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These effects of 5-HT3 receptor activation are prevented by co-administration of a D2-receptor antagonist cheap 100 mg kamagra gold being overweight causes erectile dysfunction. This is consistent with evidence that activation of 5-HT3 receptors can increase dopamine release and points to functional interactions between these two groups of neurons that affect the sleep±waking cycle safe 100mg kamagra gold impotence l-arginine. Such interactions will certainly confound any attempts to define the specific role of 5-HT in the regulation of sleep and arousal. Overall, 5-HT transmission seems to increase during waking and to decline in sleep although it may only reach its minimal level, in some neurons anyway, during REM 494 NEUROTRANSMITTERS, DRUGS AND BRAIN FUNCTION sleep. Whether its role is simply to prime target cells to enable an increase in the motor activity associated with waking, as has been suggested, remains to be seen. ADENOSINE It is perhaps not surprising that, since adenosine has been presented as an endogenous inhibitor of neuronal function with its antagonists, like theophylline, being stimulants (see Chapter 13), it should have been implicated in sleep induction. In fact EEG studies have shown that administration of an adenosine A1 agonist increases SWS in humans and induces it in sleep-deprived rats while adenosine also inhibits the important cortical activating brainstem cholinergic neurons. After that, it falls sharply within an hour as the animal enters the quiet (lights on) sleepy period (see Huston et al. AMINO ACIDS Since most excitatory transmission is mediated by glutamate this must be involved in the sleep±waking cycle. It certainly mediates the input of the retinohypothalamic tract to the SCN, apart from afferent inputs more generally to the ARAS, etc. So far, specific in vivo manipulation of the direct glutamate input to the SCN has not been possible. The fact that SCN neurons contain GABA, and that this appears to be the neurotransmitter released by the geniculohypothalamic tract onto the SCN, clearly puts it in a prime position for regulation of sleep rhythms. However, its precise role is unclear, not least because it can act as an excitatory, as well as an inhibitory, neurotransmitter in this nucleus and that these varied responses appear to follow a circadian rhythm (see Chapter 11). Again, specific manipulation of this pathway is difficult although GABA enhancement generally (e. SLEEP FACTORS In classical times, sleep was thought to be induced by sleep factors (vapours) emanating from food in the stomach. These are thought to have a pervading influence on sleep throughout the brain, although the stomach is no longer regarded as their source! This view was strongly encouraged by experiments, carried out in the early twentieth century, by Pieron in Paris, who showed that the CSF of sleep-deprived dogs contained a substance that had a somnogenic effect when infused into non-sleep- deprived animals. Since then, many candidate sleep substances have emerged, some of which are more convincing than others. Chemical extraction from thousands of rabbit brains and many gallons of human urine yielded a sleep factor and established it as a muramyl peptide. Unfortunately muramyl peptides are not synthesised by mammalian cells but are components of bacterial cell walls. Apart from the obvious possibility of mere contamination, it is not clear how the substance turned up in the CSF and brain tissue. Despite this setback, and some scepticism about whether somnogenic peptides exist at all, research still continues in this area and many candidates have been suggested. These include well-known peptides such as prolactin, CCK-8, VIP and somatostatin as well as some novel ones such as d-sleep-inducing peptide. IL-6 also reduces REM sleep and SWS in the first half of the sleep cycle but subsequently increases SWS. However, all these responses vary with dose, test species and even time of day. These factors are produced by T-cell lymphocytes but their receptors are associated with neurons, astrocytes, microglia and endothelial cells. Because these agents induce nitric oxide synthase, and there is some evidence that nitric oxide increases waking, possibly through modulation of ACh release in the medial pontine reticular formation, there is no need for them to cross the blood± brain barrier (although there is evidence that they do). Nevertheless, how these factors actually cause changes in the sleep cycle is as yet unclear. An indirect effect via changes in the rate of prostaglandin synthesis (see below) is one possibility but others include modulation of 5-HT2A-mediated serotonergic transmission and suppression of glutama- tergic neuronal activity through an adenosine-dependent process.

The embryoblast flattens into the embryonic disc (see dermal cells produce the lining of the GI tract purchase kamagra gold 100mg visa neurogenic erectile dysfunction causes, the digestive organs cheap 100 mg kamagra gold visa erectile dysfunction protocol hoax, fig. These gans and body systems that derive from each of the primary germ layers. Once they are formed, at the end of the second week, the preembryonic The period of prenatal development is referred to as gestation. Knowing this and the period is completed and the embryonic period begins. In a typical reproductive cycle, a woman ovulates 14 days prior to the onset of the next menstruation and is fertile for approxi- mately 20 to 24 hours following ovulation. Adding 9 months, or 38 weeks, to the time of ovulation gives one the estimated delivery date. Developmental © The McGraw−Hill Anatomy, Sixth Edition Development Anatomy, Postnatal Companies, 2001 Growth, and Inheritance Chapter 22 Developmental Anatomy, Postnatal Growth, and Inheritance 761 Digestive tract Amnion Amniotic fluid Skin Heart Spinal cord Chorion Body stalk with umbilical vessels Syncytiotrophoblasts Brain Yolk sac Endoderm Mesoderm Ectoderm Muscle: smooth, cardiac, and skeletal Connective tissue: embryonic, Epidermis of skin and epidermal connective tissue proper, derivatives: hair, nails, glands cartilage, bone, blood of the skin; linings of oral, nasal, Dermis of skin; dentin of teeth anal, and vaginal cavities Epithelium of blood vessels, Nervous tissue; sense organs lymphatic vessels, body Lens of eye; enamel of teeth cavities, joint cavities Pituitary gland Internal reproductive organs Adrenal medulla Kidneys and ureters Adrenal cortex Epithelium of pharynx, external acoustic canal, tonsils, thyroid, parathyroid, thymus, larynx, trachea, lungs, GI tract, urinary bladder and urethra, and vagina Liver and pancreas FIGURE 22. Developmental © The McGraw−Hill Anatomy, Sixth Edition Development Anatomy, Postnatal Companies, 2001 Growth, and Inheritance 762 Unit 7 Reproduction and Development bon dioxide can be removed; (2) establishment of a constant, Knowledge Check protective environment around the embryo that is conducive to 4. List the structural characteristics of a zygote, morula, and development; (3) establishment of a structural foundation for blastocyst. Approximately when do each of these stages of embryonic morphogenesis along a longitudinal axis; (4) provi- the preembryonic period of development occur? Discuss the process of implantation and describe the phys- through genetic expression. If these needs are not met, a sponta- iological events that ensure pregnancy. Serious developmental defects usually cause the embryo to be naturally aborted. About 25% of early aborted embryos EMBRYONIC PERIOD have chromosomal abnormalities. Other abortions may be caused by environmental factors, such as infectious agents or teratogenic The events of the 6-week embryonic period include the differentia- drugs (drugs that cause birth defects). In addition, an implanted em- tion of the germ layers into specific body organs and the formation bryo is regarded as foreign tissue by the immune system of the of the placenta, the umbilical cord, and the extraembryonic mem- mother, and is rejected and aborted unless maternal immune re- sponses are suppressed. Objective 7 Define embryo and describe the major events Extraembryonic Membranes of the embryonic period of development. At the same time that the internal organs of the embryo are Objective 8 List the embryonic needs that must be met to being formed, a complex system of extraembryonic membranes avoid a spontaneous abortion. The extraembryonic membranes are the amnion, yolk sac, allantois, and chorion. These membranes Objective 9 Describe the structure and function of each of are responsible for the protection, respiration, excretion, and the extraembryonic membranes. At parturition, Objective 10 Describe the development and functions of the placenta, umbilical cord, and extraembryonic membranes the placenta and the umbilical cord. During the embryonic period—from the beginning of the third week to the end of the eighth week—the developing organism is Amnion correctly called an embryo. It loosely envelops the embryo, forming an cord, and extraembryonic membranes. The term conceptus refers amniotic sac that is filled with amniotic fluid (fig. In to the embryo, or to the fetus later on, and all of the extraembry- later fetal development, the amnion expands to come in contact onic structures—the products of conception. The development of the amnion is initiated early in the embryonic period, at which time its margin is at- Embryology is the study of the sequential changes in an or- ganism as the various tissues, organs, and systems develop. As Chick embryos are frequently studied because of the easy access the amniotic sac enlarges during the late embryonic period (at through the shell and their rapid development. Mice and pig embryos about 8 weeks), the amnion gradually sheaths the developing are also extensively studied as mammalian models. Genetic manipu- lation, induction of drugs, exposure to disease, radioactive tagging or umbilical cord with an epithelial covering (fig. During the preembryonic period of cell division and differ- • It cushions and protects by absorbing jolts that the mother entiation, the developing structure is self-sustaining.

Several other disorders may present symptoms similar Primary idiopathic polymyositis cases comprise ap- to polymyositis; these include neurological or neuromus- proximately one third of the inflammatory myopathies buy kamagra gold 100 mg cheap erectile dysfunction 23. Early third of polymyositis cases are associated with a closely re- stages of muscular dystrophy may mimic polymyositis discount kamagra gold 100mg amex impotence diagnosis code, al- lated condition called dermatomyositis, symptoms of though the overall courses of the diseases differ consider- which include a mild heliotrope (light purple) rash around ably; the decline in function is much more rapid in un- the eyes and nose and other parts of the body, such as treated polymyositis. Nail bed abnormalities may also be produce symptoms of the disease, depending on the present. Still other cases (approximately 8%) are associ- severity of the infection. A large number of commonly ated with cancer present in the lung, breast, ovary, or gas- used drugs may produce the typical symptoms of muscle trointestinal tract. This association occurs mostly in older pain and weakness, and a careful drug history may sug- patients. Finally, about one fifth of polymyositis cases are gest a specific cause. In cases in which dermatomyositis is associated with other connective tissue disorders, such as combined with the typical symptoms of polymyositis, the rheumatoid arthritis and lupus erythematosus. Careful follow-up (by Polymyositis is thought to be primarily an autoim- direct muscle strength testing and measurement of serum mune disease. Muscle histology shows infiltration by in- CK levels) is necessary to determine the ongoing effective- flammatory cells such as lymphocytes, macrophages, ness of treatment. Muscle tissue destruction, which is al- may become inactive, but relapses can occur, and other most always present, occurs by phagocytosis. The route treatment approaches, such as the use of cytotoxic drugs, of infiltration often follows the vascular supply. Long-term physical therapy and assis- may be elevated serum levels of enzymes normally pres- tive devices are required when drug therapy is not suffi- ent in muscle, such as creatine kinase (CK). It is accomplished by the interaction of Explains Muscle Contraction the globular heads of the myosin molecules (crossbridges, which project from the thick filaments) with binding sites The structure of skeletal muscle provides important clues to on the actin filaments. The width of the A bands force and shortening are produced and where the chemical (thick-filament areas) in striated muscle remains constant, energy stored in the muscle is transformed into mechanical regardless of the length of the entire muscle fiber, while the energy. The total shortening of each sarcomere is only width of the I bands (thin-filament areas) varies directly about 1 m, but a muscle contains many thousands of sar- with the length of the fiber. These represent ma- the effect of multiplying all the small sarcomere length terial extending into the A band from the I bands. The lengths of the thin and thick myofilaments comere is small (a few hundred micronewtons), but, again, remain constant despite changes in fiber length. When the muscle is stretched be- thin filaments telescope into the array of thick filaments. This limits the CHAPTER 8 Contractile Properties of Muscle Cells 145 I I Over this small region, further interdigitation does not lead A A A to an increase in the number of attached crossbridges and the force remains constant. At shorter lengths, additional geometric and physical factors play a role in myofilament interactions. Since mus- cle is a “telescoping” system, there is a physical limit to the Least overlap amount of shortening. As thin myofilaments penetrate the I I A band from opposite sides, they begin to meet in the mid- dle and interfere with each other (1. At the A A A extreme, further shortening is limited by the thick filaments of the A band being forced against the structure of the Z lines (1. The relationship between overlap and force at short Moderate overlap lengths is more complex than that at longer lengths, since more factors are involved. It has also been shown that at I I very short lengths, the effectiveness of some of the steps in A A A the excitation-contraction coupling process is reduced. These include reduced calcium binding to troponin and some loss of action potential conduction in the T tubule system. Some of the consequences for the muscle as a whole are apparent when the mechanical behavior of mus- Most overlap cle is examined in more detail (see Chapter 9). The overall shortening is the sum of Events of the Crossbridge Cycle the shortening of the individual sarcomeres. Drive Muscle Contraction The process of contraction involves a cyclic interaction be- tween the thick and thin filaments. The steps that comprise amount of force that can be produced, since a shorter the crossbridge cycle are attachment of thick-filament length of thin filaments interdigitates with A band thick fil- crossbridges to sites along the thin filaments, production of aments and fewer crossbridges can be attached.