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Active transport always moves solute ance and a decreased capacitance associated with the against its electrochemical gradient buy 100mg lady era. All the other op- myelinated regions of the axon generic lady era 100mg with visa, both of which pro- tions are shared by both active transport and equili- mote the electrotonic spread of the positive charge brating carrier-mediated transport systems order 100 mg lady era otc. Nongated ion channels available at the terminals discount lady era 100mg without a prescription, using enzymes that reside in are not involved in the generation of action potential purchase 100mg lady era with amex. Myelin contributes substantially to by ribosomes, which are not found in axons or termi- the effective membrane resistance, Rm. The supply of peptide transmitters in the axon stant increases as Rm increases because it is more diffi- terminal must be continuously replenished via axoplas- cult for ions to flow across the membrane relative to mic transport from the cell body. When essential component of axoplasmic transport; disrupt- an axon demyelinates, its space constant decreases and ing their integrity would diminish axonal transport and conduction velocity is slowed. GABA is the major inhibitory trans- deficits associated with multiple sclerosis. Activity of the GABA system sponsible for docking and binding synaptic vesicles to is widespread in the brain, and a disruption of GABA the presynaptic membrane to prepare them for release. The acute onset of symptoms in both tion of SNARES has no direct effect on other compo- people suggests food poisoning and not a chronic dis- nents of neurochemical transmission, including action order or a stroke. A toxin that blocked nerve-muscle potential propagation, transmitter-receptor interac- transmission would produce muscle paralysis or weak- tion, or uptake mechanisms. Spatial summation of synaptic poten- suggests abnormally high excitability and firing of sen- tials can occur if they are close enough that the space sory nerves. Ciguatera toxin, the product of a dinofla- constant spans the two synapses; therefore, properties gellate that sometimes contaminates red snapper and of the cell that increase the space constant would opti- other reef fishes, is probably the cause of the sensory mize the effectiveness of the two synapses. Ciguatera constant increases with increasing membrane resist- toxin binds to voltage-gated sodium channels and re- ance or decreasing cytoplasmic resistance. Temporal summation could also increase the conduction velocity because the action potential will effectiveness of the two synapses; this would be facili- no longer “jump” from node to node. Acetylcholinesterase is the enzyme tentials) will be more spread out and will have a slower that breaks acetylcholine down into acetate and rate of rise than normal. Blocking the function of opening of voltage-gated calcium channels and entry acetylcholinesterase would prevent the breakdown of of extracellular calcium into the nerve terminals. Defi- ACh, which would accumulate in the cleft because cient acetylcholine release by motor nerve terminals there is no uptake mechanism for ACh and it diffuses could explain muscle weakness. Catecholaminergic transmission is ef- polarization phase of the nerve action potential de- ficient, in part, because there is a significant reuptake pends on voltage-gated potassium channels. The of the catecholamines for repackaging into synaptic upstroke of the nerve action potential depends on volt- vesicles to use again. Nerve excitability (and, in the cleft and do not aid in the removal of the cate- hence, nerve firing) is affected by extracellular calcium cholamines from the cleft. The postsynaptic cell may concentration (hypocalcemia results in increased ex- have an uptake mechanism (not endocytosis) for the citability), but this is because of an effect on sodium catecholamines, but the efficacy of this mechanism is channels, not calcium channels. Dopamine plays a major role in two Chapter 4 functional systems of the brain, the motor system and the limbic system. Too much dopaminergic trans- is encoded in the action potential frequency. Cessation mission can result in psychotic disorders, such as schiz- of the stimulus would lead to a rapid decrease in the ac- ophrenia. A blockade of dopaminergic transmission tion potential frequency, and adaptation of the recep- ameliorates psychosis. Cholinergic transmission is in- tor would also lead to a decrease in frequency. The constant and maintained stimulus, at least some adap- role of nitrergic transmission in cognition and behav- tation would take place, and the frequency would fall ior is unknown. Most neurotransmitters are synthe- tential velocity is a property of the nerve—not the re- sized locally within the axon terminals from precursors ceptor—and it would not be affected. Rods and cones are absent from the tended limb are best sensed by receptors that adapt area of the retina where the optic nerve exits. Likewise, sensors that adapt quickly would not blind spot is of appreciable size, but because its loca- be well suited for detecting the continued presence of tion is off-center and the eyeballs are mirror images, a chemical stimulus. Reduction in the intensity of a sensa- cause nerves are exiting there and do not make tion is largely the result of a decline in the generator synapses.

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In reality this presents a problem because overstimulation of the receptor could not only increase neuronal function up to convulsive level but even cause neurotoxicity discount lady era 100 mg free shipping. Briefly cheap lady era 100mg online, NMDA applied to rat cortex causes retrograde degeneration of cholinergic neurons in nucleus basalis while NMDA antagonists prevent anoxic destruction of cultured hippocampal neurons and brain damage caused by cerebral vascular occlusion in rodents discount lady era 100mg online. The ischaemia the latter produces causes such an excessive neuronal discharge and release of glutamate that the intense activation of NMDA receptors produces a prolonged neuronal depolarisation cheap lady era 100 mg without a prescription, Ca2‡ entry and cell death generic lady era 100mg with amex. Possibly a weak partial NMDA agonist, or a drug acting at one of the NMDA receptor subsites (see Chapter 10) like that for glycine, may be of some value. GABA Although there is no neuropathological evidence to implicate GABA in AzD it is known that agonists at the benzodiazepine receptor site not only augment GABA function but also cause amnesia. So it is possible that an inverse agonist, or perhaps even an antagonist, for the benzodiazepine receptor could have the opposite effect and improve memory. In humans, one antagonist, the b carboline derivative ZK93426, showed some improvement in learning and memory tests. It also improves acquisition in animal-learning tests and counteracts the impairment caused by scopolamine, as does the b-carboline inverse agonist DMCM. The fear of inducing anxiety or even convulsions with inverse benzodiazepine agonists has prompted the evaluation of partial inverse agonists (see Abe, Takeyama and Yoshimura 1998). OTHER NTs There have been few attempts to manipulate the monoamines in AzD and those using selegiline, the MOAB inhibitor, have shown little effect although the 5-HT3 antagonist, ondansetron, may give a slight improvement. Despite the clear loss of somatostatin in AzD a synthetic analogue L-363586 had no beneficial effect on memory loss. ATTENUATION OF DEGENERATION Even if NT manipulation had provided an effective therapy in AzD it would still be important to stop the progression of degeneration and the disease process itself. The activity of b-amyloid might be reduced by: (a) stopping its production by reducing the phosphorylation and proteolysis of APP (b) increasing its breakdown (c) counteracting its toxic effects through plaque formation APP is normally cleaved within the Ab sequence by an unidentified protease, so- called a-secretase, so that most of the extracellular APP is released in a soluble form into the extracellular fluid (see Checler 1995). When b-amyloid is formed another protease (b) splits APP so that the complete Ab sequence persists at the extracellular end of the remaining membrane and intracellular APP chain. This is then cleaved by anaother protease (g-secretase) to release the b-amyloid (Fig. 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). The b-amyloid (Ab4) sequence is partly extracellular and partly in the membrane. 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.

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It is best to jot down only important key words or phrases that help you recon- struct the conversation later 100 mg lady era with amex. Most people speak at approx 125 words per minute but are capable of assimilating approx 500 spoken words per minute buy lady era 100 mg free shipping. The extra time is often used to think about something other than what the speaker is saying lady era 100mg amex. Communica- tion is more effective if you focus only on what is being said discount lady era 100mg without a prescription. Listening Skills Patients often base their assessment of a physician’s competence more on communication skills than clinical talent purchase 100 mg lady era visa. Some doctors have the ability to make each patient feel that whatever the patient is saying is the most important thing he or she has heard all day. Other physicians who may be just as qualified may appear impatient or uninterested. Experts on effective communication agree on the following simple rules for avoiding misinterpretation. This technique informs the speaker whether or not his or her message is being heard and understood. This is accom- plished by asking questions, making statements, or offering visual cues that indicate your understanding and degree of concurrence. By remaining silent when a patient is speaking, you are less likely to be preparing or rehearsing your response while listening. For example, a too-relaxed posture can reflect disinter- est, whereas arms crossed in front of your body often signals defensive- ness. Some doctors avoid sitting behind a desk to remove a semblance of a barrier. If you lean forward slightly and look at the patient while he or she speaks, your nonverbal communication says, “I’m interested in what you have to say. SPEAKING: VERBAL AND NONVERBAL EXPRESSION After listening to the patient, you need to respond. Tempo of Speech and Tone of Voice Some physicians have a tendency to speak rapidly or to economize on words. Often, the stress that physicians experience in their daily practice is reflected unconsciously in their tone of voice. For example, the phrase, “You should have called me,” can be said in an empathic, solicitous manner or in an impatient, accusatory way. The effect that these two styles have on a patient can differ dramatically. Pause for Assimilation and Feedback When your message is complex, pause frequently, even if you do not sense confusion in the listener. A break in speech allows patients to either digest what you are saying or ask for clarification. The resulting dialogue reinforces the patients’ feeling that they are participating in their health care. Most patients will interpret this question for what it is—a sincere interest in their welfare. One of the best ways to ensure that explanations or instructions are understood is to ask patients to repeat what they have just been told. Explaining that you want to ensure their well-being can dispel the notion that you are being condescending. You might want to give the example that “50” and “15” sound very similar, but the numbers can literally spell the difference between life and death when they represent milligrams prescribed for a potent drug. Chapter 6 / Communication and Patient Safety 69 TAILOR YOUR LANGUAGE One of the most common complaints in patient attitude surveys has to do with physicians’ use of complex terminology or medical jargon. There is a substantial choice of words available for communicating with patients according to their intellectual and educational level. Whereas physicians define the stomach as a specific organ, patients complaining of a “stomach ache” might be referring to an indefinite area from the ribs to the pubis.

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Hypothalamic CRH stimulates ACTH release from corti- the ovaries and testes generic 100mg lady era fast delivery. This Tsecretes an array of peptide hormones that have im- important functional connection between the brain and the portant actions on almost every aspect of body function buy discount lady era 100mg line. Others bring about changes in body function cheap 100 mg lady era mastercard, which enable the individual to grow lady era 100 mg cheap, reproduce buy 100 mg lady era amex, and re- HYPOTHALAMIC-PITUITARY AXIS spond appropriately to stress and trauma. The pituitary hormones produce these physiological effects by either The human pituitary is composed of two morphologically acting directly on their target cells or stimulating other en- and functionally distinct glands connected to the hypo- docrine glands to secrete hormones, which, in turn, bring thalamus. The pituitary gland or hypophysis is located at about changes in body function. It sits in a depression in the sphenoid bone of may originate within or outside the body. The two morphologically perceived and processed by the brain, which signals the pi- and functionally distinct glands comprising the human pi- tuitary gland to increase or decrease the rate of secretion of tuitary are the adenohypophysis and the neurohypophysis a particular hormone. The adenohypophysis consists of the pars tu- gland to events occurring within or outside the body, beralis, which forms the outer covering of the pituitary 581 582 PART IX ENDOCRINE PHYSIOLOGY Neurohypophysis Adenohypophysis mone are then released into the nearby capillary circulation, from which they are carried into the systemic circulation. Median eminence Pars Pars tuberalis distalis (anterior lobe) Anterior Pituitary Hormones Are Synthesized Infundibular and Secreted in Response to Hypothalamic stem Releasing Hormones Carried in the Hypophyseal Portal Circulation Infundibular The anterior lobe contains clusters of histologically distinct process (posterior lobe) types of cells closely associated with blood sinusoids that drain into the venous circulation. These cells produce ante- rior pituitary hormones and secrete them into the blood si- Pars nusoids. The six well-known anterior pituitary hormones intermedia are produced by separate kinds of cells. In most vertebrates, the pituitary contains a third leasing hormones, also called hypophysiotropic hor- anatomically distinct lobe, the pars intermedia or interme- mones, synthesized by neural cell bodies in the hypothal- diate lobe. Granules containing releasing hormones are stored diate lobe is found as a thin diffuse region of cells between in the axon terminals of these neurons, located in capillary the anterior and posterior lobes. The adenohypophysis is give rise to the principal blood supply to the anterior lobe formed from an evagination of the oral ectoderm called of the pituitary. The neurohypophysis forms as an exten- The blood supply to the anterior pituitary is shown in sion of the developing hypothalamus, which fuses with Figure 32. Arterial blood is brought to the hypothalamic- Rathke’s pouch as development proceeds. The posterior pituitary region by the superior and inferior hypophyseal lobe is, therefore, composed of neural tissue and is a func- arteries. The superior hypophyseal arteries give rise to a tional part of the hypothalamus. The capil- laries converge into long veins that run down the pituitary Posterior Pituitary Hormones Are Synthesized stalk and empty into the blood sinusoids in the anterior by Hypothalamic Neurons Whose Axons lobe. They are considered to be portal veins because they deliver blood to the anterior pituitary rather than joining Terminate in the Posterior Lobe the venous circulation that carries blood back to the heart; The infundibular stem of the pituitary gland contains bun- therefore, they are called long hypophyseal portal vessels. They also penetrate into the lower in- of neurons that originate in the supraoptic nuclei and par- fundibular stem, where they form another important capil- aventricular nuclei of the hypothalamus. The capillaries of this network converge into these neurons are large compared to those of other hypo- short hypophyseal portal vessels, which also deliver blood thalamic neurons; hence, they are called magnocellular neu- into the sinusoids of the anterior pituitary. The hormones arginine vasopressin (AVP) and oxy- blood supply to the anterior lobe of the pituitary gland is tocin are synthesized as parts of larger precursor proteins known as the hypophyseal portal circulation. Prohor- When a neurosecretory neuron is stimulated to secrete, mones are then packaged into granules and enzymatically the releasing hormone is discharged into the hypophyseal processed to produce AVP and oxytocin. Releasing hormones travel transported down the axons by axoplasmic flow; they accu- only a short distance before they come in contact with their mulate at the axon terminals in the posterior lobe. Only the amount of releas- Stimuli for the secretion of posterior lobe hormones may ing hormone needed to control anterior pituitary hormone be generated by events occurring within or outside the secretion is delivered to the hypophyseal portal circulation body. These stimuli are processed by the central nervous by neurosecretory neurons. Consequently, releasing hor- system (CNS), and the signal for the secretion of AVP or mones are almost undetectable in systemic blood. Secretory granules containing the hor- synthesis and secretion of a particular anterior pituitary CHAPTER 32 The Hypothalamus and the Pituitary Gland 583 M hormone. Corticotropin-releasing hormone (CRH), thy- rotropin-releasing hormone (TRH), and growth hor- 2 Hypothalamus mone-releasing hormone (GHRH) stimulate the secretion Third and synthesis of ACTH, TSH, and GH, respectively ventricle (Table 32. Luteinizing hormone-releasing hormone 1 (LHRH), also known as gonadotropin-releasing hormone Superior (GnRH), stimulates the synthesis and release of FSH and hypophyseal LH. In contrast, somatostatin, also called somatotropin artery release inhibiting factor (SRIF), inhibits GH secretion.

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