Neuroscience 2

8/12/2019 Neuroscience 2

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Neuroscience 2

1.

A lesion at which site in the diagram below could produce weakness of muscles thatmediate swallowing, chewing, breathing, and speaking?

A. A

B. B

C. C

D. D

E.

F. !

G. "

H. #

The answer is: G

$his figure is a hori%ontal &iew of the brain at the le&el of the head of the caudate nucleus

and the internal capsule. $he posterior limb of the internal capsule '!( contains fibers thatarise from the leg region of the cerebral corte) and pro*ect to lumbar le&els of the spinal

cord, thus ser&ing as +Ns for the elicitation of &oluntar- mo&ement of the contralateral

leg. !ibers in the anterior limb of the internal capsule '#( pro*ect in large numbers todeep pontine nuclei and represent firstorder neurons in a pathwa- linking the cerebral

corte) with the cerebellum. /seudobulbar pals- is characteri%ed in part b- a weakness of

the muscles controlling swallowing, chewing, breathing, and speaking. 0t results from a

lesion of the +Ns associated with the head region of the corte), which pass through thegenu of the internal capsule '"( en route to brainstem cranial ner&e nuclei upon which

the- s-napse. $he descending column of the forni) 'B(, situated along the midline of the



brain, contains fibers that arise from the hippocampal formation and pro*ect in large part

to the mamillar- bodies.

$he head of the caudate nucleus 'D( is part of an important element of the motors-stems called the basal ganglia. 0t recei&es significant inputs from se&eral regions

associated with motor functions. $hese include the cerebral corte) and the dopamine

containing region of the substantia nigra 'i.e., the pars compacta(. $he mediodorsalthalamic nucleus '( pro*ects large uantities of a)ons to e)tensi&e regions of the rostral

half of the frontal lobe, including the prefrontal corte). 0t also recei&es significant

pro*ections from the prefrontal region of the corte).

2.

$he cerebellum is deri&ed from which of the following?

The answer is: B

$he cerebellum is formed from the dorsolateral aspects of the alar plates, which bend

mediall- and posteriorl- to form the rhombic lips.

.$he anterior pituitar- is deri&ed from which of the following?

A. Neural crest cells

B. 3hombic lips

C. esencephalon

D. 4ulcus limitans

E. $elencephalon

F. -elencephalon

G. !loor plate

H. 3athke5s pouch

The answer is: H

$he anterior lobe of the pituitar- is formed as an inpocket deri&ati&e of the ectodermal

stomodeum, called Rathke's pouch.

4.A -oung child is brought into the hospital emergenc- room because he has episodes of

&omiting, headaches, problems in acuisition of motor skills, cranial ner&e d-sfunction,and problems in breathing. $his combination of s-ndromes most closel- relates to which

of the following disorders?

A. Cleft palate



B. #-drocephalus

C. Anencephal-

D. 4-ringom-elia

E. Congenital aneur-sm

The answer is: B

$he s-mptoms described are characteristic of h-drocephalus. #-drocephalus ma- comeabout as a result of defects such as the failure of formation of the cerebellar &ermis,

foramens of agendie and 6uschka, or of the corpus callosum. $here is an enlarged

cranium as a result of the buildup of cerebrospinal fluid 'C4!(, causing brain damage.4e&eral of the s-mptoms ma- also be caused b- a compression of the posterior fossa and

the absence of a cerebellar &ermis. Cleft palate is a fissure of the medial aspect of the lip

and would not result in the s-mptoms described pre&iousl-. Anencephal- is the complete

or partial absence of the brain and is not compatible with life. 4-ringom-elia isassociated with bilateral segmental loss of pain and temperature. A congenital aneur-sm

can occur in a &ariet- of places within the CN4 and is t-picall- associated with stroke in

the adult.

7.

Apoptosis is likel- to occur following which of the following e&ents?

A. 4timulation of an afferent ner&e fiber

B. 4e&ering of an afferent ner&e fiber

C. $he beginning of m-elin formation

D. limination of ner&e growth factor

E. 3eduction in brain serotonin le&els

The answer is: D

8hen ner&e growth factor is eliminated, cell death results and in&ol&es fragmentation,

shrinkage, and ultimate phagoc-tosis of the cell. Apoptosis is belie&ed to be triggered b-a biochemical process that causes transcription of a &ariet- of genes. Ner&e growth factor

blocks the acti&ation of this process. 0t should also be noted that this form of cell death

differs from that occurring after ner&e in*ur- or trauma to the ner&e. $he other choiceslisted are unrelated to the process of apoptosis.

9.$he methods in&ol&ing microin*ections of !luoro"old or horseradish pero)idase '#3/(

ha&e been emplo-ed o&er the past few decades b- man- in&estigators. $hese methods

ha&e been used to identif- which of the following



A. Cell bodies

B. etabolic acti&it- of neurons

C. 4ensor- endings of ner&e fibers

D. Central ner&ous s-stem receptors

E. Degenerating a)ons

The answer is: A

8ith #3/ histochemistr-, the gl-coprotein en%-me #3/ is in*ected into the region of theterminal endings of the neuronal pathwa- under e)amination and is incorporated into the

a)ons through a process of micropinoc-tosis. #orseradish pero)idase is then retrogradel-

transported back to the cell bodies of origin of that pathwa-, where it is then degraded.B- reacting the tissue with an appropriate substrate, the labeled cells can be &isuali%ed

under light microscop-.

:.

4ubstances such as tritiated amino acids and phaseolus &ulgaris agglutinin microin*ected

into specific regions of the brain ha&e also been emplo-ed b- man- in&estigators for the

stud- of the ner&ous s-stem. $hese methods are specific in that the- label which of thefollowing?

A. Cell bodies

B. "lial cells

C. 4ensor- receptors

D. otor end plates

E. A)ons and a)on preterminals

The answer is: E

$he mapping of pathwa-s utili%ing anterograde tracing of fibers depends upon the

process of a)onal transport. !or e)ample, if a tritiated amino acid such as #leucine is

microin*ected into a region of the brain, it gets s-nthesi%ed into protein in the cell bodiesand transported down the respecti&e a)ons to their terminals. B- utili%ing

autoradiographic methods, one can identif- the loci of the label contained in the protein

that has been transported to the a)on terminals. $he application of phaseolus &ulgarisagglutinin also utili%es the principle of anterograde transport to map the distribution of

pathwa-s from cell bodies in*ected with this substance.

;.8hich of the following procedures would be utili%ed in order to show positi&e staining of

groups of serotonin neurons



A. lectrical brain stimulation

B. "lutamate stimulation of the brain

C. #3/ staining of neurons

D. 0mmunoc-tochemical labeling

E. etabolic staining of neurons

The answer is: D

0mmunoc-tochemical methods, including in situ h-bridi%ation, ha&e been used to identif-the presence and locali%ation of specific neurotransmitters and receptors, such as

serotonin.

<.

An indi&idual sustained a se&ere knife wound, damaging a spinal ner&e ad*oining itsentr- to the spinal cord. 0f one could e)amine this peripheral ner&e and its cell bod-,which of the following e&ents would he or she most likel- obser&e?

A. A displacement of the nucleus toward the peripher- of the cell

B. A mitotic di&ision of the neuronal cell bod-

C. A more intense staining of the cell bod-

D. Degeneration of processes along the a)on pro)imal but not distal to the lesion

E. An initial loss of mitochondria in the a)oplasm at 3an&ier5s node

The answer is: A

Damage to a ner&e fiber pro)imal to its cell bod- will cause, among other changes,retrograde degeneration of the cell bod-. A number of changes occur in the neuron during

the process of retrograde degeneration. $he cell bod- initiall- shows some swelling and

becomes distended. At the beginning of the degenerati&e process, there is anaccumulation of mitochondria in the a)oplasm at 3an&ier5s nodes. $he nucleus is then

displaced toward the peripher- of the cell. $he Nissl granules break down, first in the

center of the cell= later, the breakdown spreads outward. 0n addition, the a)onal processdistal to the site of the lesion will undergo degeneration. 0t should be noted that

retrograde degeneration procedures were used e)perimentall- prior to the ad&ent of

histochemical methods for identif-ing cell bodies of origin of gi&en pathwa-s in theCN4.

1>.

A 97-earold man is diagnosed with a form of a peripheral neuropath-. $his indi&idualwill likel- displa- which of the following

A. A loss in motor function, but sensor- functions will remain largel- intact



B. A reduction in conduction &elocit- of the affected ner&e

C. An increase in the number of 3an&ier5s nodes

D. Degeneration of m-elin but the a)on will t-picall- remain intact

E. 4igns of an upper motor neuron '+N( paral-sis

The answer is: B

0n a peripheral neuropath-, there ma- be damage to either the m-elin or the a)on directl-,although, more often, there is damage to the m-elin. Because of m-elin 'or a)onal(

damage, there is a reduction 'or loss( of conduction &elocit-. $he disorder ma- affect

both sensor- and motor components of the peripheral ner&e, thereb- causing d-sfunctionin both the sensor- and the motor processes associated with that ner&e. Because there is

peripheral neuronal damage, the motor loss will be reflected in a weakness, paral-sis, or

refle) acti&it- associated with the affected muscle, as well as impairment of sensation.

11.

During an in &itro e)periment, the membrane potential of a ner&e cell is h-perpolari%ed

to 12> m@. At that time, a transmitter, known to be inhibitor- in function, is applied tothe preparation and results in a depolari%ation of the membrane. 8hich of the following

is the most likel- reason for this occurrence?

A. 0nhibitor- transmitters normall- depolari%e the posts-naptic membrane

B.$he normal response of the posts-naptic membrane to an- transmitter isdepolari%ation

C. $he inhibitor- transmitter acti&ates ligandgated potassium channels

D. 4odium channels become inacti&ated

E. Calcium channels become acti&ated

The answer is: C

$o understand how an inhibitor- transmitter can actuall- cause a partial depolari%ation ofthe membrane, refer to the "oldman euation. $he release 'or application( of an

inhibitor- transmitter will ser&e to open specific ion channels, notabl- those of

potassium. 0f the membrane is artificiall- h-perpolari%ed to 12> m@, the opening of the

potassium channel will lead to a redistribution of the ions across the membrane to anormal le&el. 0f the normal euilibrium potential for potassium is appro)imatel- :7 m@,

then, application of an inhibitor- transmitter 'that t-picall- functions b- opening

potassium channels( will result in a redistribution of potassium ions toward the potassiumeuilibrium potential 'i.e., :7 m@(. Conseuentl-, the membrane potential will be

reduced 'i.e., depolari%ed( from 12> m@ to a &alue close to :7 m@. ther possible

answers are clearl- incorrect. 0nhibitor- transmitters normall- function to h-perpolari%ethe membrane. /osts-naptic membranes ma- either be depolari%ed or h-perpolari%ed,

depending upon the nature of the transmitter and receptor comple) present at the s-napse.



4ince the influ) of calcium during the depolari%ation phase of the action potential leads to

opposing effects, acti&ation of this channel cannot account for the obser&ed effects.

0nacti&ation of sodium channels would not result in a depolari%ation of the membrane, but, instead, ma- contribute to the h-perpolari%ation of the membrane.

12.$he passi&e spread of a pres-naptic current acorss a gap *unction that is acti&ated b-

changes in &oltage, p#, or calcium ion le&els is most closel- associated with which of the

following

A. $he resting potential

B. $he action potential

C. lectrical pres-naptic potentials

D. lectrical posts-naptic potentials

E. 3eceptor potentials

The answer is: D

lectrical posts-naptic potentials in&ol&e the passi&e spread of current across a gap

*unction that is permeable to a &ariet- of small ions. $he stimulus for such acti&ation ma- be a change in either &oltage, p#, or intracellular calcium.

1.8hich of the following characteri%es a principal feature of a)osomatic s-napses

A. 0t is referred to as a t-pe 0 s-napse

B. $he- ha&e an electrical continuit- linking the pre and posts-naptic cells

C. $he- are t-picall- inhibitor-

D. 4-naptic transmission is mediated b- glutamate

E. $he- form the predominant s-napse of cortical pro*ections to the neostriatum

The answer is: C

A)on terminals that make s-naptic contact with the soma of posts-naptic cells are

freuentl- obser&ed to be inhibitor- and are referred to as a type II synapse. A classic

e)ample of this is in the cerebellar corte), where an interneuron 'basket cell( makess-naptic contact with the soma of the /urkin*e cell. $hese are chemical and not electrical

s-napses, and their actions are freuentl- mediated b- "ABA. Acti&ation of the basket

cell results in subseuent inhibition of the /urkin*e cell. $he o&erwhelming number of

e)citator- s-napses are obser&ed to be a)odendritic. $he- are referred to as a type I synapse and are freuentl- characteri%ed b- speciali%ed e)tensions of the dendrites called

spines. $hese s-napses also displa- a dense basement membrane and a prominent



pres-naptic densit-. Cortical pro*ections to the neostriatum ha&e been shown to be

e)citator- and their functions mediated b- glutamate.

1.

8hich of the following is a second messenger s-stem directl- acti&ated b- the binding of

norepinephrine to a betaadrenergic receptor A. 0nositol 1,,7triphosphate '0/(

B. Adenosine 5,75c-clic phosphate 'cA/(

C. Diac-lgl-cerol 'DA"(

D. Arachidonic acid

E. /rostaglandins

The answer is: B

8hen norepinephrine reaches a adrenergic receptor, a " protein acti&ates aden-lc-clase, which generates a second messenger, cA/, from A$/. cA/ acti&ates a

cA/dependent kinase that alters the conformation of regulator- subunits of other

kinases. $his frees catal-tic subunits to phosphor-late specific proteins, which, in turn,

leads to the cellular response. 0/ and DA" are associated with the transmitteracet-lcholine, which binds to muscarinic receptors, and arachidonic acid is linked to

histamine, which binds to histamine receptors.

/rostaglandins are metabolites of arachidonic acid.

17.

#-perpolari%ation of the neuron is go&erned b- which of the followingA. Chloride and sodium

B. Chloride and potassium

C. /otassium and sodium

D. 4odium and calcium

E. 4odium onl-

The answer is: B

0n neurons within the CN4, an inhibitor- transmitter will open chloride channels. 0naddition, second messengers ma- also mediate inhibition. 0t is likel- that the- do so b-

opening potassium channels. 8hen a chloride channel is opened, it will lead to

mo&ement of this ion down its concentration gradient and into the cell. $his will make

the cell more negati&e 'i.e., h-perpolari%ed(. At the same time, there will be an efflu) of potassium, which will also produce h-perpolari%ation of the cell because positi&e charges



are now being remo&ed. n the other hand, sodium and calcium influ) are associated

with depolari%ation of the cell.

19.

$he release of the transmitter is directl- go&erned b- which of the following

A. 4odium influ)

B. 4odium efflu)

C. /otassium influ)

D. /otassium efflu)

E. Calcium influ)

The answer is: E

)perimental methods permit e&aluation of the relati&e contributions of different ions inthe regulation of transmitter release. Neither tetrodoto)in, which blocks &oltagegatedsodium channels, nor tetraeth-lammonium, which blocks &oltagegated potassium

channels, will block the generation of a posts-naptic potential when the pres-naptic cell

is artificiall- depolari%ed. 0n contrast, pres-naptic calcium influ) triggers the release of

the transmitter and results in a posts-naptic potential. oreo&er, when pres-napticcalcium influ) is blocked, no posts-naptic potential is produced. Action potentials at the

pres-naptic a)on terminals open up calcium channels, permitting calcium influ). $his

e&ent helps mo&e s-naptic &esicles to acti&e sites as actin filaments 'which anchor the&esicles( are dissol&ed.

1:. N-meth-lDaspartate 'NDA(, kainate, and uisualate all act on which of the

following receptors

A. "ABA receptors

B. )citator- amino acid receptors

C. Adrenergic receptors

D. pioid receptors

E. Dopamine receptors

The answer is: B

NDA, kainate, and uisualate act upon e)citator- amino acid receptors. $he NDA

receptor differs from the other t-pes of receptors in that it is blocked b- g2 and

controls a cation channel permeable to calcium, sodium, and potassium./harmacologicall-, NDA receptors can be blocked b- 2amino7phosphono&aleric

acid. $he uisualate receptor is acti&ated b- uisualic acid= it has a high affinit- for 6





a result of this defecti&e gene, there is an abundance of /he in the brain, which produces

a to)ic metabolite, thus interfering in brain de&elopment and maturation.

2>.

Fuestion 2 of 2

After an indi&idual is admitted to the hospital, it is determined that he displa-s a &ariableweakness of cranial ner&e and limb muscles but shows no clinical signs of dener&ation

from tests, which include electrom-ogram '"( recordings. $his disorder was partiall-

re&ersed b- the administration of drugs that inhibit acet-lcholinesterase.

8hich of the following is the likel- basis for this disorder?

A. $he production of e)cessi&e uantities of acet-lcholine 'ACh(

B. $he production of antibodies that act against nicotinic ACh receptors

C. A minor stroke in&ol&ing the motor strip of the cerebral corte)

D. A &itamin B deficienc-

E. @iral encephalitis

The answer is: B

-asthenia gra&is is an autoimmune disease that causes cranial ner&e and limb muscle

weakness b- producing antibodies that act against the nicotinic receptor at theneuromuscular *unction. $he result is that the action of ner&e fibers that inner&ate skeletal

muscle are affected, producing loss of the effects of ACh at the neuromuscular *unction.

$he net result is a reduction of the si%e of the action potential in the muscle, producing aweakness in the affected muscle. $his disorder is re&ersed b- administration of drugs that

inhibit the en%-me, acet-lcholinesterase, that degrades ACh. ultiple sclerosis, A64, and

combined s-stem disease 'see the chapter entitled G$he 4pinal CordG( in&ol&e damage toa)ons andHor ner&e cells within the CN4, producing much more profound damage to

motor functions and, in the case of combined s-stem disease, damage to both motor and

sensor- s-stems. uscular d-stroph- is t-picall- characteri%ed, in part, b- progressi&e

weakness of muscles and degeneration of the muscle fibers. $he other disorders listed allin&ol&e disorders affecting the CN4, and thus, the s-mptoms associated with these

disorders differ significantl- from those described in this case. )cessi&e release of ACh

is not a realistic e&ent that is likel- to occur 'e)cept from the bite of a black widowspider(. 0n theor-, if it were to occur, there is no reason to belie&e that muscular weakness

would be a s-mptom. 0nstead, there would be some rigidit- and muscle spasms.

21.

$he neuroto)in, bungaroto)in, has been utili%ed as a &aluable e)perimental tool

because it binds to which of the following?

A. "ABAA receptor



B. "ABAB receptor

C. Nicotinic receptor

D. NDA receptor

E. #istamine receptor

The answer is: C

$he to)ins, including bungaroto)in, can produce posts-naptic effects similar to thatobser&ed with curare, b- binding specificall- to the subunits of the nicotinic ACh

receptor. 0n the case of the neuromuscular *unction, the binding is to subunit of the

nicotinic ACh receptor. Because of the selecti&e actions of bungaroto)in upon the AChreceptor, it has been used effecti&el- as an e)perimental tool to stud- the properties and

actions of ACh and its associated receptors.

22.A 9>-earold male has high blood pressure and the diagnosis indicates that it is due in

part to retention of water. 8hich of the following compounds would most likel- relate to

this process

A. )-tocin

B. 4erotonin

C. #istamine

D. @asopressin

E. 4omatostatin

The answer is: D

@asopressin is produced mainl- from the magnocellular neurons of the h-pothalamus.$he hormone is released into the capillaries of the posterior pituitar-. 8hen it is released

into the &ascular s-stem, it stimulates the kidne-s to conser&e water. $he action of

o)-tocin is related to functions of the uterus and breasts. $his hormone pla-s a role in the

e)pulsion of the fetus at birth and in the milk e*ection refle) following suckling.4ubstance /, histamine, and somatostatin are not known to relate specificall- to this

process.

2.

A 97-earold man has been e)periencing considerable pain due to a chronic back

problem. 0f the patient is administered morphine to alle&iate the problem, which of thefollowing is a possible mechanism b- which morphine would pro&ide effecti&e action

A. 3elease of somatostatin

B. 3elease of histamine



C. 3elease of &asopressin

D. 3elease of ACh

E. 3elease of substance /

The answer is: B

8hen an opioid compound, especiall- a receptor agonist 'such as morphine(, is

administered in response to chronic pain, this causes the release of histamine in neurons.$his leads to the acti&ation of histamine #2 receptors, which pla- a role in the relief of

pain. 0n fact, there are ongoing attempts now to de&elop drugs, such as histamine #

receptor compounds, which ha&e been shown to mediate antinociception and ha&e antiinflammator- properties as well. $he other choices listed in this uestion are not known

to relate to the alle&iation of pain, in particular, with respect to morphine administration.

0n fact, substance / is associated with the elicitation of pain impulses.

2.

8hich of the following receptors reuires the simultaneous binding of two different

agonists for acti&ation?

A. 6A/ receptor

B. Eainate receptor

C. NDA receptor

D. A/A receptor

E. "ABAA receptor

The answer is: C

NDA receptors are uniue among receptors in that the- reuire the simultaneous binding of two different agonists for their acti&ation. NDA ion channels are opened

after such compounds as glutamate and gl-cine are applied to the membranes that include

NDA receptors. 3ecent e&idence has shown that a metabotropic glutamate receptor, 6A/, is present in the retina. Acti&ation of this receptor ma- ser&e to h-perpolari%e

bipolar neurons within the retina. "lutamate acti&ation 'of this receptor( constitutes an

unusual action because most neurons in the CN4 are depolari%ed b- glutamate. A/A isone of se&eral classes of ionotropic glutamate receptors and functions as a s-naptic

receptor for fast e)citator- s-naptic transmission mediated through glutamate. $he otherchoices, kainate and "ABA receptors, do not ha&e this propert-.

27.

Neuroscience 2

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