cause the dry mouth. We know that the drug is not
blocking cholinergic nicotinic receptors because the
skeletal muscles are not affected.
Because the membrane potential of the cells in
question depolarizes (i.e., becomes less negative)
when chloride channels are blocked, one can assume
there was net chloride diffusion into the cells through
these channels prior to treatment with the drug.
Therefore, one can also predict that this passive
inward movement was being exactly balanced by active
transport of chloride out of the cells.
Without acetylcholinesterase, more acetylcholine
would remain bound to the receptors, and all the
actions normally caused by acetylcholine would be
accentuated. Thus, there would be marked narrowing
of the pupils, airway constriction, stomach cramping
and diarrhea, sweating, salivation, slowing of the
heart, and fall in blood pressure. On the other
hand, in skeletal muscles, which must repolarize
after excitation in order to be excited again, there
would be weakness, fatigue, and ﬁ nally inability to
contract. In fact, lethal poisoning by high doses of
cholinesterase inhibitors occurs because of paralysis
of the muscles involved in respiration. Low doses of
these compounds are used therapeutically.
These potassium channels, which open after a
short delay following the initiation of an action
potential, increase potassium diffusion out of the
cell, hastening repolarization. They also account for
the increased potassium permeability that causes the
afterhyperpolarization. Therefore, the action potential
would be broader (that is, longer in duration) and
would return to resting level more slowly, and the
afterhyperpolarization would be absent.
For example, photons of light are the adequate
stimulus for photoreceptors of the eye, and sound is
the adequate stimulus for hair cells of the ear.
Receptor potentials generate only local currents in
the receptor membrane that transduces the stimulus,
but when they reach the ﬁ rst node of Ranvier, they
depolarize the membrane to threshold, and there the
voltage-gated sodium channels ﬁ rst initiate action
potentials. Beyond that point, the receptor potential
decreases with distance, whereas action potentials
propagate all the way to the central axon terminals.
Lateral inhibition increases the contrast between the
region at the center of a stimulus and regions at the
edges of the stimulus, which increases the acuity of
The occipital lobe of the cortex is the initial site of
visual processing. (Review Figure 7–14.)
Somatic sensations include those from the skin,
muscles, bones, tendons, and joints, but not encoding
of sound by cochlear hair cells.
A myopic (nearsighted) person has an eyeball that is
too long. When the ciliary muscles are relaxed and
the lens is as ﬂ at as possible, parallel light rays from
distant objects focus in front of the retina, while
diverging rays from near objects are able to focus on
the retina. (Recall that with normal vision, it takes
ciliary muscle contraction and a rounded lens to
focus on near objects.)
When the right optic tract is destroyed, perception
of images formed on the right half of the retina in
both eyes is lost, so nothing is visible at the left side
of a person’s ﬁ eld of view (Review Figure 7–29.)
Pressure waves traveling down the cochlea make the
cochlear duct vibrate, moving the basilar membrane
against the stationary tectorial membrane and bending
the hair cells that bridge the gap between the two.
With the sudden head rotation from left-to-right,
inertia of the endolymph causes it to rotate from
right-to-left with respect to the semicircular canal
that lies in the horizontal plane. This ﬂ uid ﬂ ow
bends the cupula and embedded hair cells within
the ampulla, which inﬂ uences the ﬁ ring of action
potentials along the vestibular nerve.
“Umami” is derived from the Japanese word
meaning delicious, and the stimulation of these taste
receptors by glutamate produces the perception of a
rich, meaty ﬂ avor.
Quantitative and Thought Questions
(a) Use drugs to block transmission in the pathways
that convey information about pain to the brain.
For example, if substance P is the neurotransmitter
at the central endings of the nociceptor afferent
ﬁ bers, give a drug that blocks the substance P
receptors. (b) Cut the dorsal root at the level of
entry of the nociceptor ﬁ bers to prevent transmission
of their action potentials into the central nervous
system. (c) Give a drug that activates receptors in
the descending pathways that block transmission
of the incoming or ascending pain information. (d)
Stimulate the neurons in these same descending
pathways to increase their blocking activity
(stimulation-produced analgesia or, possibly,
acupuncture). (e) Cut the ascending pathways that
transmit information from the nociceptor afferents.
(f) Deal with emotions, attitudes, memories, and so
on to decrease sensitivity to the pain. (g) Stimulate
nonpain, low-threshold afferent ﬁ bers to block
transmission through the pain pathways (TENS).
(h) Block transmission in the afferent nerve with a
local anesthetic such as Novocaine or Lidocaine.
Information regarding temperature is carried via
the anterolateral system to the brain. Fibers of this
system cross to the opposite side of the body in the
spinal cord at the level of entry of the afferent ﬁ bers
(see Figure 7–19a). Damage to the left side of the
spinal cord or any part of the left side of the brain