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The ovaries of a sexually mature female are solid cheap tadora 20 mg visa, ovoid structures about 3 buy tadora 20mg with visa. The color and texture of the ovaries vary according to the age and reproductive stage of the female. Fol- lowing puberty, the ovaries are pinkish-gray and have an irregu- lar surface because of the scarring caused by ovulation. The lateral por- tion of the ovary is positioned near the open end of the uterine FIGURE 21. The paired ovaries are positioned in the upper pelvic cav- ity, one on each lateral side of the uterus. Each ovary is situated in a shallow depression of the posterior body wall, the ovarian fossa, and secured by several membranous attachments. The principal supporting membrane of the female reproductive tract is the broad ligament. The broad ligament is the parietal peri- Knowledge Check toneum that supports the uterine tubes and uterus. Define ally supported by an ovarian ligament, which is anchored to the menstruation and ovulation. What is the usual span uterus, and a suspensory ligament, which is attached to the of a woman’s reproductive years? Distinguish between the primary sex organs, secondary sex is the thin outermost layer composed of cuboidal epithelial cells organs, and secondary sex characteristics. The principal substance of the ovary is divided into an outer ovarian cortex and a vascular inner ovar- STRUCTURE AND FUNCTION ian medulla, although the boundary between these layers is not distinct. The stroma—the material of the ovary in which folli- OF THE OVARIES cles and blood vessels are embedded—lies in both the cortical The ovary contains a large number of follicles, each of which en- and medullary layers. Some of these follicles mature during the ovarian cycle, and the ova they contain progress to the secondary oocyte Blood Supply and Innervation stage of meiosis. During ovulation, the largest follicle ruptures and releases its secondary oocyte. The ruptured follicle becomes a Blood is supplied by ovarian arteries that arise from the lateral corpus luteum and regresses to become a corpus albicans. These sides of the abdominal aorta,just below the origin of the renal ar- cyclic changes in follicular development are accompanied by teries. An additional supply comes from the ovarian branches of changes in hormone levels. The right ovarian vein empties into the inferior vena cava, Objective 4 Describe the position of the ovaries and the whereas the left ovarian vein drains into the left renal vein. Objective 5 Describe the structural changes in the ovaries that lead to and follow ovulation. Female Reproductive © The McGraw−Hill Anatomy, Sixth Edition Development System Companies, 2001 Chapter 21 Female Reproductive System 729 Ampulla Uterine tube of uterine Suspensory Ovarian ligament tube ligament of Body of uterus ovary Mesovarium Fundus of uterus Ovary Infundibulum of uterine tube Round Fimbriae ligament Egg cell Broad Follicle Endometrium ligament of uterus Myometrium Perimetrium Fornix of vagina Cervix of uterus Vagina Waldrop FIGURE 21. The ovaries have both sympathetic and parasympathetic a newborn girl contain about 2 million oocytes, this number de- innervation from the ovarian plexus. Innervation to the ovaries, clines to 300,000 to 400,000 by the time she enters puberty. On however, is only to the vascular networks and not to the follicu- average, 400 oocytes are ovulated during a woman’s reproductive lar substance within the stroma. Follicle Formation Normal, healthy ovaries usually cannot be palpated either by Primary oocytes that are not stimulated to complete the first vaginal or abdominal examination. If the ovaries become meiotic division are contained within tiny follicles called pri- swollen or displaced, however, they are palpable through the vagina. There are many types of nonmalignant tumors of the ovaries, most of mordial follicles. In response to stimulation by gonadotropic which cause swelling and some localized tenderness. The ovaries at- hormones, some of these oocytes and follicles get larger, and the rophy during menopause, and ovarian enlargement in post- follicular cells divide to produce the follicular epithelium that menopausal women is usually cause for concern. At The germ cells that migrate into the ovaries during early embry- this point, they are called secondary follicles (fig. The mound is called the cumulus oogonia stops at this point and never resumes. Under stimulation of follicle-stimulating of the first meiotic division, and therefore the primary oocytes are still diploid (have 46 chromosomes). Female Reproductive © The McGraw−Hill Anatomy, Sixth Edition Development System Companies, 2001 730 Unit 7 Reproduction and Development Primary follicles Vesicle Secondary follicle (a) Granulosa cells Antrum Corona radiata Secondary oocyte Zona pellucida Cumulus oophorus Theca interna (b) FIGURE 21. In- By about the tenth to the fourteenth day following day 1 of a terestingly, the follicular cells produce estrogen from its precursor menstrual period, usually just one follicle has matured fully to be- testosterone, which is supplied by a layer of cells immediately come a vesicular ovarian (graafian) follicle (fig. This does not form two complete cells, that it forms a bulge on the surface of the ovary. Under proper however, because only one cell—the secondary oocyte—gets al- hormonal stimulation (a sudden burst of luteinizing hormone most all of the cytoplasm. The other cell formed at this time be- from the anterior pituitary, triggered by a peak level of estrogen), comes a small polar body (fig. The secondary oocyte enters the second meiotic and extrude its secondary oocyte into the peritoneal cavity near division, but meiosis is arrested at metaphase II and is never the opening of the uterine tube in the process of ovulation (ov-yu˘- completed unless fertilization occurs. Female Reproductive © The McGraw−Hill Anatomy, Sixth Edition Development System Companies, 2001 Chapter 21 Female Reproductive System 731 (a) (b) FIGURE 21.
Skeletal System: The © The McGraw−Hill Anatomy order 20 mg tadora with mastercard, Sixth Edition Appendicular Skeleton Companies purchase 20 mg tadora with mastercard, 2001 186 Unit 4 Support and Movement Base of patella Articular surface Anterior surface Medial Apex of patella condyle Intercondylar eminence Intercondylar eminence Lateral condyle Articular surface of fibular head Head of fibula Tibial tuberosity Fibular articular Neck of fibula surface Anterior border Body of Body of tibia fibula Patella Tibia Fibula Medial malleolus Lateral malleolus Lateral malleolus (a) (b) FIGURE 7. Anterior to differ in shape, however, because of their load-bearing role. The remaining four The metatarsal bones are numbered I to V, starting with the tarsal bones form a distal series that articulate with the medial (great toe) side of the foot. The proximal bases of the first, second, and third metatarsals ar- Metatarsus ticulate proximally with the cuneiform bones. The heads of the metatarsals articulate distally with the proximal phalanges. The The metatarsal bones and phalanges are similar in name and proximal joints are called tarsometatarsal joints, and the distal number to the metacarpals and phalanges of the hand. The ball of the foot is formed by the heads of the first two calcaneus: L. Skeletal System: The © The McGraw−Hill Anatomy, Sixth Edition Appendicular Skeleton Companies, 2001 Chapter 7 Skeletal System: The Appendicular Skeleton 187 Sesamoid bone Distal Metatarsal Talus phalanx bones Distal phalanx Cuneiform Tibia Phalanges Proximal bone Middle phalanx Fibula phalanx Navicular Proximal phalanx bone Calcaneus Metatarsal Medial I II cuneiform bone bones III IV V Intermediate cuneiform bone Lateral cuneiform bone Tarsal Navicular bone bones Cuboid bone Talus Calcaneus (a) (b) I II III Distal phalanx IV Phalanges Proximal phalanx V Distal phalanx Middle phalanx Head Proximal phalanx First metatarsal bone Body Metatarsal bones Medial cuneiform Fifth metatarsal bone bone Base Intermediate cuneiform bone Lateral cuneiform bone Navicular bone Cuboid bone Talus Calcaneus Tarsal bones Tuberosity of calcaneus (c) (d) FIGURE 7. Each digit (toe) is indicated by a Roman numeral, the first digit, or great toe, being Roman numeral I. Skeletal System: The © The McGraw−Hill Anatomy, Sixth Edition Appendicular Skeleton Companies, 2001 188 Unit 4 Support and Movement Phalanges The 14 phalanges are the skeletal elements of the toes. As with the fingers of the hand, the phalanges of the toes are arranged in a proximal row, a middle row, and a distal row. The great toe, or hal- Cuneiform lux (adjective, hallucis) has only a proximal and a distal phalanx. They are formed by the structure and Talus arrangement of the bones and maintained by ligaments and ten- Calcaneus dons (fig. The arches are not rigid; they “give” when Navicular bone weight is placed on the foot, and they spring back as the weight Transverse arch is lifted. Longitudinal arch The longitudinal arch is divided into medial and lateral parts. The talus First metatarsal bone is keystone of the medial part, which originates at the calcaneus, rises at the talus, and descends to the first three metatarsal bones. Phalanges of big toe The shallower lateral part consists of the calcaneus, cuboid, and (a) fourth and fifth metatarsal bones. The transverse arch extends across the width of the foot Bases of and is formed by the calcaneus, navicular, and cuboid bones pos- metatarsal bones teriorly and the bases of all five metatarsal bones anteriorly. A weakening of the ligaments and tendons of the foot may cause the arches to “fall”—a condition known as pes planus, or, Transverse arch more commonly, “flatfoot. Skeletal System: The © The McGraw−Hill Anatomy, Sixth Edition Appendicular Skeleton Companies, 2001 Chapter 7 Skeletal System: The Appendicular Skeleton 189 FIGURE 7. It is the most common congenital deformity of the foot, al- though it also occurs in the hand. Syndactyly is the condition in which two or more digits are webbed together. It is a common con- genital deformity of the hand, although it also occurs in the foot. The condition can be effectively treated surgically if the procedure is done at an early age. Describe the structure of each of the long bones of the lower ing or breaking of a bone. Radiographs are often used to diagnose extremity and the position of each of the tarsal bones. Which bones of the foot contribute to the formation of the classified in several ways, and the type and severity of the frac- arches? Pathologic fractures, for example, result from diseases that weaken the bones. Most fractures, however, are called traumatic fractures because they are caused by injuries. The following are descriptions of several kinds of traumatic fractures (fig. The fractured bone is exposed to the Minor defects of the extremities are relatively common malfor- outside through an opening in the skin. The fracture has separated the bone into two an extra digit is incompletely formed and does not function. The bone is splintered into Polydactyly is inherited as a dominant trait, whereas syndactyly several fragments. An incomplete break (partial fracture), in is not certain whether it is abnormal positioning or restricted which one side of the bone is broken, and the other side movement in utero that causes this condition, but both genetics is bowed. Skeletal System: The © The McGraw−Hill Anatomy, Sixth Edition Appendicular Skeleton Companies, 2001 190 Unit 4 Support and Movement A greenstick fracture is incomplete, A partial (fissured) fracture A comminuted fracture is and the break occurs on the convex involves an incomplete break. A transverse fracture is complete, An oblique fracture is complete, A spiral fracture is and the fracture line is horizontal. A fracture of either or both of the distal ends of the Certain fractures seem to resist healing, however, even with this tibia and fibula at the level of the malleoli. New techniques for treating fractures include applying weak electrical currents to fractured bones. The broken portion of the bone is driven in- cantly reducing the time of immobilization. A fracture in which the bone fragments are not ultimate repair of the bone occurs naturally within the bone it- in anatomical alignment. When a bone is fractured, the surrounding periosteum is main in anatomical alignment. A disrupted aligning the broken ends and then immobilizing them until new blood supply to osteocytes and periosteal cells at the frac- bone tissue has formed and the fracture has healed.
This was first shown at peripheral noradrenergic synapses where the amount of noradrenaline released from nerve terminals is reduced by applied exogenous noradrenaline and increased by appropriate (alpha) adrenoceptor antagonists discount tadora 20 mg overnight delivery. Thus through presynaptic (alpha) adrenoreceptors 20mg tadora with mastercard, which can be distinguished from classical postsynaptic (alpha) adrenoreceptors by relatively specific agonists and antagonists, neuronal-released noradrenaline is able to inhibit its own further (excessive) release. It is a mechanism for controlling the synaptic concentration of noradrenaline. This inhibition does not necessarily involve any change in membrane potential but the receptors are believed to be linked to and inhibit adenylate cyclase. Whether autoinhibition occurs with all NTs is uncertain but there is strong evidence for it at GABA, dopamine and 5-HT terminals. There is also the interesting possibility that presynaptic inhibition of this form, with or without potential changes, need not be restricted to the effect of the NT on the terminal from which it is released. Numerous studies in which brain slices have been loaded with a labelled NT and its release evoked by high K or direct stimulation show NEUROTRANSMITTER SYSTEMS AND FUNCTION: OVERVIEW 17 Figure 1. A noradrenergic terminal has been shown to possess receptors for a wide range of substances, so-called heteroceptors (see Langer 1981, 1997) and although this may be useful for developing drugs to manipulate noradrenergic transmission it seems unlikely that in vivo all of the receptors could be innervated by appropriate specific synapses or reachable by their NT. They may be pharmacologically responsive but not always physiologically active (see Chapter 4). CONTROL OF SYNAPTIC NT CONCENTRATION Having briefly discussed the presynaptic control of NT release it is necessary to consider how the concentration of a NT is controlled at a synapse so that it remains localised to its site of release (assuming that to be necessary) without its effect becoming too excessive or persistent. Although one neuron can receive hundreds of inputs releasing a number of different NTs, the correct and precise functioning of the nervous system presumably requires that a NT should only be able to act on appropriate receptors at the site of its release. This control is, of course, facilitated to some extent by having different NTs with specific receptors so that even if a NT did wander it could only work where it finds its receptors and was still present in sufficient concentration to meet their affinity requirements. Normally the majority of receptors are also restricted to the immediate synapse. Nevertheless, from release (collection) studies we know that enough NT must diffuse (overflow) to the collecting system, be that a fine probe in vivo or the medium of a perfusion chamber in vitro, to be detected. Thus one must assume that either the concentration gradient from the collecting site back to the active synaptic release site is so steep that the NT can only reach an effective concentration at the latter, or it is not unphysiological for a NT to have an effect distal from its site of release. Released NT, if free to do so, would diffuse away from its site of release at the synapse down its concentration gradient. The structure of the synapse and the narrow gap between pre- and postsynaptic elements reduces this possibility but this means that there must be other mechanisms for removing or destroying the NT so that it, and its effects, do not persist unduly at the synapse but are only obtained by regulated impulse controlled release. ACh, this is achieved by localised metabolising enzymes but most nerve terminals, especially those for the amino acids and monoamines, possess very high-affinity NT uptake systems for the rapid removal of released NT. In fact these are all Na- and Cl7-dependent, substrate-specific, high- affinity transporters and in many cases their amino-acid structure is known and they have been well studied. Transport can also occur into glia as well as neurons and this may be important for the amino acids. Of course, a further safeguard against an excessive synaptic concentration of the NT is the presence of autoreceptors to control its release. Thus there are mechanisms to ensure that NTs neither persist uncontrollably at the synapse nor produce dramatic effects distal from it. Studies of glutamate release always show a measurable basal level (1±3 mM), although this may not all be of NT origin, and yet it is very difficult to increase that level even by quite intense stimulation. Whether this is a safeguard against the neurotoxicity caused by the persistent intense activation NEUROTRANSMITTER SYSTEMS AND FUNCTION: OVERVIEW 19 of neurons by glutamate (see Chapter 9), or just to ensure that neurons remain responsive to further stimulation is unclear, as is the mechanism by which it is achieved. Despite the above precautions, it is still possible that NT spillover and extrasynaptic action may occur and indeed could be required in some instances. Thus the diffusion of glutamate beyond the synapse could activate extrasynaptic high-affinity NMDA or metabotropic receptors (Chapter 9) to produce long-lasting effects to maintain activity in a network. Crosstalk between synapses could also act as a back-up to ensure that a pathway functions properly (see Barbour and Hausser 1997). MORPHOLOGICAL CORRELATES OF SYNAPTIC FUNCTION Obviously different NTs have different synaptic actions and it is of interest to see to what extent there are morphological correlates for these differing activities. As mentioned previously, an axon generally makes either an axo-dendritic or axo- somatic synapse with another neuron. Gray (1959) has described subcellular features that distinguish these two main types of synapse. Under the electron microscope, his designated type I synaptic contact is like a disk (1±2 mm long) formed by specialised areas of opposed pre- and postsynaptic membranes around a cleft (300 A) but showing an asymmetric thickening through an accumulation of dense material adjacent to only the postsynaptic membrane. A type II junction is narrower (1 mm) with a smaller cleft (200 A) and a more even (symmetric) but less marked membrane densification on both sides of the junction. In addition the presynaptic vesicles are generally large (300±600 A diameter), spherical and numerous at the asymmetric type I synapse but smaller (100±300 A), fewer in number and somewhat flattened or disk-like at the symmetric type II. Vesicles of varying shape can sometimes be found at both synapses, and while some differences are due to fixation problems, the two types of synapse described above are widely seen and generally accepted. They appear to be associated with fast synaptic events so that type I synapses are predominantly axo-dendritic, i. Asymmetric excitatory synapses outnumber GABA inhibitory symmetric synapses by up to 4:1, even though at such synapses there is usually only one actual synaptic junction whereas at the symmetrical inhibitory synapse there can be a number of such junctions Ð presumably to ensure adequate inhibitory control. Unfortunately in routine EM (electron microscope) preparations one cannot identify the NT at individual synapses although structural features (shape of vesicle, asymmetric or symmetric specialisations) may provide a clue. At cholinergic synapses the terminals have clear vesicles (200±400 A) while monoamine terminals (especially NA) have distinct large (500±900 A) dense vesicles.
The existence of co-transmitters order tadora 20 mg visa, especially substance P generic tadora 20mg line, thyrotropin releasing hormone (TRH) and enkephalin, gives further options for functional specialisation of different neurons but, as yet, the distribution of these peptides within different nuclei has provided no specific clues as to how this might occur. In any case, species differences in the distribution of co-transmitters is a confounding factor. In short, although the 5-HT system seems to have a rather non-specific influence on overall brain function, in terms of the brain areas to which these neurons project, there is clearly much to be learned about possible functional and spatial specialisations of neurons projecting from different nuclei. SYNTHESIS The first step in the synthesis of 5-HT is hydroxylation of the essential amino acid, tryptophan, by the enzyme tryptophan hydroxylase (Fig. This enzyme has several features in common with tyrosine hydroxylase, which converts tyrosine to l-DOPA in 5-HYDROXYTRYPTAMINE 191 Figure 9. The primary substrate for the pathway is the essential amino acid, tryptophan and its hydroxylation to 5-hydroxytryptophan is the rate- limiting step in the synthesis of 5-HT. The cytoplasmic enzyme, monoamine oxidase (MAOA), is ultimately responsible for the catabolism of 5-HT to 5-hydroxyindoleacetic acid the noradrenaline synthetic pathway. First, it has an absolute requirement for O2 and the reduced pterin co-factor, tetrahydrobiopterin. Second, hydroxylation of trypto- phan, like that of tyrosine, is the rate-limiting step for the whole pathway (reviewed by Boadle-Biber 1993) (see Chapter 8). However, unlike the synthesis of noradrenaline, the availability of the substrate, tryptophan, is a limiting factor in the synthesis of 5-HT. Indeed, the activated form of tryptophan hydroxylase has an extremely high Km for tryptophan (50 mM), which is much greater than the concentration of tryptophan in the brain (10±30 mM). This means that not only is it unlikely that this enzyme ever becomes saturated with its substrate but also that 5-HT synthesis can be driven by giving extra tryptophan. First, it predicts that a dietary deficiency of tryptophan could lead to depletion of the neuronal supply of releasable 5-HT. Indeed, this has been confirmed in humans to the extent that a tryptophan-free diet can cause a resurgence of depression in patients who were otherwise in remission (see Chapter 20). In contrast, a tryptophan-high diet increases synthesis and release of 5-HT. In fact, when given in combination with other drugs that augment 5-HT transmission (e. Transport of tryptophan across the blood±brain barrier and neuronal membranes relies on a specific carrier for large neutral amino acids (LNAAs). Thus, although an increase in the relative concentration of plasma tryptophan, either through dietary intake or its reduced metabolism in a diseased liver, increases its transport into the brain, other LNAAs (such as leucine, isoleucine or valine) can compete for the carrier. It is known that consumption of carbohydrates increases secretion of insulin which, in addition to its well-known glucostatic role, promotes uptake of LNAAs by peripheral tissues. However, it seems that tryptophan is less affected by insulin than the other LNAAs in this respect and so its relative concentration in the plasma increases, thereby increasing its transport into the brain (see Rouch, Nicolaidis and Orosco 1999). The resulting increase in synthesis and release of 5-HT is claimed to enhance mood. Although this scheme is rather controversial, it has been suggested as an explanation for the clinical improvement in some patients, suffering from depression or premenstrual tension, when they eat carbohydrates. It has also been suggested to underlie the carbohydrate-craving experienced by patients suffering from Seasonal Affective Disorder (Wurtman and Wurtman 1995). Not a great deal is known about factors that actually activate tryptophan hydroxylase. In particular, the relative contribution of tryptophan supply versus factors that specifically modify enzyme activity under normal dietary conditions is unknown. However, removal of end-product inhibition of tryptophan hydroxylase has been firmly ruled out. Also, it has been established that this enzyme is activated by electrical stimulation of brain slices, even in the absence of any change in tryptophan concentration, and so other mechanisms are clearly involved. So far, it has been established from in vitro studies that the enzyme undergoes phosphorylation, a process that changes the conformation of the enzyme protein and leads to an increase in its activity. This involves Ca2/calmodulin-dependent protein kinase II and cAMP-dependent protein kinase which suggests a role for both intracellular Ca2 and enzyme phosphorylation in the activation of tryptophan hydroxylase. Indeed, enzyme purified from brain tissue innervated by rostrally projecting 5-HT neurons, that have been stimulated previously in vivo, has a higher activity than that derived from unstimulated tissue but this increase rests on the presence of Ca2 in the incubation medium. Also, when incubated under conditions which are appropriate for phosphorylation, the Km of tryptophan hydroxylase for its co-factor and substrate is reduced whereas its Vmax is increased unless the enzyme is purified from neurons that have been stimulated in vivo, suggesting that the neuronal depolarisation in vivo has already caused phosphorylation of the enzyme. This is supported by evidence that the enzyme activation caused by neuronal depolarisation is blocked by a Ca2/calmodulin protein kinase inhibitor. However, whereas depolarisation 5-HYDROXYTRYPTAMINE 193 alone increases enzyme Vmax, it does not appear to affect the enzyme Km and so a firm link between neuronal depolarisation and enzyme phosphorylation has yet to be established. The apparent reliance of enzyme activation on phosphorylation and intracellular Ca2 gives a clue as to how the rate of 5-HT synthesis might be coupled to its impulse- evoked release. Certainly, the impulse-induced increase in intracellular Ca2, and/or activation of the G protein-coupled receptors that govern synthesis of cAMP, could modify the activity of tryptophan hydroxylase. Indeed, this could explain why activation of either somal 5-HT1A autoreceptors in the Raphe nuclei (which depress the firing rate of 5-HT neurons) or terminal 5-HT1B autoreceptors (which depress 5-HT release) can reduce the production of cAMP and attenuate 5-HT synthesis. The product of the hydroxylation of tryptophan, 5-hydroxytryptophan, is rapidly decarboxylated to 5-HT by a specific decarboxylase enzyme. This is generally thought to be a soluble enzyme which suggests that 5-HT is synthesised in the cytoplasm, before it is taken up into the storage vesicles. If this is the case, then considerable losses might be incurred from its metabolism by monoamine oxidase before it reaches the storage vesicles. Indeed, this could explain why 5-HT turnover seems to greatly exceed its rate of release.
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