine onto smooth
muscle of some organs leads to contraction (e.g., walls of the
gastrointestinal tract), and release onto other organs leads
to relaxation (e.g., sphincters in the gastrointestinal tract).
For some targets innervated by the ANS, one can shift from
contraction to relaxation by switching from activation of
the parasympathetic nervous system to activation of the