By V. Kirk. Cleary University. 2018.

Parasympathetic efferents to the small and large neurons are second- or third-order neurons representing intestinal musculature are predominantly stimulatory as a re- the efferent arm of the reflex circuit discount 20mg cialis super active with amex erectile dysfunction kidney. They are the final sult of their input to the enteric microcircuits that control the common pathways out of the brain to the enteric circuits activity of excitatory motor neurons purchase cialis super active 20 mg on line erectile dysfunction and high blood pressure. The dorsal vagal complex consists of the dorsal motor Efferent vagal fibers form synapses with neurons in the nucleus of the vagus, nucleus tractus solitarius, area ENS to activate circuits that ultimately drive the outflow of postrema, and nucleus ambiguus; it is the central vagal in- signals in motor neurons to the effector systems. This center in the brain is more effector system is the musculature, its innervation consists directly involved in the control of the specialized digestive of both inhibitory and excitatory motor neurons that par- functions of the esophagus, stomach, and the functional ticipate in reciprocal control. If the effector systems are cluster of duodenum, gallbladder, and pancreas than the gastric glands or digestive glands, the secretomotor neu- distal small intestine and large intestine. The circuits in the rons are excitatory and stimulate secretory behavior. The generalized Abdominal Early satiety symptoms of both disorders overlap (Fig. Surgical Heartburn Pallor vagotomy results in a rapid emptying of liquids and a de- Anorexia Rapid pulse layed emptying of solids. As mentioned earlier, vagotomy Weight loss Perspiration impairs adaptive relaxation and results in increased con- Syncope tractile tone in the reservoir (see Fig. Increased pressure in the gastric reservoir more forcefully presses liquids into the antral pump. Paralysis with a loss of Delayed Rapid propulsive motility in the antrum occurs after a vagotomy. A Symptoms of disordered gastric empty- layed emptying of solids after a vagotomy. Some of the symptoms of delayed vagotomy is performed as a treatment for peptic ulcer dis- and rapid gastric emptying overlap. Delayed gastric emptying with no demonstrable un- absence of inhibitory motor neurons and the failure of derlying condition is common. Up to 80% of patients the circular muscles to relax account for the obstructive with anorexia nervosa have delayed gastric emptying of stenosis. Another such condition is idiopathic gastric Rapid gastric emptying often occurs in patients who stasis, in which no evidence of an underlying condition have had both vagotomy and gastric antrectomy for the can be found. These individuals have are used successfully in treating these patients. The pathological ef- dren, hypertrophic pyloric stenosis impedes gastric fects are referred to as the dumping syndrome, which re- emptying. This is a thickening of the muscles of the py- sults from the “dumping” of large osmotic loads into the loric canal associated with a loss of enteric neurons. Memory, the processing of incoming information ercise and stressful environmental change, coinciding with from outside the body, and the integration of propriocep- the suppression of digestive functions, including motility tive information are ongoing functions of higher brain cen- and secretion. The release of norepinephrine (NE) from ters responsible for the logical organization of outflow to sympathetic postganglionic neurons is the principal media- the skeletal muscles by way of the basic spinal reflex circuit. NE acts directly on sphincteric muscles The basic connections of the vago-vagal reflex circuit are to increase tension and keep the sphincter closed. Presy- like somatic motor reflexes, in that they are “fine-tuned” naptic inhibitory action of NE at synapses in the control from moment to moment by input from higher integrative circuitry of the ENS is primarily responsible for inactiva- centers in the brain. Suppression of synaptic transmission by the sympathetic nerves occurs at both fast and slow excitatory synapses in the Autonomic Sympathetic Neurons Project to neural networks of the ENS. This inactivates the neural cir- the Gut From Thoracic and Upper Lumbar cuits that generate intestinal motor behavior. Activation of Segments of the Spinal Cord the sympathetic inputs allows only continuous discharge of inhibitory motor neurons to the nonsphincteric muscles. Sympathetic innervation to the gut is located in thoracic The overall effect is a state of paralysis of intestinal motility and lumbar regions of the spinal cord (Fig. Efferent this state occurs transiently, it is called physiological ileus sympathetic fibers leave the spinal cord in the ventral roots and, when it persists abnormally, is called paralytic ileus. The prevertebral ganglia are the celiac, superior mesen- Splanchnic Nerves Transmit Sensory Information teric, and inferior mesenteric ganglia.

The aura of neurological symptoms and/or signs in migraine is thought to be caused by a vascular or a neuronal mechanism trusted cialis super active 20mg erectile dysfunction diet pills, or a combination of the two buy cialis super active 20mg visa erectile dysfunction and diabetic neuropathy. One theory suggests that changes in the vasculature are responsible for causing migraine whereas a second theory proposes that the vascular changes only mediate the pain and symptoms of migraine. A third theory suggests the primary abnormality is neuronal and originates within the brain itself. The original hypothesis was that vasoconstriction of intracranial vessels leads to a reduced blood flow, which results in cerebral hypoxia. Wolff, who proposed this idea, stated that following the vasoconstriction of the cranial vessels, vasodilatation of these vessels occurred which gave rise to the pain (via the stretching of nerve endings in the vascular walls), and which also resulted in a change in regional cerebral blood flow. There are some weaknesses in the theory that the primary problem is within the vasculature. As the progression of the symptoms does not respect vascular territories it is unlikely to be primarily due to spasm within the vasculature. The blood flow changes are more consistent with a primary neuronal event causing secondary vascular changes. Another factor that makes the theory of a primary vascular abnormality untenable is that the headache may begin while cortical blood flow is still reduced. A related idea is that peripheral nerves are the source of the problem and then cause the associated vascular changes via release of 5-HT and other inflammatory mediators. Here, the primary abnormality is 458 NEUROTRANSMITTERS, DRUGS AND BRAIN FUNCTION within the brain itself, a spreading decrease in electrical activity, that moves at a rate of 2±3 mm/min from the site of origin across the cortex. This transient wavefront suppresses both evoked and spontaneous neuronal activity. In spreading depression, the depolarisation is limited to one hemisphere, and there is a refractory period for further spreading depression of up to 3 min. Any decrease in neuronal firing leads to an increase in metabolism which would result in a decrease in rCBF, via autoregulation. Stimulation of the presynaptic inhibitory 5-HT1D receptors on trigeminal Ad-fibres inhibits the release of calcitonin gene related peptide (CGRP) which on release forms peripheral ends of sensory fibres via the antidromic axon reflex, causes vasodilatation. Direct attenuation of the excitability of neurons in the trigeminal nuclei, as 5-HT1B/ 5-HT1D receptors on pain transmission neurons in the trigeminal nucleus caudalis and in the upper cervical cord, are activated. Stimulation of these receptors is caused by second-generation triptans that cross the blood±brain barrier such as zolmitriptan, naratriptan, rizatriptan and eletriptan. Direct vasoconstriction is mediated by the stimulation of vascular 5-HT1B receptors. These receptors are also found systemically, so coronary arteries also undergo vaso- constriction. Sumatriptan constricts cerebral arteries, but if the vasculature is normal, this does not affect rCBF. Mast cells, as well as releasing 5-HT, can also release histamine which causes vaso- dilatation, oedema and itch and ATP and adenosine are also involved in inflammatory conditions. Substance P and CGRP released from the peripheral terminals of primary afferents (via axon reflex) can also cause the mast cells to degranulate and release 5-HT. The peptides cause a number of effects including vasodilatation, plasma extravasation and mast cell degranulation and ATP can result in a direct nociceptor activation via activation of P2X receptors. Other factors such as Nerve Growth Factor (NGF) and cytokines are also important at the peripheral level and resultant changes in the phenotype of the sensory neurons have been shown to be one of the resultant effects. Thus, NGF is upregulated in the area of tissue damage and then binds to its high- affinity receptor, the trkA receptor, one of the tyrosine kinase family. NGF and the receptor are then internalised and transported to the cell body in the dorsal root ganglion. Here, there is a resultant change in gene expression so that the gene for pre- pro tachykinins is turned on. Thus tissue damage causes complex changes in the transduction of painful stimuli. NERVE DAMAGE Neuropathic pain states are thought to be generated in the peripheral sensory neurons by events within the nerve itself and so are independent of peripheral nociceptor activation. Damage to peripheral nerves can be caused by a number of pathological, metabolic and viral causes. According to the terminology guide of the International PAIN AND ANALGESIA 459 Figure 21.

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Stratified epithelia have a primarily evidence indicates that sperm introduced into the female protective function that is enhanced by rapid cell divisions cialis super active 20mg sale erectile dysfunction milkshake. They vagina during sexual intercourse may be moved along the return cur- rents cheap cialis super active 20 mg with amex male erectile dysfunction pills, or eddies, generated by ciliary movement. This greatly en- are classified according to the shape of the surface layer of cells, hances the likelihood of fertilization. Pseudostratified Ciliated Columnar Epithelium Stratified Squamous Epithelium As the name implies, this type of epithelium has a layered ap- pearance (strata = layers). Actually, it is not multilayered (pseudo Stratified squamous epithelium is composed of a variable number = false), because each cell is in contact with the basement mem- of cell layers that are flattest at the surface (fig. Histology © The McGraw−Hill Anatomy, Sixth Edition of the Body Companies, 2001 84 Unit 3 Microscopic Structure of the Body Larynx Trachea Bronchiole Lung Secondary bronchi (b) (b) Cilia Goblet cell Bronchus Nucleus (a) Basement membrane Connective tissue (c) FIGURE 4. Uterine tube Ovary Uterus Urinary bladder Cervix Urethra Rectum Vagina Anus (b) (a) Stratified squamous epithelium (c) FIGURE 4. In the moistened areas, such as in the vagina (a), it is nonkeratinized, whereas in the epidermis of the skin it is keratinized. Histology © The McGraw−Hill Anatomy, Sixth Edition of the Body Companies, 2001 Chapter 4 Histology 85 Parotid gland Nuclei Lumen of parotid duct Basement (b) membrane (c) Parotid duct (a) FIGURE 4. Stratified Cuboidal Epithelium As the newly produced cells grow in size, they are pushed toward Stratified cuboidal epithelium usually consists of only two or the surface, where they replace the cells that are sloughed off. This type of epithelium is Movement of the epithelial cells away from the supportive base- confined to the linings of the large ducts of sweat glands, salivary ment membrane is accompanied by the production of keratin (ker′a˘- glands, and the pancreas, where its stratification probably pro- tin) (described below), progressive dehydration, and flattening. There are two types of stratified squamous epithelial tis- sues: keratinized and nonkeratinized. Keratinized stratified squamous epithelium contains ker- atin, a protein that strengthens the tissue. Keratin makes Transitional epithelium is similar to nonkeratinized stratified the epidermis (outer layer) of the skin somewhat waterproof squamous epithelium except that the surface cells of the former and protects it from bacterial invasion. The outer layers of are large and round rather than flat, and some may have two nu- the skin are dead, but glandular secretions keep them soft clei (fig. Nonkeratinized stratified squamous epithelium lines the permit distension (stretching) of the urinary bladder as it fills oral cavity and pharynx, nasal cavity, vagina, and anal with urine. This type of epithelium, called mucosa (myoo-ko′sa˘), being rounded when the urinary bladder is empty to being some- is well adapted to withstand moderate abrasion but not what flattened as it distends with urine. The cells on the exposed surface are alive and are A summary of membranous epithelial tissue is presented in always moistened. Stratified squamous epithelium is the first line of defense against the entryof living organisms into the body. Stratification, Body Membranes rapid mitotic activity, and keratinization within the epidermis of the skin are important protective features. An acidic pH along the surfaces of Body membranes are composed of thin layers of epithelial tissue this tissue also helps to prevent disease. Body membranes cover, separate, and sup- gion is about 6, and the pH along the vaginal lining is 4 or lower. The two basic types of body membranes, mucous membranes and serous membranes, are described in detail in chapter 2 under the heading “Body keratin: Gk. Histology © The McGraw−Hill Anatomy, Sixth Edition of the Body Companies, 2001 86 Unit 3 Microscopic Structure of the Body Ureter (b) Urinary bladder (b) Lumen of urinary bladder Transitional epithelium Urethra Smooth muscle tissue (a) (c) FIGURE 4. Histology © The McGraw−Hill Anatomy, Sixth Edition of the Body Companies, 2001 Chapter 4 Histology 87 Secretion Lumen Mucus Liver Cell membrane Stomach Gallbladder Golgi complex Large intestine Small intestine Nucleus of goblet cell Rough endoplasmic reticulum Creek (a) (b) (c) FIGURE 4. Multicellular glands, as their name implies, are composed of both secretory cells and cells that form the walls of the As tissues develop in the embryo, tiny invaginations (infoldings) ducts. Multicellular glands are classified as simple or com- or evaginations (outfoldings) of membranous epithelia give rise to pound glands. The ducts of the simple glands do not specialized secretory structures called exocrine (ek′so˘-krin) glands.

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Phospholipase C calcium synergizes with the action of DAG in the activa- (PLC) catalyzes the breakdown of PIP2 to inositol trisphosphate tion of some forms of protein kinase C and may also acti- (IP ) and diacylglycerol (DAG) cheap cialis super active 20mg free shipping new erectile dysfunction drugs 2014, which are used for signaling and 3 vate many other calcium-dependent processes buy 20 mg cialis super active mastercard erectile dysfunction doctors in coimbatore. Mechanisms exist to reverse the effects of DAG and IP3 B, The generation of IP3 and DAG and their intracellular signaling by rapidly removing them from the cytoplasm. The binding of hormone (H) to a G-protein-coupled receptor dephosphorylated to inositol, which can be reused for phos- (R) can lead to the activation of PLC. The DAG is converted to phospha- Gq, 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. Lowering cytosolic calcium • It binds directly to an effector molecule, such as protein concentrations shifts the equilibrium in favor of the release kinase C, to participate in its activation. Calmodulin then dissociates • It binds to an intermediary cytosolic calcium-binding from the various proteins that were activated, and the cell protein, such as calmodulin. Calmodulin is a small protein (16 kDa) with four bind- ing sites for calcium.

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