USMLE Step 1 Qs (10)

Vasopressin is produced mainly from the magnocellular neurons of the hypothalamus. The hormone is released into the capillaries of the posterior pituitary. When it is released into the vascular system, it stimulates the kidneys to conserve water. The action of oxytocin is related to functions of the uterus and breasts. This hormone plays a role in the expulsion of the fetus at birth and in the milk ejection reflex following suckling. Substance P, histamine, and somatostatin are not known to relate specifically to this process.

In this case, disruption of the root fibers of C5–C6 involve components of the brachial plexus and affect muscle groups such as the deltoid, supraspinatus, intraspinatus, biceps, and flexor carpi radialis. These muscles govern abduction of the arm, rotation of the arm at the shoulder, flexion of the elbow and wrist. Reflex activity would also be affected due to disturbance of both alpha and gamma motor neurons serving the biceps muscle. Lesions involving the cerebral cortex or pons, especially the region of the pyramidal tracts, would produce a UMN paralysis, which would include hyperreflexia and hypertonia. An LMN paralysis involving the ventral horn cells at C1 would not affect the brachial plexus and the muscle groups indicated in this question. The triceps muscle is not involved in producing the movements affected by the injury.

Myasthenia gravis is an autoimmune disease that causes cranial nerve and limb muscle weakness by producing antibodies that act against the nicotinic receptor at the neuromuscular junction. The result is that the action of nerve fibers that innervate skeletal muscle are affected, producing loss of the effects of ACh at the neuromuscular junction. The net result is a reduction of the size of the action potential in the muscle, producing a weakness in the affected muscle. This disorder is reversed by administration of drugs that inhibit the enzyme, acetylcholinesterase, that degrades ACh. Multiple sclerosis, ALS, and combined system disease (see the chapter entitled "The Spinal Cord") involve damage to axons and/or nerve cells within the CNS, producing much more profound damage to motor functions and, in the case of combined system disease, damage to both motor and sensory systems. Muscular dystrophy is typically characterized, in part, by progressive weakness of muscles and degeneration of the muscle fibers. The other disorders listed all involve disorders affecting the CNS, and thus, the symptoms associated with these disorders differ significantly from those described in this case. Excessive release of ACh is not a realistic event that is likely to occur (except from the bite of a black widow spider). In theory, if it were to occur, there is no reason to believe that muscular weakness would be a symptom. Instead, there would be some rigidity and muscle spasms.

When norepinephrine reaches a beta -adrenergic receptor, a G protein activates adenyl cyclase, which generates a second messenger, cAMP, from ATP. cAMP activates a cAMP-dependent kinase that alters the conformation of regulatory subunits of other kinases. This frees catalytic subunits to phosphorylate specific proteins, which, in turn, leads to the cellular response. IP3 and DAG are associated with the transmitter acetylcholine, which binds to muscarinic receptors, and arachidonic acid is linked to histamine, which binds to histamine receptors.
Prostaglandins are metabolites of arachidonic acid.

In this case, there is a loss of superficial abdominal reflexes, which require that spinal segments T8–T12 are intact. The test for these reflexes is to stroke a quadrant of the abdominal wall with an object such as a wooden stick. The normal response is for the muscle of the quadrant stimulated to contract and for movement of the umbilicus in the direction of the stimulus

Multiple sclerosis is a demyelinating autoimmune disease that affects CNS function. This disorder produces a wide variety of symptoms, including sudden sensory dysfunction and loss, which affect vision and the somatosensory system, causing tingling, pain, and hypesthesia. Broad functional motor disturbances also occur, including weakness of the upper or lower limbs, UMN signs, and gait impairment. There is also bladder dysfunction as well as an increase in CSF protein and IgG synthesis. Diffuse cerebellar degeneration would produce gait ataxia and deficits in the accuracy of intentional movements. As noted earlier, ALS would produce both a UMN and an LMN paralysis, which typically does not extend to sensory functions. Likewise, a peripheral neuropathy would not produce UMN signs, visual deficits, and extensive motor disturbances as described in this case. A tumor of the prefrontal cortex would affect some cognitive and emotional functions, but it would not affect sensory processes such as vision and somatosensation, nor would it produce signs of a UMN disorder or muscle weakness.

The anterior lobe of the pituitary is formed as an in-pocket derivative of the ectodermal stomodeum, called Rathke's pouch.

Lithium has been used for a number of years as an effective drug for the treatment of bipolar disorders. It has been shown to decrease the length, severity, and recurrence of manic states as well as the depressive components of this disorder. The mechanism of action of lithium in effectively combating bipolar disorder is not absolutely clear since it has a wide variety of biological effects. In part, these include: changes in the expression of some G proteins and subtypes of adenyl cyclase, alteration of the coupling of G proteins to neurotransmitter receptors, alterations of monoamine levels and receptors, and effects upon ion channels. Monoaminergic drugs are generally used for the treatment of panic disorders and, to some extent, to treat anxiety. Anxiety attacks are also treated with benzodiazepine drugs. Drugs for the treatment of epilepsy generally include those that increase or maintain GABA levels or decrease glutamate levels. For schizophrenia, a wide range of drugs has been used; these include those which affect monoaminergic, cholinergic, and GABAergic systems.

The symptoms described are characteristic of hydrocephalus. Hydrocephalus may come about as a result of defects such as the failure of formation of the cerebellar vermis, foramens of Magendie and Luschka, or of the corpus callosum. There is an enlarged cranium as a result of the buildup of cerebrospinal fluid (CSF), causing brain damage. Several of the symptoms may also be caused by a compression of the posterior fossa and the absence of a cerebellar vermis. Cleft palate is a fissure of the medial aspect of the lip and would not result in the symptoms described previously. Anencephaly is the complete or partial absence of the brain and is not compatible with life. Syringomyelia is associated with bilateral segmental loss of pain and temperature. A congenital aneurysm can occur in a variety of places within the CNS and is typically associated with stroke in the adult.

Experimental methods permit evaluation of the relative contributions of different ions in the regulation of transmitter release. Neither tetrodotoxin, which blocks voltage-gated sodium channels, nor tetraethylammonium, which blocks voltage-gated potassium channels, will block the generation of a postsynaptic potential when the presynaptic cell is artificially depolarized. In contrast, presynaptic calcium influx triggers the release of the transmitter and results in a postsynaptic potential. Moreover, when presynaptic calcium influx is blocked, no postsynaptic potential is produced. Action potentials at the presynaptic axon terminals open up calcium channels, permitting calcium influx. This event helps move synaptic vesicles to active sites as actin filaments (which anchor the vesicles) are dissolved.

Phenylketonuria results in severe mental retardation and is caused by a defect in the gene that provides the code for Phe hydroxylase, the enzyme that converts Phe to tyrosine. As a result of this defective gene, there is an abundance of Phe in the brain, which produces a toxic metabolite, thus interfering in brain development and maturation.

In a peripheral neuropathy, there may be damage to either the myelin or the axon directly, although, more often, there is damage to the myelin. Because of myelin (or axonal) damage, there is a reduction (or loss) of conduction velocity. The disorder may affect both sensory and motor components of the peripheral nerve, thereby causing dysfunction in both the sensory and the motor processes associated with that nerve. Because there is peripheral neuronal damage, the motor loss will be reflected in a weakness, paralysis, or reflex activity associated with the affected muscle, as well as impairment of sensation.

The biosynthesis of catecholamines includes the following steps: tyrosine is converted into L-dihydroxyphenylalanine (L-DOPA) by tyrosine hydroxylase. L-DOPA is then decarboxylated by a decarboxylase to form dopamine (and CO2). The conversion of dopamine to norepinephrine comes about by the action of the enzyme dopamine beta-hydroxylase. The rate-limiting enzyme in the biosynthesis of serotonin is tryptophan hydroxylase. In this process, tryptophan is converted to 5-hydroxytryptophan by tryptophan hydroxylase and by 5-hydroxytryptophan decarboxylase into serotonin.

Guillain-Barré syndrome is an acute polyneuropathy whose occurrence frequently follows a respiratory infection. It results in myalgia of the lower limbs, loss of muscle tone and tendon reflexes, and some flaccidity. The disorder can also affect the seventh cranial nerve. The disorder can produce diffuse demyelination of the peripheral nerves with an increase in lymphocytes present at the sites of demyelination. The other disorders listed are generally progressive where eventual recovery without intervention is not known to occur. Myasthenia gravis and lumbar disk prolapse would not show demyelination and lymphocyte increases near the sites of demyelination. Multiple sclerosis involves central nervous system (CNS) structures; therefore, the constellation of symptoms would be different. As indicated earlier, MD is progressive with effects upon both proximal muscles and later in distal muscles.

Inability to move the eyes up or down when they are displaced laterally would result from a lesion of the midbrain involving cranial nerve III. Because the somatomotor neurons of cranial nerve III supply, in part, the superior and inferior recti muscles as well as the inferior oblique muscle, cranial nerve III is responsible for up-and-down movements of the eye when they are positioned laterally. Recall that when the eye is positioned medially, it is the superior oblique that is innervated by cranial nerve IV that pulls the eye downward.

NMDA, kainate, and quisqualate act upon excitatory amino acid receptors. The NMDA receptor differs from the other types of receptors in that it is blocked by Mg2+ and controls a cation channel permeable to calcium, sodium, and potassium. Pharmacologically, NMDA receptors can be blocked by 2-amino-5-phosphonovaleric acid. The quisqualate receptor is activated by quisqualic acid; it has a high affinity for L-glutamate and alpha-amino-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA). The kainate receptor is activated by kainic acid. It regulates a channel that is permeable to sodium and potassium, binds AMPA, and is important in the process of excitotoxicity

There are three mechanisms by which a transmitter is removed from the region of the synaptic cleft. The most common one is reuptake, in which transporter molecules mediate high-affinity reuptake that is specific for the transmitter in question. Other mechanisms include diffusion, which removes some components of the transmitter substance, and enzymatic degradation of the amine achieved by the enzymes monoamine oxidase and catechol-O-methyltransferase.

The reflex described in this question is the corneal reflex. It involves the reflex activation of the ophthalmic division of the sensory component of cranial nerve V in response to touching of the cornea and the motor division of the facial (cranial nerve VII), which produces the motor component (i.e., the blinking response). The sensory component of cranial nerve V is classified as a general somatic afferent fiber and the somatic motor component of cranial nerve VII is classified as a special visceral efferent fiber.

The most likely cause of the condition in this patient is a cervical disk prolapse. This disorder would produce pain in the neck and arm, which increases with movement of the head. It would also cause loss of some sensation in the thumb and other fingers, as well as weakness in both finger extension and of the biceps reflex. Syringomyelia would produce bilateral segmental loss of pain and temperature. A knife wound completely severing the nerve would result in a functional loss similar to that experienced with an LMN paralysis. Polio results in loss of LMNs, thus also producing an LMN paralysis. One of the effects of AIDS is that it produces damage to the lateral and dorsal columns, resulting in the appearance of a UMN disorder.

When nerve growth factor is eliminated, cell death results and involves fragmentation, shrinkage, and ultimate phagocytosis of the cell. Apoptosis is believed to be triggered by a biochemical process that causes transcription of a variety of genes. Nerve growth factor blocks the activation of this process. It should also be noted that this form of cell death differs from that occurring after nerve injury or trauma to the nerve. The other choices listed are unrelated to the process of apoptosis.

In neurons within the CNS, an inhibitory transmitter will open chloride channels. In addition, second messengers may also mediate inhibition. It is likely that they do so by opening potassium channels. When a chloride channel is opened, it will lead to movement of this ion down its concentration gradient and into the cell. This will make the cell more negative (i.e., hyperpolarized). At the same time, there will be an efflux of potassium, which will also produce hyperpolarization of the cell because positive charges are now being removed. On the other hand, sodium and calcium influx are associated with depolarization of the cell.

Gamma motor neurons innervate the polar regions of the muscle spindle and, when excited, cause resetting of the spindle by stretching it, resulting in a lowering of the threshold for activation of that receptor by an external force. Unmyelinated C fibers mediate nociceptive sensations from the periphery to the spinal cord and thus do not relate to this question. 1A fibers arise from the nuclear region of the spindle and mediate spindle activity to the spinal cord and thus form the afferent limb of the monosynaptic stretch reflex. Alpha motor neurons arise in the ventral horn of spinal cord and innervate extrafusal muscle fibers, causing movement of the limb when excited. It does not innervate the polar regions of the spindle. General visceral afferent fibers exit from the intermediolateral cell columns (at T1–L3 for sympathetics and S2–S4 for parasympathetics) of the spinal cord and innervate postganglionic neurons for these respective autonomic systems. Such fibers, therefore, do not relate to muscle spindles, including their polar regions.

The nerves innervating the knee and hip exit the spinal cord between L4–S1. Typical characteristics of a peripheral neuropathy include muscle weakness directed in a more pronounced manner upon the proximal muscles. Depression of tendon reflexes is generally not seen, and muscle wasting might occur only at a very late stage of the disease. Damage to the neuromuscular junction, such as myasthenia gravis, produces a different constellation of deficits. These include muscle fatigue and weakness that is fluctuating. This disorder also typically affects cranial nerves. In addition, the spinal segments indicated (T8–L3) are not associated with the muscle groups in question. Damage to the ventral horn would produce an LMN (flaccid) paralysis, which is not characteristic of the muscle weakness of this patient. Likewise, damage to the lateral funiculus would produce a UMN (spastic) paralysis, and dorsal horn damage would produce sensory deficits as well as affect muscle tone. In addition, the spinal segments indicated in this last choice (e) do not relate to the muscle groups affected in the patient.

NMDA ion channels are opened by both glutamate and glycine. On the other hand, Mg2 generates a voltage-dependent block of this ion channel. The drug of abuse, phencyclidine (PCP), also utilizes a similar mechanism to block NMDA-receptor channels. The other choices do not relate to this mechanism with respect to PCP

Damage to a nerve fiber proximal to its cell body will cause, among other changes, retrograde degeneration of the cell body. A number of changes occur in the neuron during the process of retrograde degeneration. The cell body initially shows some swelling and becomes distended. At the beginning of the degenerative process, there is an accumulation of mitochondria in the axoplasm at Ranvier's nodes. The nucleus is then displaced toward the periphery of the cell. The Nissl granules break down, first in the center of the cell; later, the breakdown spreads outward. In addition, the axonal process distal to the site of the lesion will undergo degeneration. It should be noted that retrograde degeneration procedures were used experimentally prior to the advent of histochemical methods for identifying cell bodies of origin of given pathways in the CNS.

their activation. NMDA ion channels are opened after such compounds as glutamate and glycine are applied to the membranes that include NMDA receptors. Recent evidence has shown that a metabotropic glutamate receptor, L-AP4, is present in the retina. Activation of this receptor may serve to hyperpolarize bipolar neurons within the retina. Glutamate activation (of this receptor) constitutes an unusual action because most neurons in the CNS are depolarized by glutamate. AMPA is one of several classes of ionotropic glutamate receptors and functions as a synaptic receptor for fast excitatory synaptic transmission mediated through glutamate. The other choices, kainate and GABA receptors, do not have this property.

Hemisection of the right side of the spinal cord that involves segments T8 to T12 will result in contralateral loss of pain and temperature sensation below the level of the lesion and ipsilateral loss of conscious proprioception below the level of the lesion. Thus, this patient will experience loss of pain and temperature in the left leg and loss of conscious proprioception in the right leg. In addition, there will be damage to the descending corticospinal fibers that normally are essential for activation of the LMNs that control muscles of the right leg (i.e., UMN paralysis of the right leg). However, since the lesion is situated below the entry of sensory fibers as well as the origin of anterior horn cells that innervate the upper limbs, no loss of sensation to the upper limbs will ensue, nor will there be an LMN or UMN paralysis of the upper limbs. The pain and temperature fibers ipsilateral to the site of the lesion are unaffected because the second-order neurons decussate at the approximate level of their cell bodies of origin and ascend on the side contralateral to the lesion, leaving this system intact.

The medial vestibulospinal tract arises from the medial vestibular nucleus and descends in the medial longitudinal fasciculus to cervical levels where it controls LMNs, which innervate (flexor) muscles controlling the position of the head. The lateral vestibulospinal tract facilitates extensor motor neurons of the limbs; the rubrospinal tract facilitates flexor motor neurons of the limbs; and the reticulospinal tracts modulate muscle tone of the limbs.

Conjugate lateral gaze requires the simultaneous contractions of the lateral rectus muscle of one eye and the medial rectus of the other eye. Recent studies have indicated that there is a region that integrates and coordinates such movements and that the site is part of the nucleus of cranial nerve VI. It is likely that it accomplishes this phenomenon, in part, because ascending axons from the abducens nucleus pass through the medial longitudinal fasciculus to the contralateral nuclei of cranial nerve III. Thus, the abducens nucleus serves not only to innervate the lateral rectus muscle but also to integrate signals necessary for conjugate deviation of the eyes. The abducens nucleus appears to be the only cranial nerve structure where lesions of the root fibers and nucleus fail to display identical effects.

Reserpine interferes with the uptake-storage mechanism associated with amine granules, which results in destruction of these granules. Administration of this drug will produce long-lasting depletion of norepinephrine. Amphetamine blocks the reuptake mechanism and, thus, produces a net increase in the release of norepinephrine. Apomorphine is a nonspecific dopamine agonist; clonidine is an alpha2-receptor agonist, and yohimbine is an alpha2-receptor antagonist.

To understand how an inhibitory transmitter can actually cause a partial depolarization of the membrane, refer to the Goldman equation. The release (or application) of an inhibitory transmitter will serve to open specific ion channels, notably those of potassium. If the membrane is artificially hyperpolarized to –120 mV, the opening of the potassium channel will lead to a redistribution of the ions across the membrane to a normal level. If the normal equilibrium potential for potassium is approximately –75 mV, then, application of an inhibitory transmitter (that typically functions by opening potassium channels) will result in a redistribution of potassium ions toward the potassium equilibrium potential (i.e., –75 mV). Consequently, the membrane potential will be reduced (i.e., depolarized) from –120 mV to a value close to –75 mV. Other possible answers are clearly incorrect. Inhibitory transmitters normally function to hyperpolarize the membrane. Postsynaptic membranes may either be depolarized or hyperpolarized, depending upon the nature of the transmitter and receptor complex present at the synapse. Since the influx of calcium during the depolarization phase of the action potential leads to opposing effects, activation of this channel cannot account for the observed effects. Inactivation of sodium channels would not result in a depolarization of the membrane, but, instead, may contribute to the hyperpolarization of the membrane

The alpha-toxins, including alpha-bungarotoxin, can produce postsynaptic effects similar to that observed with curare, by binding specifically to the alpha-subunits of the nicotinic ACh receptor. In the case of the neuromuscular junction, the binding is to alpha-subunit of the nicotinic ACh receptor. Because of the selective actions of alpha-bungarotoxin upon the ACh receptor, it has been used effectively as an experimental tool to study the properties and actions of ACh and its associated receptors.

In general, first-order sensory neurons form ganglia outside the CNS. There is one exception, the mesencephalic nucleus of cranial nerve V, which transmits unconscious proprioception (i.e., muscle spindle activity) from jaw muscles. These inputs serve as the first-order neurons for a disynaptic pathway to the cerebellum, as well as for a monosynaptic pathway with the motor nucleus of cranial nerve V for the jaw-closing reflex

The cerebellum is formed from the dorsolateral aspects of the alar plates, which bend medially and posteriorly to form the rhombic lips.

Both the lateral and anterior spinothalamic tracts cross over to the contralateral white matter of the cord relatively close to their cell bodies of origin and ascend to the thalamus. Similarly, the ventral spinocerebellar tract crosses over to the contralateral side and ascends as a distinct fiber pathway in the far lateral aspect of the white matter immediately below the position occupied by the dorsal spinocerebellar tract. The anterior corticospinal tract represents approximately 10 percent of the fibers descending from the cortex as corticospinal fibers. These fibers pass ipsilaterally through the brainstem to the spinal cord, reaching the anterior funiculus of the cord. Near the level at which these fibers terminate, most anterior corticospinal fibers cross over in the commissure of the spinal cord to supply the intermediate gray of the ventral horn. Posterior spinocerebellar fibers, which arise from Clarke's nucleus dorsalis, do not cross in the spinal cord. Instead, they pass laterally from their cell of origin and ascend within the dorsal half of the far lateral aspect of the white matter to the cerebellum. Lateral vestibulospinal fibers arise from the lateral vestibular nucleus and descend ipsilaterally within the ventral funiculus to all levels of the spinal cord, where they terminate upon neurons in the ventral horn. Dorsal column fibers are first-order neurons that arise from the periphery and enter the spinal cord at all levels. They ascend ipsilaterally in the fasciculus gracilis and cuneatus to the level of the dorsal column nuclei of the medulla, where they terminate.

The primary projection pathway of the inferior olivary nucleus exits this nucleus, enters the inferior cerebellar peduncle of the contralateral side of the brain, and passes into the cerebellar cortex, terminating on apical dendrites of Purkinje cells throughout the cerebellar cortex in a somatotopic manner. As indicated previously in the explanation of the previous question, this pathway represents an important source of input to the cerebellum from significant regions mediating sensory and motor information (via the inferior olivary nucleus). Other suggested answers do not include known projection targets of the inferior olivary nucleus.

Cranial nerve X is a highly complex nerve. It contains a few general somatic afferents from the back of the ear that enter the brain as cranial nerve X but terminate in the trigeminal complex. Special visceral afferents include fibers from chemoreceptors for taste associated with the epiglottis and chemoreceptors in the aortic bodies that sense changes in O2-CO2 levels in the blood. General visceral afferent fibers arise from the trachea, pharynx, larynx, and esophagus and signal changes in blood pressure to the brainstem. Special visceral efferent fibers innervate the constrictor muscles of the pharynx and the intrinsic muscles of the larynx. General visceral efferent fibers constitute part of the cranial aspect of the parasympathetic nervous system; thus, they are preganglionic parasympathetic fibers that innervate the heart, lung, esophagus, and stomach.

For a lesion to produce both an ipsilateral gaze paralysis and contralateral hemiplegia, it must be situated in a location where fibers regulating both lateral gaze and movements of the contralateral limbs lie close to each other. The only such location is the ventrocaudal aspect of the pons, where fibers of cranial nerve VI descend toward the ventral surface of the brainstem and where corticospinal fibers are descending toward the spinal cord. The other regions listed in the question do not meet this condition.

Immunocytochemical methods, including in situ hybridization, have been used to identify the presence and localization of specific neurotransmitters and receptors, such as serotonin.

A primary characteristic of a lesion of the dorsolateral medulla is loss of pain and temperature sensation on the contralateral side of the body and ipsilateral half of the face. Damage to the descending tract of the trigeminal nerve and to the spinal nucleus of cranial nerve V will produce loss of sensation on the ipsilateral side of the face. There also will be damage to the lateral spinothalamic tract, which has already crossed at the level of the spinal cord and which conveys pain and temperature sensation from the contralateral side of the body. In addition, fibers arising from the nucleus ambiguus exit laterally from the medulla, and these fibers, which innervate the larynx and pharynx, would also be affected, causing dysphonia. Hemiparesis would not result from this lesion since the pyramidal tract would remain intact. The cerebellum would also be spared and intention tremor associated with cerebellar damage would not occur.

This figure is a horizontal view of the brain at the level of the head of the caudate nucleus and the internal capsule. The posterior limb of the internal capsule (F) contains fibers that arise from the leg region of the cerebral cortex and project to lumbar levels of the spinal cord, thus serving as UMNs for the elicitation of voluntary movement of the contralateral leg. Fibers in the anterior limb of the internal capsule (H) project in large numbers to deep pontine nuclei and represent first-order neurons in a pathway linking the cerebral cortex with the cerebellum. Pseudobulbar palsy is characterized in part by a weakness of the muscles controlling swallowing, chewing, breathing, and speaking. It results from a lesion of the UMNs associated with the head region of the cortex, which pass through the genu of the internal capsule (G) en route to brainstem cranial nerve nuclei upon which they synapse. The descending column of the fornix (B), situated along the midline of the brain, contains fibers that arise from the hippocampal formation and project in large part to the mamillary bodies.
The head of the caudate nucleus (D) is part of an important element of the motor systems called the basal ganglia. It receives significant inputs from several regions associated with motor functions. These include the cerebral cortex and the dopamine-containing region of the substantia nigra (i.e., the pars compacta). The mediodorsal thalamic nucleus (E) projects large quantities of axons to extensive regions of the rostral half of the frontal lobe, including the prefrontal cortex. It also receives significant projections from the prefrontal region of the cortex.

The combined deficit in which the patient loses ability to (use his lateral rectus muscle) abduct his right eye and display facial expression on the right side of the face means that the lesion is located in the dorsal pons at the site where the facial nerve curves around (just above) the motor nucleus of cranial nerve VI. Thus, a lesion at this site will affect both cranial nerves, causing the combined deficits described previously.

The group called special visceral afferent fibers is limited to those cranial nerves that convey impulses to the brain associated with olfaction (I) and taste (VII, IX, and X). Since olfaction and taste involve chemical senses, some authors also include cranial nerves IX and X in the group because these nerves contain components involved in signaling changes in O2 and CO2 levels in the blood.

With HRP histochemistry, the glycoprotein enzyme HRP is injected into the region of the terminal endings of the neuronal pathway under examination and is incorporated into the axons through a process of micropinocytosis. Horseradish peroxidase is then retrogradely transported back to the cell bodies of origin of that pathway, where it is then degraded. By reacting the tissue with an appropriate substrate, the labeled cells can be visualized under light microscopy.

The mapping of pathways utilizing anterograde tracing of fibers depends upon the process of axonal transport. For example, if a tritiated amino acid such as 3H-leucine is microinjected into a region of the brain, it gets synthesized into protein in the cell bodies and transported down the respective axons to their terminals. By utilizing autoradiographic methods, one can identify the loci of the label contained in the protein that has been transported to the axon terminals. The application of phaseolus vulgaris agglutinin also utilizes the principle of anterograde transport to map the distribution of pathways from cell bodies injected with this substance.

Axon terminals that make synaptic contact with the soma of postsynaptic cells are frequently observed to be inhibitory and are referred to as a type II synapse. A classic example of this is in the cerebellar cortex, where an interneuron (basket cell) makes synaptic contact with the soma of the Purkinje cell. These are chemical and not electrical synapses, and their actions are frequently mediated by GABA. Activation of the basket cell results in subsequent inhibition of the Purkinje cell. The overwhelming number of excitatory synapses are observed to be axodendritic. They are referred to as a type I synapse and are frequently characterized by specialized extensions of the dendrites called spines. These synapses also display a dense basement membrane and a prominent presynaptic density. Cortical projections to the neostriatum have been shown to be excitatory and their functions mediated by glutamate.

Electrical postsynaptic potentials involve the passive spread of current across a gap junction that is permeable to a variety of small ions. The stimulus for such activation may be a change in either voltage, pH, or intracellular calcium.

Because the deficit includes a homonymous hemianopsia, the lesion has to be located somewhere in the forebrain, such as in the region that includes the optic tract and internal capsule on the right side of the brain. The motor neurons of cranial nerve VII, as well as spinal cord motor neurons, receive cortical fibers that are crossed, which accounts for the fact that motor dysfunctions of the lower face and body involve lesions on the same side.

When an opioid compound, especially a mu-receptor agonist (such as morphine), is administered in response to chronic pain, this causes the release of histamine in neurons. This leads to the activation of histamine H2 receptors, which play a role in the relief of pain. In fact, there are ongoing attempts now to develop drugs, such as histamine H3-receptor compounds, which have been shown to mediate antinociception and have anti-inflammatory properties as well. The other choices listed in this question are not known to relate to the alleviation of pain, in particular, with respect to morphine administration. In fact, substance P is associated with the elicitation of pain impulses.

The solitary nucleus of the medulla plays a significant role in the neural control of autonomic functions because it receives input from several different regions of the brain that regulate such functions. These inputs include fibers that arise from the hypothalamus, central nucleus of the amygdala, midbrain periaqueductal gray, and sensory processes (i.e., visceral afferents) of the glossopharyngeal and vagus nerves. The last signal changes in blood pressure and levels of oxygen and carbon dioxide in the blood. The ventrolateral nucleus of the thalamus, red nucleus of the midbrain, and ventral horn cells of the spinal cord are associated with somatomotor rather than autonomic function. The nucleus accumbens is believed to be associated with motivational processes.