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The Central Nervous Sys- Schnitzlein HN abilify 15 mg otc depression legere definition, Hartley EW buy abilify 10 mg amex anxiety x blood and bone lyrics, Murtagh FR, Grundy L, Fargher JT. Computed Tomography of the Head and Spine: A Photographic Noback CR, Strominger NL, Demarest RJ. The Human Brain: An Introduction to its Functional A Photographic Color Atlas of MRI, CT, Gross, and Microscopic Anatomy, 5th ed. Inter- and intra-laminar dis- to the hippocampus mediated by stellate cells in the entorhinal cor- tribution of tectospinal neurons in 23 mammals. Baltimore: Urban & projections in primate as studied by retrograde double-labeling Schwarzenberg, 1981. Pernkopf Atlas of Topographic and Applied Human neurones of the substantia nigra receive a GABA-containing input Anatomy, 3rd ed. Atlas of Cross Section Anatomy of the Brain: Guide to anterograde tracing method. J Comp Neurol 1990;294: the Study of the Morphology and Fiber Tracts of the Human Brain. New York: Blakiston Division, McGraw-Hill Book Company, Inc, Strata P (ed). Illustrated Guide to the Central bulbospinal axons that contain serotonin and either enkephalin or Nervous System. Localization of enkephalin- Tatu L, Moulin T, Bogousslavsky J, Duvernoy H. Arterial territories ergic neurons in the dorsolateral pontine tegmentum projecting to of human brain: Brainstem and cerebellum. The posterior cranial fossa: Microsurgical anatomy and Terzian H, Ore GD. Neurosurgery 2000; 47 (Supplement); by bilateral removal of the temporal lobes. The supratentorial cranial space: Microsurgical Tieman SB, Butler K, Neale JH. Identification of cells of origin of non-pri- walk, CT: Appleton & Lange, 1995. Sylvian fissure morphology and asymmetry in munoreactive terminals synapse on primate spinothalamic tract men and women: Bilateral differences in relation to handedness in cells. Baltimore: Urban & Woolsey TA, Hanaway J, Gado MH: The Brain Atlas: A Visual Guide Schwarzenberg, 1982. The Pain System: The Neural Basis of Nociceptive Basal Cisterns and Vessels of the Brain, Diagnostic Studies, Gen- Transmission in the Mammalian Nervous System, Volume 8, Pain eral Operative Techniques and Pathological Considerations of and Headache. Bringing connection content into your WebCT courses As a first step, you will want to download from connection the files that you want to use in your courses. Please refer to the other Help information available at http://connection. Typically these files will be images, PowerPoint presentations, Word documents, and/or Adobe Acrobat (PDF) files. The steps below are also appropriate for bringing your own files into WebCT. Note: Spaces or punctuation characters other than the underscore in file names are not allowed in WebCT. Tip: If you are ever adding multiple files to WebCT during the same session, such as a group of images, or an HTML PowerPoint presentation, try zipping the files together. There are several products on the market, such as WinZip and StuffIt that can combine and compress several files into one. This means that you don’t need to upload each file separately, and your upload time may be reduced, if the files you are adding are compressible. Zipped files can be unzipped again using WebCT’s built- in Unzip utility within Manage Files. For further information on any of the WebCT tools mentioned here, please refer to the online help in WebCT, or visit the WebCT documentation index, which is located at: http://help. From there, you can provide students with access to images in several different ways. One way is to add images into an Image Database that students can access in the course. The Image Database tool allows you to add many images and their descriptions in a single, searchable tool, without any knowledge of HTML.

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Since receptors can be expressed in cell lines the affinity of drugs for the different receptors can discount abilify 15mg with mastercard depression symptoms for males, however buy cheap abilify 20 mg online depression symptoms rating scale, be established, as can their cellular actions. Detection of appropriate mRNA also makes it possible to map the distribution of the receptors. The main characteristics of the DA receptors are summarised below and in Table 7. D1 receptor family D1 Highest expression in human striatum and nucleus accumbens and olfactory tubercle but also some in cortex and hypothalamus. In the striatum 50% of medium sized striato-nigral neurons, which also express substance P, express them. Antagonists [ [ Clozapine Number High Low High Low Low Distribution Striatum [ [ Nuc. See Sibley and Monsma (1997), Sokoloff and Schwartz (1995) and Strange (1996). D5 Highest concentration in hippocampus and hypothalamus but much lower expression overall. Also linked to stimulation of adenylate cyclase but higher submicromolar affinity for DA (K1$200 nM). D2 receptor family D2 Mostly in striatum, nucleus accumbens and olfactory tubercle but also on neuron cell bodies in substantia nigra and ventral tegmentum where they are the auto- receptors for locally (dendritic) released DA. The loss of specific D2 antagonist binding in the striatum after lesions of the afferent nigro-striatal tract indicates their presynaptic autoreceptor role on terminals there. Other lesion studies have also established D2 receptors on other inputs such as the cortico striatal tract. As with D1 receptors some 50% of striatal medium-sized cells contain them but they are different neurons as they co-express enkephalin rather than substance P. The importance of this difference in the therapy of Parkinsonism is taken up later (Chapter 15). Although linked to inhibition of adenylate cyclase (and IP3 turnover) this is not their primary action. They increase K‡ conductance (hyperpolarise neurons) but also inhibit Ca2‡ entry through voltage-sensitive channels, probably directly. When functioning as autoreceptors, these effects would also reduce DA release. The affinity for DA is slightly higher for the D2 (K1$400 nM) than for D1 receptors. No pharmacological differences have been established between the long or short forms of the D2 receptor. Mainly in limbic regions (nucleus accumbens and olfactory tubercle) but also in hypothalamus. Some in caudate and cortex and also expressed on DA neurons in substantia nigra, presumably as autoreceptors. No effect on adenylate cyclase but inhibits Ca2‡ entry (autoreceptor role). D4 Again very few in number compared with D2 but located in frontal cortex, mid- brain and amygdala. Comparison of the K1 values of various agonists and antagonists for the different receptors (Table 7. Some differences that have been exploited are the low affinity of raclopride for D4 receptors (compared with D2 and D3), the high affinity of clozapine and the benzamide derivative YM 43611 for the D4 (cf. Since only the latter is an agonist, however, their value in establishing the roles of the D3 and D4 receptors is limited, although the high affinity of clozapine for D4 receptors and their location in the frontal cortex has been considered, somewhat controversially, to be of significance in the aetiology and therapy of schizophrenia (see Chapter 17). D2,D3 and D4) receptors (a) D1 D5 D2 D3 D4 Agonist Bromocriptine 440* 440* 8* 5* 290* Quinpirole 1900 ± 5 24* 30* 7-OH-DPAT 5000* ± 10 1* 650 SKF 38393 1 0. SYNAPTIC EFFECTS Because DA is very much localised to one brain area (striatum) and as there is such a pronounced DA pathway from the substantia nigra to the striatum it would be reasonable to assume that the effect of this pathway on striatal neuron activity is well established.

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Hemostasis can be viewed as four separate but potent activator of platelet adherence and secretion abilify 15mg fast delivery depression symptoms minor. Rup- interrelated events: tured cells at the site of tissue injury release adenosine • Compression and vasoconstriction abilify 20 mg lowest price depression symptoms hygiene, which act immedi- diphosphate (ADP), which causes platelets to aggregate at ately to stop the flow of blood the damaged site. These aggregates effectively stop the • Formation of a platelet plug flow of blood from the ruptured vessels. The fibrin network traps red cells, leuko- exerted by the tissue around the injured area, and vasocon- cytes, platelets, and serum at sites of vascular damage, striction. The degree of compression varies in different tis- thereby forming a blood clot. The stable, fibrin-based sues; for example, bleeding below the eye is not readily de- blood clot eventually replaces the unstable platelet ag- terred because the skin in this area is easily distensible. Fibrin is Back-pressure increases as blood which leaks out of the dis- an insoluble polymer of proteolytic products of the rupted capillaries accumulates. Fibrin molecules are cleaved uterus after childbirth, contraction of underlying muscles from fibrinogen by thrombin, which is generated in compresses blood vessels supplying the tissue and mini- plasma during clotting. Damaged cells at the site of tissue injury mation, thrombin cleaves four small peptides (fib- release potent substances that directly cause blood vessels rinopeptides) from each molecule of fibrinogen. The fib- to constrict, including serotonin, thromboxane A2, epi- rinogen molecule devoid of these fibrinopeptides is nephrine, and fibrinopeptide B. The fibrin monomers sponta- neously assemble into ordered fibrous arrays of fibrin, resulting in an insoluble matrix of fibrous strands. At this Platelets Form a Hemostatic Plug stage, the clot is held together by noncovalent forces. First, they form plasma enzyme, fibrin stabilizing factor (Factor XIII), multicellular aggregates linked by protein strands at sites of catalyzes the formation of covalent bonds between CHAPTER 11 Blood Components, Immunity, and Hemostasis 207 strands of polymerized fibrin, stabilizing and tightening the blood clot. Blood clotting is mediated by the sequential activation of a series of coagulation factors, proteins synthesized in the liver that circulate in the plasma in an inactive state. They are referred to by number (designated by a Roman numeral) in a sequence based on the order of the discovery of each factor. The plasma coagulation factors and their common names are listed in Table 11. The sequential activation of a series of inactive mole- cules resulting in a biological response is called a metabolic cascade. The sequential activation of coagulation factors resulting in the conversion of fibrinogen to fibrin (and, hence, clotting) is called the coagulation cascade. The de- ficiency or deletion of any one factor of the cascade has se- vere consequences. Individuals deficient in factor VIII (an- tihemophilic factor), for example, display prolonged bleeding time on tissue injury, as a result of delayed clot- ting. Those who lack factor VIII have hemophilia, a condi- tion resulting in severe coagulation defects. Two separate coagulation cascades result in blood clotting in different circumstances. The two systems are the intrinsic coagulation pathway and the extrinsic co- agulation pathway (Fig. The ex- trinsic pathway is initiated by tissue factor (fac- pathway, all the factors required for coagulation are pres- 2 tor III) released from damaged cells. For initiation of the extrinsic path- tor III converts factor VII to factor VIIa, which then forms a way, a factor extrinsic to blood but released from injured complex with factor III and Ca2. This complex converts factor X tissue, called tissue thromboplastin or tissue factor (fac- to factor Xa. In the intrinsic system, factor XII is first converted to tor III), is required. Phospholipids are required for activa- factor XIIa following its exposure to foreign surfaces, such as tion of both coagulation pathways. Factor XIIa initiates a cascade of events, in- vide a surface for the efficient interaction of several cluding activation of factor X, subsequent conversion of pro- factors. A component of tissue factor provides the neces- thrombin to thrombin, and, finally, fibrin formation. Phospho- lipids required for the activation of the intrinsic pathway are found on platelet membranes. The final events leading to fibrin formation by both pathways result from the activation of the common path- way.

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