Answers to Test & Quantitative and Thought Questions
terminals is necessary for neurotransmitter release.
Stimulating the smooth muscle cell membrane
would also not cause a response in the absence of
calcium because in all of the various types of smooth
muscle, calcium must enter from outside the cell
to trigger contraction. In some cases, the external
calcium directly initiates contraction, and in others it
triggers the release of calcium from the sarcoplasmic
reticulum (calcium-induced calcium release).
The simplest model to explain the experimental
observations is as follows. Upon parasympathetic
nerve stimulation, a neurotransmitter is released
that binds to receptors on the membranes of smooth
muscle cells and triggers contraction. The substance
released, however, is not acetylcholine (ACh) for the
Action potentials in the parasympathetic nerves
are essential for initiating nerve-induced contraction.
When the nerves were prevented from generating
action potentials by blockage of their voltage-gated
sodium channels, there was no response to nerve
stimulation. ACh is the neurotransmitter released
from most, but not all, parasympathetic endings.
When the muscarinic receptors for ACh were blocked,
however, stimulation of the parasympathetic nerves
still produced a contraction, providing evidence that
some substance other than ACh is being released by
the neurons and producing contraction.
Elevation of extracellular ﬂ uid calcium concentration
would increase the amount of calcium entering
the cytosol through L-type calcium channels. This
would result in a greater depolarization of cardiac
muscle cell membranes during action potentials. The
strength of cardiac muscle contractions would also
be increased because this larger calcium entry would
trigger more calcium release through ryanodine
receptor channels, and thus there would be a greater
activation of cross-bridge cycling.
The basal nuclei, sensorimotor cortex, thalamus,
brainstem, and cerebellum are all middle-level
structures that create a motor program based on the
intention to carry out a voluntary movement.
When a given muscle is stretched, muscle-spindle
stretch receptors send action potentials along afferent
ﬁ bers that synapse directly on alpha motor neurons
to extrafusal ﬁ bers to that muscle, causing it to
contract back toward the prestretched length.
Afferent action potentials from pain receptors in
the injured left foot would stimulate the withdrawal
reﬂ ex of the left leg (activation of ﬂ exor muscles and
inhibition of extensors) and the opposite pattern in
the right leg (the crossed-extensor reﬂ ex).
Activating the gamma motor neurons would cause
contraction of the ends of intrafusal muscle ﬁ bers,
stretching the muscle-spindle receptors, and the
resulting action potentials would monosynaptically
excite the alpha motor neurons innervating the
extrafusal ﬁ bers of the stretch receptors.
See Figure 10–10.
Most descending corticospinal pathways cross the
midline of the body in the medulla oblongata.
Upper motor neuron disorders are typically
characterized by hypertonia and spasticity.
The reverse is actually true.
In Parkinson’s, a deﬁ cit of dopamine from neurons
of the substantia nigra results in “resting tremors.”
toxin speciﬁ cally blocks
the release of neurotransmitter from neurons that
normally inhibit motor neurons. The resulting
imbalance of excitatory and inhibitory inputs causes
spastic contractions of muscles.
Quantitative and Thought Questions
None. The gamma motor neurons are important
in preventing the muscle spindle stretch receptors
from going slack, but when this reﬂ ex is tested,
the intrafusal ﬁ bers are not ﬂ accid. The test is
performed with a bent knee, which stretches the
extensor muscles in the thigh (and the intrafusal
ﬁ bers within the stretch receptors). The stretch
receptors are therefore responsive.
The efferent pathway of the reﬂ ex arc (the alpha
motor neurons) would not be activated, the effector
cells (the extrafusal muscle ﬁ bers) would not be
activated, and there would be no reﬂ ex response.
The drawing must have excitatory synapses on the
motor neurons of both ipsilateral extensor and
ipsilateral ﬂ exor muscles.
A toxin that interferes with the inhibitory synapses on
motor neurons would leave unbalanced the normal
excitatory input to these neurons. Thus, the otherwise
normal motor neurons would ﬁ re excessively, which
would result in increased muscle contraction. This
is exactly what happens in lockjaw as a result of the
toxin produced by the tetanus bacillus.
In mild cases of tetanus, agonists (stimulators)
of the inhibitory interneuron neurotransmitter
gamma-aminobutyric acid (GABA) can shift the
balance back toward the inhibition of alpha motor
neurons. In more severe cases, paralysis can be
induced by administering long-lasting drugs that
block the nicotinic acetylcholine receptors at the