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The amygdala in the tem- bladder fullness is perceived is an example of higher CNS poral lobe coordinates the autonomic components of centers inhibiting a spinal cord reflex cheap kamagra oral jelly 100mg. Episodes of hypertension and piloerection volved with the control of autonomic functions are collec- in spinal cord injury patients are another example of unin- tively termed the central autonomic network (see Fig generic kamagra oral jelly 100 mg with visa. The Brainstem Is a Major Control Center for Autonomic Reflexes Insular cortex Areas within all three levels of the brainstem are important Cerebral hemisphere in autonomic function (Fig. The periaqueductal gray and hypothalamus matter of the midbrain coordinates autonomic responses to Hypothalamus painful stimuli and can modulate the activity of the sensory tracts that transmit pain. The parabrachial nucleus of the Amygdala pons participates in respiratory and cardiovascular control. The nu- Periaqueductal cleus of the tractus solitarius receives afferent input from gray matter Midbrain cardiac, respiratory, and gastrointestinal receptors. The ventrolateral medullary area is the major center for control of the preganglionic sympathetic neurons in the spinal cord. Neurons that Parabrachial control specific functions like blood pressure and heart rate Pons region are clustered within this general region. The descending paths for regulation of the preganglionic sympathetic and spinal parasympathetic neurons are not yet fully delineated. The Hypothalamus and Cerebral Hemispheres Provide the Highest Levels of Autonomic Control Spinal cord Intermediolateral The periventricular, medial, and lateral areas of the hy- horn pothalamus in the diencephalon control circadian rhythms, and homeostatic functions such as thermoregu- The central autonomic network. Because of the major role of cerebral, hypothalamic, brainstem, and spinal the hypothalamus in autonomic function, it has at times cord components. A hierarchy of reflexes initiated from these dif- been labeled the “head ganglion of the ANS. REVIEW QUESTIONS DIRECTIONS: Each of the numbered (A) Presynaptic axons that travel in the 2. Which effects would destruction of the items or incomplete statements in this oculomotor nerve lumbar paravertebral ganglia by a section is followed by answers or by (B) Postsynaptic axons that travel in gunshot cause in the ipsilateral leg? Select the the facial nerve (A) It would be cold and clammy ONE lettered answer or completion that is (C) Acetylcholine delivered by the (B) It would be weak BEST in each case. Impaired dilation of the pupil when paravertebral ganglia (D) It would be warm and dry entering a dark room is due to (E) Postsynaptic axons arising from (E) There would be no detectable deficient functioning of prevertebral ganglia change (continued) 118 PART II NEUROPHYSIOLOGY 3. Which of these is not a (E) There is no parasympathetic (B) Preganglionic to postganglionic neurotransmitter in the autonomic innervation to the sweat glands parasympathetic nervous system? Which statement correctly describes (C) Postganglionic axon-target tissue (A) Acetylcholine the relationship between preganglionic nicotinic (B) Norepinephrine and postganglionic sympathetic axons? A concurrent increase in receptors of the parasympathetic is much greater than the number of parasympathetic and decrease in postganglionic target tissue synapse presynaptic axons sympathetic outflow to the heart share general structural similarity? A patient who is being treated with a (D) Gray matter of the upper thoracic (E) The receptor at the neuromuscular medication complains of the adverse spinal cord junction effect of difficulty adjusting his eyes to (E) Reticular formation of the medulla 5. How is the medication supplied with parasympathetic modifying autonomic function? Philadelphia: Lippincott- paravertebral ganglion to cutaneous (C) Mimicking the action of Raven, 1997. Carpenter’s Human Neu- (B) Vagal preganglionics to (D) Inhibiting cholinergic activity roanatomy. Media, PA: prevertebral ganglion to cutaneous (E) Inhibiting adrenergic activity Williams & Wilkins, 1996. The activation of which type of Siegel GJ, Agranoff BW, Albers RW, (C) Spinal preganglionics to para- synapse could alter cyclic AMP levels Fisher SK, Uhler MD. Phila- (D) Spinal gray ramus to cutaneous (A) Preganglionic to postganglionic delphia: Lippincott Williams & nerve sympathetic Wilkins, 1999. The limbic system receives distributed monoaminergic and learning and memory. In most of the brain, capillary en- Tstimuli from the body and the outside world and dothelial cells are connected by tight junctions that prevent processes that information in neural networks or centers of substances in the blood from entering the brain. These integration to mediate an appropriate response or learned tight junctions are part of the blood-brain barrier.

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Unlike autonomic ganglia elsewhere in the body 100 mg kamagra oral jelly fast delivery, where they function mainly as relay-distribution centers for signals transmitted from the brain and spinal cord buy discount kamagra oral jelly 100 mg on line, enteric The Enteric Division of the ANS Functions as a ganglia are interconnected to form a nervous system with Minibrain in the Gut mechanisms for the integration and processing of informa- tion like those found in the CNS. This is why the ENS is The ENS is a minibrain located close to the effector sys- sometimes referred to as the “minibrain-in-the-gut. Effector systems of the digestive tract are the musculature, secretory glands, and blood vessels. Rather than crowding the vast numbers of neurons required Myenteric and Submucous Plexuses for controlling digestive functions into the cranium as part Are Parts of the ENS of the cephalic brain and relying on signal transmission over long and unreliable pathways, the integrative micro- The ENS consists of ganglia, primary interganglionic fiber circuits are located at the site of the effectors. The circuits tracts, and secondary and tertiary fiber projections to the CHAPTER 26 Neurogastroenterology and Gastrointestinal Motility 457 effector systems (i. These structural components of the ENS are inter- ing several seconds can be recorded in cell bodies of enteric laced to form a plexus. These synaptic events may be excitatory most obvious constituents of the ENS (see Fig. The postsynaptic potentials (EPSPs) or inhibitory postsynaptic myenteric plexus, also known as Auerbach’s plexus, is lo- potentials (IPSPs). They can be evoked by experimental cated between the longitudinal and circular muscle layers stimulation of presynaptic axons, or they may occur spon- of most of the digestive tract. Presynaptic inhibitory and facilitatory events known as Meissner’s plexus, is situated in the submucosal can involve axoaxonal, paracrine, or endocrine forms of region between the circular muscle and mucosa. The sub- transmission, and they occur at both fast and slow synaptic mucous plexus is most prominent as a ganglionated net- connections. Neurons in submucosal submucous plexus and applying electrical shocks to stimu- ganglia send fibers to the myenteric plexus and also receive late presynaptic axons and release the neurotransmitter at synaptic input from axons projecting from the myenteric the synapse. The interconnections link the two networks into a functionally integrated nervous system. Enteric Slow EPSPs Have Specific Properties Mediated by Metabotropic Receptors Sensory Neurons, Interneurons, and Motor The slow EPSP in Figure 26. The heuristic model for the ENS is the same as that for the Slowly activating depolarization of the membrane poten- brain and spinal cord (Fig. In fact, the ENS has as tial with a time course lasting longer than 2 minutes after many neurons as the spinal cord. Repetitive dis- rons, interneurons, and motor neurons in the ENS are con- charge of action potentials reflects enhanced neuronal ex- nected synaptically for the flow of information from sensory citability during the EPSP. The record shows hyperpolariz- neurons to interneuronal integrative networks to motor neu- ing after-potentials associated with the first four spikes of rons to effector systems. As the slow EPSP develops, the hyperpolarizing the activity of each effector system into meaningful behavior after-potentials are suppressed and can be seen to recover of the integrated organ. Bidirectional communication occurs at the end of the spike train as the EPSP subsides. Slow EPSPs are mediated by multiple chemical messen- SYNAPTIC TRANSMISSION gers acting at a variety of different metabotropic receptors. Multiple kinds of synaptic transmission occur in the micro- Different kinds of receptors, each of which mediates slow circuits of the ENS. Both fast synaptic potentials with du- synaptic-like responses, are found in varied combinations Central nervous system Enteric Effector nervous system systems Interneurons Muscle Sensory Reflexes Motor Secretory epithelium neurons FIGURE 26. Sensory Information processing neurons, interneurons, and motor neu- rons are synaptically interconnected to form the microcircuits of the ENS. As Gut behavior in the CNS, information flows from Motility pattern sensory neurons to interneuronal inte- Secretory pattern grative networks to motor neurons to Circulatory pattern effector systems. B, The fast EPSPs were SPs, fast EPSPs, and slow IPSPs all occur in en- also evoked by single electrical shocks applied to the axon that teric neurons. A, The slow EPSP was evoked by repetitive electri- synapsed with the recorded neuron. Two fast EPSPs were evoked cal stimulation of the synaptic input to the neuron. C, The slow IPSP was evoked by the stimula- During the slow EPSP, repetitive discharge of action potentials tion of an inhibitory input to the neuron. A common mode of signal trans- tatory motor neurons to the intestinal musculature or the duction involves receptor activation of adenylyl cyclase mucosa results in prolonged contraction of the muscle or and second messenger function of cAMP, which links sev- prolonged secretion from the crypts. The occurrence of eral different chemical messages to the behavior of a com- slow EPSPs in inhibitory motor neurons to the musculature mon set of ionic channels responsible for generation of the results in prolonged inhibition of contraction. Serotonin, substance P, and acetyl- sponse is observed as a decrease in contractile tension.

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It is lo- The medial muscles that move the hip joint include the gracilis cated deep to the other two adductor muscles order kamagra oral jelly 100 mg visa. The adductor pectineus purchase 100mg kamagra oral jelly fast delivery, adductor longus, adductor brevis, and adductor magnus longus, adductor brevis, and the adductor magnus are synergistic muscles (figs. Muscular System © The McGraw−Hill Anatomy, Sixth Edition Companies, 2001 278 Unit 4 Support and Movement TABLE 9. Tensor fasciae latae Anterior border of ilium and iliac crest Iliotibial tract Abducts thigh at the hip joint Superior gluteal n. Muscular System © The McGraw−Hill Anatomy, Sixth Edition Companies, 2001 Chapter 9 Muscular System 279 Patellar tendon FIGURE 9. The muscles that adduct the hip joint are summarized in Anterior, or Extensor, Muscles table 9. The anterior muscles that move the knee joint are the sartorius and quadriceps femoris muscles (fig. It can act the Knee Joint on both the hip and knee joints to flex and rotate the hip The muscles that move the knee originate on the pelvic girdle or laterally, and also to assist in flexing the knee joint and ro- thigh. They are surrounded and compartmentalized by tough fas- tating it medially. The sartorius is the longest muscle of the cial sheets, which are a continuation of the fascia lata and iliotib- body. These muscles are divided according to function and helps effect the cross-legged sitting position in which tailors position into two groups: anterior extensors and posterior flexors. Muscular System © The McGraw−Hill Anatomy, Sixth Edition Companies, 2001 280 Unit 4 Support and Movement FIGURE 9. The quadriceps femoris muscle is actually a composite of veloped buttock and shoulder muscles. The vastus medialis four distinct muscles that have separate origins but a common in- muscle occupies a medial position along the thigh. The four muscles of the quadriceps femoris muscle are the rectus femoris, vastus lateralis, vastus medialis, and vastus intermedius. Posterior, or Flexor, Muscles The rectus femoris muscle occupies a superficial position There are three posterior thigh muscles, which are antagonistic to and is the only one of the four quadriceps that functions in both the quadriceps femoris muscles in flexing the knee joint. The laterally positioned vastus lateralis muscles are known as the hamstrings (fig. It is a common The name derives from the butchers’ practice of using the tendons intramuscular injection site in infants who have small, underde- of these muscles at the knee of a hog to hang a ham for curing. Muscular System © The McGraw−Hill Anatomy, Sixth Edition Companies, 2001 Chapter 9 Muscular System 281 The biceps femoris muscle occupies the posterior lateral aspect of the thigh. It has a superficial long head and a deep short head, and causes movement at both the hip and knee joints. The superficial semitendinosus muscle is fusiform and is located on the posterior medial aspect of the thigh. The flat semimembranosus muscle lies deep to the semitendinosus on the posterior medial aspect of the thigh. The posterior thigh muscles that move the leg at the knee joint are summarized in table 9. The relative positions of the muscles of the thigh are illustrated in figure 9. The injury usually occurs when sudden lateral or medial stress to the knee joint tears the muscles or tendons. Because of its struc- ture and the stress applied to it in competition, the knee joint is highly susceptible to injury. Altering the rules in contact sports could reduce the incidence of knee injury. At the least, additional support and pro- tection should be provided for this vulnerable joint. Muscles of the Leg That Move the Joints of the Ankle, Foot, and Toes The muscles of the leg, the crural muscles, are responsible for the movements of the foot.

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Here kamagra oral jelly 100 mg line, the activation of opioid receptors on GABA neurons results in removal of GABA-mediated inhibition and so leads to facilitation cheap kamagra oral jelly 100 mg without a prescription. The four opioid receptors display in vivo binding preference for mu-endorphins and endomorphins, delta-enkephalins, kappa-dynorphin and ORL1-nociceptin/orphanin FQ (Table 12. These peptides are not completely selective for each type of receptor since the opioid peptides show a degree of sequence homology, although modified synthetic agonists are more selective. Investigation of mu receptor-mediated controls has been hampered by the lack of an endogenous ligand for the receptor in many areas, and in particular, within the spinal cord. Very recently, two peptides (endomorphin-1 and -2) have been isolated with high affinity and selectivity for m-opioid receptors, making it likely that they are the natural endogenous ligands for the receptor for morphine itself. Morphine acts on the mu receptor, and so do most of the clinically used opioid drugs. The detailed structure of these receptors has been described and we now have a reasonable understanding of their relative roles in physiological functions and in different pain states. The best-understood sites of action of morphine are at spinal and brainstem/ midbrain loci, producing both the wanted and unwanted effects of the opioid. The spinal actions of opioids and their mechanisms of analgesia involve (1) reduced transmitter release from nociceptive C-fibres so that spinal neurons are less excited by incoming painful messages, and (2) postsynaptic inhibitions of neurons conveying information from the spinal cord to the brain. At supraspinal sites, morphine can act to alter descending pathways from the brain to the cord which involve noradrenaline and serotonin and these pathways then act to reduce spinal nociceptive activity. In addition, these sites form a link between emotions, depression and anxiety, and the level of pain and analgesia in a patient. An intriguing area of research on opioids has been the accumulating evidence for plasticity in opioid controls. The degree of effectiveness of morphine analgesia is subject to modulation by other transmitter systems in the spinal cord and by pathological changes induced by peripheral nerve injury. Thus in neuropathic states, pain after nerve injury, morphine analgesia can be reduced (but can still be effective) and tactics other than dose-escalation to circumvent this will be briefly discussed in Chapter 21. Finally, there is little or no clinical evidence that morphine causes psychological dependence or drug-seeking behaviour, tolerance or problematic respiratory depression in patients. The reason is likely to be that the actions of morphine and the context of its use in a person in pain are neurobiologically quite different from the effects of opioids in street use. TACHYKININS These are a family of peptides which include substance P, isolated in 1931 but only sequenced in 1971. This peptide has been extensively studied since it was the first major peptide to be extracted from brain but only now are useful antagonists becoming available. Two closely related peptides were then isolated from mammalian tissues and can be added to a number of other tachykinins, many of which are found in amphibians. The name tachykinins originated from the vasoactive effects of substance P but the nomenclature has been resolved into calling the three major mammalian peptides substance P, neurokinin A (NKA) and neurokinin B (NKB) with the corresponding receptors being numbered 1 to 3. The order of potencies at the three receptors as follows: 260 NEUROTRANSMITTERS, DRUGS AND BRAIN FUNCTION NK1 receptor: SP 4 NKA 4 NKB NK2 receptor: NKA 4 NKB 4 SP NK3 receptor: NKB 4 NKA 4 SP The peptides have the following amino-acid sequences: SP: Arg±Pro±Lys±Pro±Gln±Gln±Phe±Phe±Gly±Leu±Met NKA: His±Lys±Thr±Asp±Ser±Phe±Val±Gly±Leu±Met NKB: Asp±Met±His±Asp±Phe±Phe±Val±Gly±Leu±Met A single gene gives rise to substance P but it can be produced from three different mRNAs derived from alternative splicing (a, b and g prepro-tachykinins). Neurokinin A has the same gene and shares two of the same mRNAs as substance P whereas neurokinin B has a different gene. High levels of the tachykinins are found in many parts of the CNS including the caudate, nucleus accumbens, olfactory bulb, colliculus and spinal cord. Early indications suggest that the peptide and its receptor play important roles in pain (see Chapter 21), inflammation and possibly stress, emesis, anxiety, depression and reward. This is generally backed up by studies with antagonists, although some of the early NK1 receptor antagonists lacked specificity and several blocked calcium channels. Coupling of the receptors is very similar with all three coupling to Gq and increasing IP3/DAG and in a number of neuronal systems it has been shown that the receptors produce slow depolarising responses via the closing of potassium channels. CHOLECYSTOKININ Cholecystokinin (CCK) and gastrin are members of a family that share a similar C- terminal sequence (Gly±Trp±Met±Asp±Phe), the biologically active end of the molecule. Early problems on the localisation of CCK stemmed from the overlap of antibodies with CGRP. There is now consensus that CCK-8 is the main transmitter in the CNS although larger forms, CCK-58 and 33, and smaller versions have been located (CCK-7, 5 and 4). Interestingly, CCK-8 is sulphated at the tyrosine residue: CCK-8: Asp±Tyr±SO3±Met±Gly±Trp±Met±Asp±Phe This peptide itself has no selectivity for the two CCK receptors, CCK-A and B, which have so far been established to stimulate IP3/DAG while, like substance P, can close potassium channels to increase neuronal activity.

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