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The olfactory nerves are minute and diffuse strands of nerve fibers that attach to the olfactory bulb (see fig buy generic chloroquine 250 mg line. Peripheral Nervous © The McGraw−Hill Anatomy generic chloroquine 250 mg online, Sixth Edition Coordination System Companies buy 250 mg chloroquine with mastercard, 2001 Chapter 12 Peripheral Nervous System 403 conducted. Sensory nerves consists of sensory (afferent) neurons Finn and German viewed a hop. Motor nerves consist pri- jingle corresponds to the initial letter of each pair of cranial nerves. A problem with this classic verse is that the eighth cranial nerve repre- marily of motor (efferent) neurons that convey impulses away sented by and in the jingle, which used to be referred to as auditory, from the CNS. Hence, the are motor only; all motor nerves contain some proprioceptor following topical mnemonic: “On old Olympus’s towering top, a fat vi- fibers (see fig. Actually, numerous olfactory nerves relay sensory impulses of smell from the mucous membranes of the nasal cavity Knowledge Check (fig. Olfactory nerves are composed of bipolar neurons that function as chemoreceptors, responding to volatile chemical 1. The tongue responds to tastes and pain and moves to ma- particles breathed into the nasal cavity. Make a quick sketch of the brain and the bodies of olfactory neurons are positioned within the mucosa, tongue to depict the relationship between the CNS and primarily that which covers the superior nasal conchae and ad- the PNS. The axons of these neurons pass through motor innervation of the tongue. List the structures of the nervous system that are consid- ered part of the PNS. II Optic Nerve The optic nerve, another sensory nerve, conducts impulses from the photoreceptors (rods and cones) in the retina of the eye. Each CRANIAL NERVES optic nerve is composed of an estimated 125 million nerve fibers that converge at the back of the eyeball and enter the cranial cav- Twelve pairs of cranial nerves emerge from the inferior surface ity through the optic canal. The optic nerve fibers pass posteriorly from the optic chiasma to the thalamus via the optic tracts. In the thala- Objective 3 Describe the clinical methods for determining mus, a majority of the fibers terminate within certain thalamic cranial nerve dysfunction. A few of the ganglion-cell axons that reach the thalamic nuclei have collaterals that convey impulses to the superior colli- culi. Synapses within the thalamic nuclei, however, permit im- Structure and Function pulses to pass through neurons to the visual cortex within the of the Cranial Nerves occipital lobes. Other synapses permit impulses to reach the nu- clei for the oculomotor, trochlear, and abducens nerves, which Of the 12 pairs of cranial nerves, 2 pairs arise from the forebrain regulate intrinsic (internal) and extrinsic (from orbit to eyeball) and 10 pairs arise from the midbrain and brain stem (fig. The visual pathway into the eyeball functions reflex- The cranial nerves are designated by Roman numerals and ively to produce motor responses to light stimuli. The Roman numerals refer to the order in which the is damaged, the eyeball served by that nerve is blinded. The names indicate the structures innervated or the principal functions of the nerves. A summary of the cranial nerves is pre- III Oculomotor sented in table 12. Nerve impulses through the oculomotor nerve produce certain Although most cranial nerves are mixed, some are associ- extrinsic and intrinsic movements of the eyeball. The oculomo- ated with special senses and consist of sensory neurons only. Peripheral Nervous © The McGraw−Hill Anatomy, Sixth Edition Coordination System Companies, 2001 404 Unit 5 Integration and Coordination TABLE 12. It divides into superior and inferior branches as it of the muscles they serve. A person whose oculomotor nerve is passes through the superior orbital fissure in the orbit (fig. The nerve enter the eyeball to supply parasympathetic autonomic trochlear nerve innervates the superior oblique muscle of the motor innervation to the intrinsic smooth muscles of the iris for eyeball with both motor and sensory fibers (fig.

This is then cleaved by anaother protease (g-secretase) to release the b-amyloid (Fig cheap chloroquine 250mg free shipping. Potentiation of a- or blockage of b- and g-secretase could reduce the production of Ab which becomes insoluble and is precipitated (see Hardy 1997) buy cheap chloroquine 250mg on-line. The b-amyloid (Ab4) sequence is partly extracellular and partly in the membrane effective 250 mg chloroquine. NEUROTROPHIC FACTORS Whether or not the production of b-amyloid can be curtailed, it would be desirable to either replace the damaged neurons or encourage the remaining functional ones to ramify further and exhibit more influence. The former, which requires tissue or cell line grafts, is currently not feasible and barely investigated experimentally but there is much interest in the possible use of neurotrophic proteins (neurotrophins) that encourage neuronal growth and differentiation. A number of these have been isolated and identified but the first to be discovered (see Levi-Montalcini 1987), and the most studied, is nerve growth factor (NGF) which, despite its name, is not universally effective on all neurons. In the periphery it is mainly released in tissues containing sympathetic nerves that take it up and transport it retrogradely to the cell body where it acts. In the brain, however, it has more influence on cholinergic than noradrenergic or other neurons so that NGF protein and MRNA expression is highest in cholinergic innervated areas of the brain such as the hippo- campus and cortex while its binding sites (receptors) are mainly in subcortical regions with cholinergic neurons like the nucleus basalis. So it may be assumed that normally the cortically produced NGF is transported back to cholinergic subcortical neurons where it exerts its trophic action. Certainly NGF increases ChAT production when added to cultured cholinergic neurons and its intraventricular infusion in rats and primates prevents the loss of ChAT activity in and degeneration of, cholinergic neurons caused by transection of the septal hippocampal cholinergic pathway, or ibotenic acid injection into the nucleus basalis. Intraventricular NGF has also been shown to improve learning and memory in aged rats and those with lesions to cholinergic pathways. So if NGF is so important for the growth and function of the cholinergic neurons, that appear so vulnerable in AzD, can they be restored and AzD controlled by administering NGF? Before that question can be answered some practical problems have to be overcome, namely how to obtain and administer it. If immune reactions are to be avoided then recombinant human factor should be used and that cannot be produced in large quantities. In any case, it is a large protein that will have to be injected directly into the brain. Even if these problems can be overcome the spread and intensity of any NGF effect has to be restricted so that excessive neuritic growth and inappropriate increases in synaptic connections do not occur. In addition to these problems there is no evidence of reduced NGF in AzD although levels and receptor number are lower in the nucleus basalis. In fact the levels of NGF were found to be increased in the cortex and hippocampus (Scott et al. At least it throws doubt on the value of augmenting NGF as a therapy for AzD. The younger showed no change in memory performance; the older some improvement after one month, which ceased after the infusion was stopped. Both patients had various reversible side-effects such as back pain and weight loss. OTHER DRUG THERAPY In the face of the failure of rational approaches in the treatment of AzD it is perhaps not surprising that there have been many less rational ones. The former, such as hydergine, a mixture of ergot alkaloids, are intended to increase cerebral blood flow and neuronal metabolism despite some reduction in blood pressure, while the latter, like piracetam, are metabolic stimulants that increase cerebral metabolism and ATPproduction. Although there is no evidence that the neuronal degeneration of AzD results, as in cardiovascular ischaemia, from the excitotoxicity of increased intracellular Ca2‡, some calcium channel blockers have been tried in AzD. They have had little effect but surprisingly a pyrrolidone derivative nefiracetam, which opens L-type voltage-sensitive calcium channels (VSCCs) reduces both scopolamine- and b-amyloid-induced impair- ments of learning and memory in rats (Yamada et al. This effect can be overcome by VSCC antagonists, but nefiracetam has not been tried in humans. SUMMARY Clearly there is a long way to go in the treatment of AzD particularly as even the most active of the generally ineffective therapies discussed above have only addressed the early symptoms of memory loss.

CASE STUDY FOR CHAPTER 37 Answers to Case Study Questions for Chapter 38 Steroid Abuse 1 buy 250 mg chloroquine with mastercard. There are two laboratory tests that indicate a problem buy 250mg chloroquine fast delivery, the A 30-year-old man and his 29-year-old wife have been try- low late follicular phase plasma estradiol concentration and ing to have a baby cheap 250mg chloroquine amex. She has been having regular menstrual the low midluteal phase plasma progesterone concentra- cycles. The low estradiol could be due to the development of a time of her ovulation. The reduced number of granulosa cells The husband’s physical examination reveals a muscular would not contain sufficient aromatase to synthesize the man with an excellent physique who works out regularly to high levels of estradiol required during the late follicular build his body. In addition, low estradiol could be due to inadequate sults indicate that his plasma testosterone is 1850 ng/dL FSH receptors on the granulosa cells or inadequate FSH se- (normal, 300 to 100 ng/dL) and LH 2 U/mL (normal, 3 to cretion. What is the major reason for the failure of the wife to get The low progesterone during the luteal phase might be due pregnant? What is a reasonable explanation for the abnormal hor- follicle that was not fully developed. Since he is a body builder with small, soft testes, high number of LH receptors could be due to insufficient priming testosterone levels, and low LH levels, the physician should of the developing follicle with FSH. Finally, the LH surge may suspect androgen abuse or possibly androgen-producing be insufficient for maximal progesterone secretion. Theoretical treatment options for the patient include exoge- suppress LH secretion and reduce intratesticular testos- nous progesterone during the luteal phase, which would terone levels. The low LH and intratesticular testosterone raise the overall circulating progesterone to levels compati- would correlate well with small testes and low sperm count, ble with maintaining pregnancy, allowing implantation of respectively. Another option would be to use exogenous FSH to stimulate follicular development to produce larger follicle(s) with suffi- CASE STUDY FOR CHAPTER 38 cient estradiol secretion and LH receptors. Follicles with ade- Early Spontaneous Pregnancy Termination quate LH receptors would respond to an LH surge with in- creased progesterone in the normal range. Another option is A 35-year-old woman visited her obstetrician/gynecolo- the administration of hCG during the periovulatory period for gist and complained that she was unable to get pregnant. The latter would Upon taking a medical history, the physician notes that the overcome any deficiency in the endogenous LH surge. Finally, patient had regular 28- to 30-day cycles during the past year, the use of clomiphene, an antiestrogen, would increase FSH during which time she had regular unprotected intercourse. Exogenous hCG could be given during uterus appear normal in size for her age. Laboratory tests in- the ovulatory phase to ensure full luteinization of the corpus dicate that her preovulatory (late follicular phase) estradiol is luteum with sufficient progesterone to maintain pregnancy. What are the clinical indications of a fertility problem with A 25-year-old woman and her 29-year-old husband this patient? Based on the clinical signs, what basic physiological princi- ular menstrual cycles of 26 to 28 days in length. Serum LH should be measured band’s semen analysis reveals a semen volume of 4 mL; pH during the anticipated preovulatory period. Low levels of LH may lead to an un- 26 days versus 28 days), the wife’s plasma progesterone ruptured dominant follicle that fails to ovulate but luteinizes, level during the midluteal phase is assessed and determined leading to progesterone levels in the normal range for the to be 10 ng/mL, which is considered normal (4 to 20 ng/mL, luteal phase. Therapies such as gonadotropins and clomiphene why the patient is not able to get pregnant? Based on the hormone measurements, what treatment development, estradiol secretion, and ovulation. Estradiol should be measured at the end of the anticipated ferred over LH and GnRH for ovulation induction because of follicular phase. APPENDIX A Answers to Review Questions the action of either adenylyl or guanylyl cyclase on ATP or GTP, respectively. For example, cAMP Chapter 1 can activate protein kinase A, which will phosphory- 1.

The binding of hormone (H) to a G-protein-coupled receptor dephosphorylated to inositol buy 250 mg chloroquine with mastercard, which can be reused for phos- (R) can lead to the activation of PLC generic 250mg chloroquine amex. The DAG is converted to phospha- Gq discount 250 mg chloroquine with visa, a G protein that couples receptors to PLC. The activation of tidic acid by the addition of a phosphate group to carbon PLC results in the cleavage of PIP2 to IP3 and DAG. IP3 interacts with calcium release channels in the endoplasmic reticulum, causing number 3. Like inositol, phosphatidic acid can be used for the release of calcium to the cytoplasm. Increased intracellular cal- the resynthesis of membrane inositol phospholipids (see cium can lead to the activation of calcium-dependent enzymes. On removal of the IP3 signal, calcium is quickly accumulation of DAG in the plasma membrane leads to the activa- pumped back into its storage sites, restoring cytoplasmic tion of the calcium- and phospholipid-dependent enzyme protein calcium concentrations to their low prestimulus levels. These are formed by the hydrolysis of appro- priate phosphatidylinositol phosphate precursors found in the cell membrane. Evidence suggests that the hydrolysis of PLC other phospholipids, such as phosphatidylcholine, may play GPCR an analogous role in hormone-signaling processes. This large gradient of calcium is main- 2+ Ca /CaM- tained by the limited permeability of the plasma membrane PK to calcium, by calcium transporters in the plasma mem- brane that extrude calcium, by calcium pumps in intracellu- lar organelles, and by cytoplasmic and organellar proteins FIGURE 1. Several plasma membrane ion channels serve to in- pendent protein kinases. Levels of intracellular calcium are regu- lated by membrane-bound ion channels that allow the entry of cal- crease cytosolic calcium levels. Either these ion channels cium from the extracellular space or release calcium from internal are voltage-gated and open when the plasma membrane de- stores (e. Calcium can also be released from in- protein kinase A or protein kinase C. IP3 causes the release of calcium from the en- endoplasmic reticulum has two other main types of ion doplasmic or sarcoplasmic reticulum in muscle cells by interaction channels that, when activated, release calcium into the cy- with calcium ion channels. When intracellular calcium rises, four toplasm, causing an increase in cytoplasmic calcium. The calcium ions complex with the dumbbell-shaped calmodulin pro- tein (CaM) to induce a conformational change. Ca2 /CaM can small water-soluble molecule IP3 activates the IP3-gated 2 calcium release channel in the endoplasmic reticulum. The then bind to a spectrum of target proteins including Ca /CaM- PKs, which then phosphorylate other substrates, leading to a re- activated channel opens to allow calcium to flow down a sponse. IP3, inositol trisphosphate; PLC, phospholipase C; CaM, concentration gradient into the cytoplasm. The IP3-gated 2 calmodulin; Ca /CaM-PK, calcium-calmodulin-dependent protein channels are structurally similar to the second type of cal- kinases; ER/SR, endoplasmic/sarcoplasmic reticulum. Ryanodine recep- tors release calcium to trigger muscle contraction when an action potential invades the transverse tubule system of contraction (myosin light-chain kinase; see Chapter 9) and skeletal or cardiac muscle fibers (see Chapter 8). Both types hormone synthesis (aldosterone synthesis; see Chapter 34), of channels are regulated by positive feedback, in which and ultimately result in altered cellular function. This causes the calcium to The IP3 generated by the activation of PLC can be dephos- be released suddenly in a spike, followed by a wave-like phorylated and, thus, inactivated by cellular phosphatases. In addition, the calcium that enters the cytosol can be rap- Increasing cytosolic free calcium activates many differ- idly removed. The plasma membrane, endoplasmic reticu- ent signaling pathways and leads to numerous physiologi- lum, sarcoplasmic reticulum, and mitochondrial mem- cal events, such as muscle contraction, neurotransmitter se- branes all have ATP-driven calcium pumps that drive the cretion, and cytoskeletal polymerization. Calcium acts as a free calcium out of the cytosol to the extracellular space or second messenger in two ways: into an intracellular organelle.

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