Page 236 - Anatomy and Physiology of Farm Animals, 8th Edition

Physiology of the Nervous System / 221

receptors because the hormone epineph- Neural Control of Skeletal Muscle
rine, also called adrenaline, likewise binds
VetBooks.ir to these receptors. Adrenergic receptors As described in Chapter 9, each contrac­

are not ion channels that open to change
polarization; rather, they are linked to tion of skeletal muscle requires stimulation
of the muscle by a somatic motor neuron.
proteins within the cell that indirectly A somatic motor neuron has its cell body
produce depolarization or hyperpolariza­ within the CNS, and its axon extends from
tion, depending on the type of adrenergic the CNS to contact a skeletal muscle cell
receptor. at the neuromuscular junction. A single
Both the neurotransmitter norepineph­ motor neuron can stimulate more than one
rine and the endocrine hormone epi­ skeletal muscle cell, but a single skeletal
nephrine are classified as catecholamines muscle cell receives input from only one
because of their chemical structure, which motor neuron. A motor neuron and all the
is derived from the amino acid tyrosine. muscle cells it innervates together are
Dopamine is another catecholamine that called a motor unit.
functions as a neurotransmitter within the A clinical classification applied to the
central and peripheral nervous systems, motor neuron that extends from the CNS
and specific dopamine receptors also exist. to skeletal muscle fibers is the lower
Gamma‐aminobutyric acid (GABA) is motor neuron (LMN). (More specifically,
the most prevalent inhibitory amino acid this is the somatic LMN, but somatic is
neurotransmitter in the CNS. Binding of often omitted in common usage.) Any
GABA to its receptor produces neuronal contraction of skeletal muscle – whether
hyperpolarization (inhibition). Several voluntary or reflex – depends on an
agents that act as sedatives, tranquilizers, intact and properly functioning LMN.
and general muscle relaxants have part Typically, a single neuron receives inputs
of their effect via promoting GABA’s from many other neurons because of con­
effects on the CNS. These include alcohol, vergence in neural networks. Therefore, a
barbiturates, and the benzodiazepines single LMN is subject to regulation by
(e.g., diazepam or Valium®). Some of multiple inputs from other neurons within
these agents bind directly to GABA the CNS. Upper motor neuron (UMN) is
receptors; others seem to facilitate the the general term applied to a neuron within
action of endogenous GABA. The GABA the CNS that acts to regulate the activity of
receptors may also be a principal target a LMN. UMNs are responsible for initiat­
for some general anesthetics. ing voluntary movement and maintaining
Glutamate, an amino acid, is the pre­ relatively stable body posture and position
dominant excitatory neurotransmitter in relative to gravity so that voluntary move­
the CNS, and several subtypes of gluta­ ments are normal. If the LMNs to a muscle
mate receptors have been identified. The are intact but the UMNs that normally
primary receptor, the AMPA receptor, is a regulate those LMNs are dysfunctional,
classic ligand‐gated sodium ion channel, voluntary movements may be reduced or
and its opening allows positive ions to absent. As long as local reflex connections
flow into the cell’s interior to depolarize are intact, however, reflexes will still be
(excite) it. Another subtype of glutamate present (see later).
receptor, the NMDA receptor (named for A total lack of voluntary movement is
the agonist N‐methyl‐d‐aspartate), is called paralysis. A reduction in volun-
involved with memory and learning. tary movement is called paresis. Muscles
Stimulation of NMDA receptors makes can be paralyzed and also have no reflex
the postsynaptic membrane respond more movement (as when LMNs are damaged),
vigorously to subsequent stimulation, a or they can be paralyzed and still have
process which is the physiological corre­ reflex movement (as when UMNs are
late of “remembering” activity. damaged).