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Regulation of GAD Of key importance in the synthesis of GABA is the short-term regulation of GAD activity cheap accutane 10mg with mastercard. Increasing the availability of glutamate does not lead to an increase in the production of GABA cheap 30mg accutane mastercard,suggesting that GAD may normally be saturated with its substrate 40mg accutane amex. GAD exists in two states; an inactive apoenzyme (apoGAD) lacking the co-factor and active 228 NEUROTRANSMITTERS order 5 mg accutane free shipping,DRUGS AND BRAIN FUNCTION Figure 11 order accutane 30 mg visa. GABA produced by both GAD67 and GAD65 can be used as a neurotransmitter but GAD65 is preferentially associated with synaptic vesicles. Synaptically released GABA is recovered into neurons and glia by GABA transporters (not shown is the possible release of GABA by reversal of these transporters). Glutamine produced in glial cells is exported to neurons and converted to glutamate (after Soghomonian and Martin 1998) holoenzyme (holoGAD) complexed with PLP. During the synthetic process GAD can undergo cycles of interconversion between these states. Traditionally,two processes have been considered important with respect to the regulation of GAD. First,GABA may promote conversion of GAD from its active to its inactive state,and so cause feedback inhibition of GABA synthesis. Second,ATP appears to inhibit,while inorganic phosphate promotes,the reactivation of GAD by PLP. During periods of increased neuronal activity,when the consumption of ATP increases,a rise in the level of phosphate should stimulate the conversion of inactive to active GAD,thereby increasing GABA synthesis. More recently,it has been suggested that soluble and membrane-bound forms of GAD may be differentially regulated. The soluble form of GAD is activated by a phosphatase that causes dephosphorylation while the membrane-bound form is activated following phosphorylation by a vesicular protein kinase (Hsu et al. Active GAD (GAD-PLP) combines with glutamate (1) to form a complex (GAD-PLP±GLU). PMP dissociates from GAD (5) leaving inactive enzyme,which requires additional PLP to be reactivated (6),a process that is affected by ATP and inorganic phosphate Two isoforms of GAD In addition to the inactive and active states of GAD,there are two distinct forms of the enzyme. The two isoforms,GAD67 and GAD65,named for their respective molecular masses ($67 and $65 kDa),are encoded by separate,independently regulated genes, GAD1 and GAD2 (Erlander et al. GAD67 and GAD65 differ substantially in their amino-acid sequence,their interaction with PLP,their kinetic properties,and their regulation (Soghomonian and Martin 1998). Individual cells contain both forms of GAD but the ratio of the two differs among different neuronal populations. GAD65 is located preferentially in nerve terminals,both in the cytosol and as a membrane-bound form closely associated with synaptic vesicles into which the newly synthesised GABA is accumulated (see below). GAD65,unlike GAD67,is not saturated with PLP and forms the majority of the apoenzyme present in brain (about half of the total GAD). This has led to the view that a proportion of GAD65 exists as a pool of inactive enzyme,ready to combine with PLP in response to cellular signals for increased GABA synthesis. Further insights into the role of GAD isoforms in the synaptic release of GABA have been provided by the techniques of gene manipulation. Mice lacking the GAD67 gene have a greatly reduced level of brain GABA (Asada et al. The neurological significance of this reduction is difficult to ascertain: GABA appears essential for the normal development of the palate and one consequence of the reduced production in GABA in these mice is a cleft palate that is responsible for their death soon after birth. In contrast, mice lacking the GAD65 gene show only a modest reduction in total brain GABA but exhibit spontaneous seizures and a greater susceptibility to chemical convulsants (Asada et al. In these mice basal GABAergic transmission is normal but GABA release during sustained synaptic activation is reduced (Obata et al. Together these results suggest that GAD67 is responsible for the synthesis of 230 NEUROTRANSMITTERS,DRUGS AND BRAIN FUNCTION most brain GABA,but GAD65 is intimately involved in synthesis of GABA required for the refilling of the releasable pool of synaptic vesicles. Inhibitors of GAD Several drugs are known to inhibit GAD,either directly or through interaction with the co-factor PLP. The largest group of inhibitors are the hydrazides,such as isoniazid, semicarbazide and thiosemicarbazide. These are carbonyl-trapping agents that react with the aldehyde group of PLP; as many other enzymes use PLP as a co-factor,these agents are not specific for GAD. Two other agents,allylglycine and 3-mercaptopropionic acid, are competitive inhibitors of GAD.

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Acute called continuous ambulatory peritoneal dialysis (CAPD) accutane 30mg with visa, can be renal failure is the sudden loss of kidney function caused by performed several times a day by the patients themselves on an shock and hemorrhage discount accutane 40mg otc, thrombosis generic accutane 5mg on line, or other physical trauma outpatient basis generic accutane 10mg fast delivery. Urinary System © The McGraw−Hill Anatomy order 30mg accutane amex, Sixth Edition Body Companies, 2001 694 Unit 6 Maintenance of the Body Urinary Incontinence The inability to voluntarily retain urine in the urinary bladder is Clinical Case Study Answer known as urinary incontinence. It has a number of causes and may The hematuria experienced by the patient is probably the result of lacer- be temporary or permanent. Emotional stress is a cause of tempo- ation caused by the upper abdominal knife wound. Permanent incontinence may result quadrant stab most likely did not violate the urinary tract. The course of blood seen in the catheter begins and proceeds as follows: abdominal from neurological trauma, various urinary diseases, tissue damage aorta → right renal artery → smaller parenchymal artery → through the within the urinary bladder or urethra, or weakness of the pelvic lacerated vessel(s) → into the lacerated urinary collecting system, either floor muscles. Remarkable advances have been made in treating at the calyx or the renal pelvis or proximal right ureter → urinary blad- permanent urinary incontinence through the implantation of an der → into catheter. During the operation, the surgeon should keep in artificial urethral sphincter. If, therefore, she is prompted to remove the damaged kidney, she should first confirm the presence of a second functioning kidney. If a second kidney is not present, every effort should be made to correct the prob- lem without performing a nephrectomy, which would consign the pa- tient to chronic hemodialysis or kidney transplant. A routine urinalysis reveals red blood cells too numerous to count, no white blood cells, and no bacte- ria. You order an intravenous urogram (IVU) (a), which is an injection of intravenous con- trast material for an exam of the urinary sys- tem, and CT scan (b). What is the large dark mass (filling defect) seen in the urinary bladder (indicated with the letter B) on the IVU? On the CT, white contrast fills the lumen of the urinary bladder (indicated with an arrow). Synchronous tumors are tumors of the (a) same cell type occuring at the same time in separate locations. Urinary System © The McGraw−Hill Anatomy, Sixth Edition Body Companies, 2001 Chapter 19 Urinary System 695 CLINICAL PRACTICUM 19. She describes the pain as intermittent and crampy, but de- nies any fever or blood in her urine. Physical exam shows a nontender ab- domen and no evidence of costovertebral angle tenderness. Routine urinalysis shows minimal red blood cells, no white blood cells, and no bacteria. What effect does this have on the ureter as demonstrated by the postcontrast image? Precontrast image Postcontrast image Chapter Summary Introduction to the Urinary System 3. The end product of the deliver blood to peritubular capillaries which is folded into rugae. These urinary system is urine, which is voided surrounding the nephron tubules. Each kidney is contained by a renal tubules are drained into papillary during ejaculation. The female capsule and divided into an outer renal ducts that extend through the renal urethra is much shorter than that of a cortex and an inner renal medulla. Micturition is controlled by reflex centers the minor calyces and then into the major calyces, which drain into the 1. Urine is channeled from the kidneys to in the second, third, and fourth sacral renal pelvis. From there, urine flows the urinary bladder by the ureters and segments of the spinal cord. Urinary System © The McGraw−Hill Anatomy, Sixth Edition Body Companies, 2001 696 Unit 6 Maintenance of the Body Review Activities Objective Questions (c) the urinary bladder. Which of the following statements about development process lead to a better concave medial border of the kidney metanephric kidneys is true? List four common congenital (c) They are the third pair of kidneys to malformations of the urinary system. Essay Questions pyuria, oliguria, polyuria, uremia, and (d) adipose capsules.

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TRYPTAMINE Although tryptamine can be detected in brain there has been much debate over whether it exists separately from 5-HT or merely co-exists with it order 40mg accutane with mastercard. Specific high-affinity binding sites have been demonstrated for tryptamine in rat cortex discount accutane 10mg mastercard. These appear to be different from 5-HT sites but until appropriate antagonists are found it remains possible that they form a subset of the ever-increasing number of 5-HT receptors (see Chapter 9) discount 40 mg accutane with mastercard. The behavioural response in rats to tryptophan plus a MAO inhibitor (Grahame-Smith 1971) is accompanied by an elevation of brain tryptamine as well as 5-HT and is less marked if the synthesis of tryptamine is reduced by a decarboxylase inhibitor that does not have a significant effect on 5-HT levels discount accutane 40mg with visa. In fact after a MAOI buy accutane 40mg mastercard, tryptamine produces a behavioural response in rats similar to that of tryptophan apart from the absence of certain features like tremor and wet-dog shake. The complexity of the situation is illustrated by studies of the effect of intra-hypothalamic injections of 5-HT and tryptamine on rat body temperature (Cox, Lee and Martin 1981). In these it was shown that 5-HT decreased temperature while tryptamine actually increased it but it was not possible to block one effect preferentially with a whole range of antagonists, despite 278 NEUROTRANSMITTERS, DRUGS AND BRAIN FUNCTION Figure 13. These are all formed by decarboxylation rather than hydroxylation of the precursors of the established monoamine neurotransmitters, dopamine and 5-HT. Also although it was the tryptamine and not the 5-HT response, which was abolished after destruction of 5-HT neurons with 5,7- dihydroxytryptamine and implies that tryptamine was releasing 5-HT, it was found that raphe (5-HT) neuron stimulation produces hyperthermia, like tryptamine, rather than hypothermia, like 5-HT. These opposing effects of tryptamine and 5-HT are also seen when they are applied directly to cortical neurons by iontopheresis. Surprisingly, the 5-HT antagonist metergoline is more effective against tryptamine and the depressant effects. When the medial Raphe nucleus OTHER TRANSMITTERS AND MEDIATORS 279 is stimulated this produces inhibition of cortical neurons followed by excitation but it is the inhibition (tryptamine-like) that is blocked by metergoline. In keeping with this finding is the observation that depletion of 5-HT with pCPA reduced only the excitatory (5-HT) response while 5,7-dihydroxytryptamine, which destroys the neurons, abolished both effects (see Jones 1983). The inference from these studies and those on temperature is that some neurons in the raphe nucleus release something other than 5- HT. This might be tryptamine but if it is not, then its effects are presumably modified by tryptamine. Possibly there is a subclass of 5-HT receptors that would be preferentially activated by tryptamine if its endogenous concentrations were ever adequate. PHENYLETHYLAMINE The relationship of phenylethylamine to dopamine is not unlike that of tryptamine to 5- HT. Present in low concentrations in the brain there is some evidence for distinct binding sites but not for specific neurons. When injected icv it causes stereotyped behaviour similar to, but more marked than, that seen with amphetamine. These effects are blocked by neuroleptics (DA antagonists) and since phenylethylamine does not bind directly to DA receptors it is assumed to release DA, like amphetamine. This is substantiated by the fact that in rats with unilateral 6-OHDA lesions of the SN its systemic administration causes ipsilateral rotation like amphetamine (see Chapter 6). Phenylethylamine certainly increases the overflow of [3H]-DA from striatal synapto- somes and slices and of endogenous DA in vivo, but part of this may be due to block of DA uptake. In any case such effects only occur with concentrations of 5  10À5 M, which are not likely to be encountered in vivo and it is not Ca2‡-dependent. Peripherally phenylethylamine causes contractions of the rat fundus just like amphetamine, tryptamine and 5-HT. These are reduced by some 5-HT antagonists, like methysergide, but not by DA antagonists. Thus some of its central effects may be mediated through a tryptamine receptor. Needless to say, the DA and amphetamine-like activity and structure of phenylethylamine, together with the facility for its synthesis in the CNS, has led to unproven suggestions of its involvement in schizophrenia. In fact there is some evidence for increased excretion of its metabolite (phenyl acetic acid) in the subgroup of paranoid schizophrenics. TYRAMINE p-Tyramine is produced by decarboxylation of tyrosine and is present in the CNS in higher (threefold) concentrations than m-tyramine, the hydroxylated derivative of phenylethylamine.

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