A-37

Appendix G

indicated. Following is an illustration of theright and left visual fields.

7. First, let us define perfect pitch and tonedeaf. Perfect pitch is the ability to repro-duce a pitch precisely just by being told itsname or reading it on a sheet of music, withno other musical support, such as pianoaccompaniment. Tone deafness is the com-plete inability to recognize or reproducemusical pitches. Both of these characteristicscan be due to variation in the structure ofthe basilar membrane, the inhibitory reflexfrom the superior olivary nucleus to thespiral organ, and the auditory cortex. Recallthat the basilar membrane is structurallydifferent from the base to the apex, allowingdifferent segments to be sensitive to differentfrequencies (see figure 15.34). In individualswith perfect pitch, the structure of the basilarmembrane may be such that tones areadequately spaced along the cochlearduct to facilitate clear separation of tones,whereas in tone-deaf individuals the spacingis inadequate to clearly separate tones.We also learned that the superior olivarynucleus of the medulla oblongata has aninhibitory effect that only allows actionpotentials from regions of the basilar mem-brane with maximum vibration to be con-ducted to the auditory cortex. This allowsan individual to distinguish specific soundfrequencies. For people with perfect pitch,the reflex from the superior olivary nucleusto the spiral organ may have a very narrow“window of function,” whereas for indi-viduals that are tone deaf, the reflex maynot function well enough.Finally, at the auditory cortex, actionpotentials that originate in the spiral organ aretranslated to perceived sounds. Variationin translation accuracy would explain thedifference between individuals with perfectpitch and those with tone deafness.8. Recall that the sound wave amplitudedetermines the volume of a sound, whereaswave frequency determines the pitch of thesound. Loud sounds have sound waves withgreater amplitude. This greater amplitudecauses the basilar membrane to vibratemore violently over a wider range. Thespreading of the wave in the basilar mem-brane to some extent counteracts the reflexfrom the superior olivary nucleus that isresponsible for enabling a person to hearsubtle tone differences.

9. We learned that the brain compares sensoryinput from the semicircular canals, eyes,and proprioceptors in the back and lowerlimbs and that conflicting information cancause motion sickness. If you close youreyes, one of these sources of information iseliminated and the brain has less conflictinginput to compare, reducing the probabilityof motion sickness. We can perceive moremotion in close objects than in distantobjects, so looking at the horizon wouldalso reduce the visual input of perceivedmotion to the brain and reduce theprobability of motion sickness.

Chapter 16

2. This question is referring to the differ-ent types of cholinergic receptors: nico-tinic receptors and muscarinic receptors.Remember that, even though these arecholinergic receptors to which acetylcholinenormally binds, they were classified basedon laboratory findings that nicotine bindsto one type of cholinergic receptor and mus-carine binds to the other type of cholinergicreceptor. Also recall that all preganglionicneurons of the sympathetic and parasympa-thetic divisions and all postganlionic neuronsof the parasympathetic division release acetyl-choline. Also, the postganglionic neuronsof the sympathetic division that innervatesweat glands also release acetylcholine.Figure 16.7 allows us to determine which ofthese synapses would be affected by nico-tine and which of these synapses would beaffected by muscarine. Nicotinic receptorsare located within the autonomic ganglia inthe membranes of postganglionic neurons ofboth the sympathetic and parasympatheticdivisions. Consumption of nicotine wouldresult in stimulation of the postganglionicneurons, and consequently, the stimulationof the effectors of both the sympathetic andparasympathetic divisions. Again, figure 16.7illustrates that muscarinic receptors arelocated on the effectors of the parasympa-thetic division. After the consumption ofmuscarine, only the effectors that respondto acetylcholine would be affected. Thisincludes all the effectors innervated bythe parasympathetic division and thesweat glands, which are innervated bythe sympathetic division.3. Muscarinic receptors are associated withall effectors innervated by the parasympa-thetic division as well as the sweat glands.We can assume that bethanechol chloridebinding to muscarinic receptors results ineffects similar to those of parasympatheticstimulation of organs. Contraction of theurinary bladder is a normal response to

the parasympathetic division, so we wouldexpect the same result when bethanecholchloride is administered. Side effects ofbethanechol chloride can be produced bythe stimulation of muscarinic receptorselsewhere in the body. The stimulation ofsmooth muscle in the digestive tract canproduce abdominal cramps, and stimula-tion of the air passageways can cause anasthmatic attack. Decreased tear productionand salivation as well as dilation of thepupils are not expected side effects becauseparasympathetic stimulation causes increasedtear production and salivation as well asconstriction of the pupils. Recall that, eventhough the sympathetic division innervatessweat glands, these glands have muscarinicreceptors, so we would expect increasedsweating as a side effect of bethanecolchloride.4. a. Dilation of the pupil is caused by thecontraction of the dilator pupillae,which are the radial muscles of the iris.b. Recall from the discussion of the iristhat the sympathetic division innervatesand therefore controls the radial muscles(dilator pupillae). The parasympatheticdivision innervates and therefore controlsthe circular muscles (sphincter pupillae).c. A drug that mimics sympathetic stimu-lation, such as an adrenergic drug, couldactivate α 1 receptor on the radial musclesof the iris and cause Sally’s pupils todilate. On the other hand, a drug thatblocks parasympathetic stimulation,such as a muscarinic blocking agent,would prevent constriction of the pupiland therefore cause dilation.d. Remember from chapter 15 that theciliary muscles constrict, changing theshape of the lenses when viewing closeobjects. Blurred vision indicates theeyedrops are inhibiting ciliary musclecontraction. From table 16.3 we can seethat ciliary muscle contraction is a para-sympathetic effect, so we would predictthat the eyedrops contain a muscarinicblocking agent, one that would affectparasympathetic effectors.e. Notice that this scenario is essentiallythe opposite as that described in part c.Based on our answer for part c, wewould expect that an adrenergic block-ing agent that binds to α 1 receptors andprevents sympathetic stimulation wouldcause the pupils to constrict. Similarly,a muscarinic agent could stimulate thecircular muscles of the iris, causing thepupils to constrict.f. Recall that sympathetic stimulation ofblood vessels normally keeps them in a