429
CHAPTER ELEVEN
Nervous System II
cells, as in the case of stimulation at neuromuscular junc-
tions (see chapter 9, p. 290) and synapses (see chapter 10,
p. 365). Receptor binding alters the membrane. For example,
the membrane’s permeability to certain ions may increase,
and in smooth muscle cells, an action potential followed by
muscular contraction may result. Similarly, a gland cell may
respond to a change in its membrane by secreting a product.
Acetylcholine can combine with two types of cholinergic
receptors, called
muscarinic receptors
and
nicotinic receptors.
These receptor names come from
muscarine,
a toxin from
a fungus that can activate muscarinic receptors, and
nico-
tine,
a toxin of tobacco that can activate nicotinic receptors.
The muscarinic receptors are in the membranes of effector
cells at the ends of all postganglionic parasympathetic nerve
± bers and at the ends of the cholinergic sympathetic ± bers.
Responses from these receptors are excitatory and relatively
slow. The nicotinic receptors are in the synapses between
the preganglionic and postganglionic neurons of the para-
sympathetic and sympathetic pathways. They produce rapid,
excitatory responses (see Table 11.10). (Receptors at neuro-
muscular junctions of skeletal muscles are also nicotinic.)
Epinephrine and norepinephrine are the two chemical
mediators of the sympathetic nervous system. The adrenal
gland releases both as hormones, but only norepinephrine is
released as a neurotransmitter by the sympathetic nervous
system. These biochemicals can then bind adrenergic recep-
tors of effector cells.
rons, however, secrete norepinephrine (noradrenalin) and are
called
adrenergic
(ad
ren-er
jik) (± g. 11.40). Exceptions to
this include the sympathetic postganglionic neurons that stim-
ulate sweat glands and a few sympathetic neurons to blood
vessels in skin (which cause vasodilation); these neurons
secrete acetylcholine and therefore are cholinergic (adrenergic
sympathetic ± bers to blood vessels cause vasoconstriction).
Most organs receive innervation from both sympathetic
and parasympathetic divisions, usually with opposing actions.
For example, the sympathetic nervous system increases heart
rate and dilates pupils, whereas parasympathetic stimulation
decreases heart rate and constricts pupils. However, this is not
always the case. For example, the diameters of most blood
vessels lack parasympathetic innervation and are thus reg-
ulated by the sympathetic division. Smooth muscles in the
walls of these vessels are continuously stimulated by sym-
pathetic impulses; they are thereby maintained in a state of
partial contraction called
sympathetic tone.
Decreasing sym-
pathetic stimulation allows the muscular walls of such blood
vessels to relax, increasing their diameters (vasodilation).
Conversely, increasing sympathetic stimulation vasoconstricts
vessels.
Table 11.10
summarizes the effects of autonomic
stimulation on various visceral effectors.
Actions of Autonomic Neurotransmitters
The actions of autonomic neurotransmitters result from their
binding to protein receptors in the membranes of effector
FIGURE 11.40
Most sympathetic f
bers are adrenergic and secrete norepinephrine at the ends oF the postganglionic f
ber; parasympathetic f
bers
are cholinergic and secrete acetylcholine at the ends oF the postganglionic f
bers. Two arrangements oF parasympathetic postganglionic f
bers are
seen in both cranial and sacral portions. Similarly, sympathetic paravertebral and collateral ganglia are seen in both the thoracic and lumbar portions
oF the nervous system. (Dendrites not shown.)
Brain
Cranial
parasympathetic
neurons
Paravertebral
ganglion
Postganglionic fiber (axon)
Preganglionic fiber (axon)
Collateral
ganglion
Visceral
effectors
Ganglion
Sacral
parasympathetic
neurons
Sympathetic neurons
ACh = acetylcholine (cholinergic)
NE = norepinephrine (adrenergic)
ACh
ACh
ACh
ACh
ACh ACh
NE
NE
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