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When directly com­ placements are associated with an antidepressant efficacy pared to ECT buy cialis jelly 20mg low price, 4 weeks of rTMS appears to be as effective comparable to standard bilateral placement buy cheap cialis jelly 20mg online, with fewer cog­ as ECT in nonpsychotic buy cialis jelly 20 mg low price, but not psychotic generic 20mg cialis jelly fast delivery, depression nitive side effects, but there are insufficient data thus far to (112). In this study there may have been a bias for the ECT recommend them as a replacement for standard BL or RUL group because over half of the patients in the ECT group placements (94,95). Two weeks of either RUL ECT or one ECT treatment followed by four rTMs NONCONVULSIVE STIMULI IN THE sessions were also shown to be equivalent in the treatment TREATMENT OF DEPRESSION of 22 depressed outpatients (113). To date there have been no seizures reported using fast Repetitive transcranial magnetic stimulation (rTMS) and rTMS within the established safety guidelines (114) and no vagal nerve stimulation (VNS) are two new treatments for cognitive side effects in patient populations (109). The most depression that, unlike ECT, use subconvulsive stimuli to common side effects are pain at the treatment site and head- treat depressive symptoms. Compared to ECT, these treat­ aches usually relieved by acetaminophen. Although early studies using slow TMS demon­ rTMS was first used in 1985 as a noninvasive method strated poor outcomes (115–117), and are often cited as of stimulating brain neurons (96). More recent trials of slow rTMS have different effects on neuronal firing, depending on the over the right DLPFC have shown benefit. Klein and col- 1104 Neuropsychopharmacology: The Fifth Generation of Progress leagues (118) randomized 71 depressed patients to 2 weeks effective in given individuals by evaluating the functional of slow, active or sham treatment over the right prefrontal neuroimaging before and after rTMS stimulation. Speer and cortex and 41% of active-treatment subjects had a 50% or associates have shown that patients with hypometabolism greater drop in Hamilton depression scores compared to on baseline PET scans utilizing [18F]-Fluorodeoxyglucose only 17% of sham-treatment subjects. Similarly, Tormos in the left prefrontal cortex responded preferentially to 2 and associates (119) showed a significant antidepressant re­ weeks of fast rTMS (20 Hz) as compared with patients with sponse to fast left DLPFC stimulation and slow right DLPFC hypermetabolism who responded at a higher rate to slow stimulation, but not fast right DLPFC stimulation or sham. Individual characteristics may be a key Slow left stimulation was not administered. Trials of slow factor in determining treatment response. Padb­ Vagal nerve stimulation (VNS) is another new and prom­ erg and colleagues (120) randomized 18 nonpsychotic pa­ ising treatment for major depression. VNS has been success- tients to treatment over the left DLPFC using fast, slow, fully used to treat patients with intractable seizures since or sham treatments. They showed a statistically significant 1994 and was noticed to have positive effects on mood (but clinically insignificant) response to fast and slow stimu­ that were not simply secondary to the decrease in seizure lation compared to placebo. The VN has both parasympathetic efferent and Nahas demonstrated that lower frequency stimulation fibers to the heart and GI tract and sensory afferent fibers (5 Hz) might be more effective at 20 Hz TMS. Patients (approximately 20% and 80% of the fibers, respectively). The fibers passing 10 versus 3/10 responders, respectively) and placebo (0/10 through the PN/LC (which are adjacent to one another) responders) (121,122). Slow TMS (�1 Hz) has never been connect to the hypothalamus and thalamus and, central to associated with seizures or any other adverse consequences the antidepressant properties of VNS, the bed nucleus of in neurologically normal individuals; therefore, it is poten­ the stria terminalis and amygdala. George and associates tially safer than fast stimulations (114). First, although half the patients respond to the treat­ tions to the limbic system as well as PET data showing ments (defined as a 50% improvement in the HDRS), a activation of limbic structures (132) and increases in CNS much smaller percentage obtains remission (HDRS �10). Second, and perhaps of more concern, is the fact that a The first open trial of VNS by Rush and colleagues in­ majority of patients (up to 100% in some studies) relapse in cluded 30 nonpsychotic patients with treatment-resistant the month after treatment. Both the antidepressant response unipolar or bipolar depression (136). Szuba, personal communication) and relapse rate (109) of epilepsy, the stimulator was attached to the left vagal are improved by increasing the number of weeks of treat­ nerve, which can be accessed peripherally in a procedure ments but, as with ECT, the most severely ill patients may similar to implanting a cardiac pacemaker, and compared respond partially and relapse quickly. Combination treat­ to the right VN has fewer afferent fibers to the autonomic ment strategies (slow right and fast left) and maintenance system controlling cardiac and gastric physiologic functions rTMS strategies are being employed to improve response (137). Twelve of 30 patients (40%) met criteria for treat­ and keep patients in remission. None of the patients discontinued techniques are being developed to assist in focusing the mag­ treatment because of adverse events. The most common netic impulse on specific cortical structures. VNS may be an effective treatment in resistant depres­ Using these techniques, rTMS can help in elucidating sion. The two variables that predicted clinical response to the neuronal pathways involved in depression. Initial studies VNS included previous response to ECT (only one of 19 using functional neuroimaging and rTMS have shown that patients who had received ECT had a sustained response many of the effects of rTMS occur at brain regions distant to VNS) and decreased stimulator output. Encouragingly, from the site of stimulation including the caudate, orbito­ of the ten responders with available follow-up data over 4 frontal cortex bilaterally, and cerebellum (124). These stud­ to 9 months, all have demonstrated continued response. The Chapter 76: Electroconvulsive Therapy 1105 adverse side effect profile and costs could be dramatically 7. Multiple monitored electroconvulsive reduced if a method of stimulating the VN could be treatment. Textbook trodes is $9,200, and the additional cost of the surgical of psychopharmacology. Washington, DC: American Psychiatric procedure raises the total costs to approximately $12,000 Press, 1995:523–543. Convuls Ther 1997; be expected for acute and 1-year maintenance treatment 13(3):125–127. ECT, research, and professional ambivalence [edito­ for ECT; however, insurance coverage may depend on the rial] [see comments]. VNS is approved The clinical science of electroconvulsive therapy, vol. Some researchers have questioned the benefit of electrical 12. Experimental studies of the mode of action of electroconvulsive therapy. Acta Psychiatr Neurol Scand 1960;35: stimulation, which does not produce a seizure (138), argu­ 1–141. Monitoring the duration of electroconvul­ to provide any clinical benefit (139). Arch vulsant hypothesis assumes that the beneficial effects from Gen Psychiatry 1982;39(10):1189–1191. ECT derive not from the convulsion, but the anticonvulsant 14. Seizure duration and clinical effect in electrocon­ vulsive therapy. Slow rTMS dampens neuronal excitability (100) and of ECT in endogenous depression. Br J Psychiatry 1976;129: theoretically may be useful in treating epilepsy (140).

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Interrupt amphotericin B therapy effective 20 mg cialis jelly, yes resume on improvement Is K level purchase cialis jelly 20mg without a prescription,3 20mg cialis jelly free shipping. Use oral or intravenous yes supplementation No Continue amphotericin B therapy and routine monitoring Close follow-up of serum electrolytes 11 buy 20mg cialis jelly with visa. The diagnosis of cyclosporine-induced acute renal dysfunction is not difficult when the patient has no other reason for reduced renal function (eg, psoriasis, rheum atoid arthritis). In renal trans- plant recipients, however, the situation is com pletely different. In this clinical setting, the clinician m ust differentiate between cyclo- sporine injury and acute rejection. The incidence of this acute cyclosporine renal injury can be enhanced by extended graft preser- vation, preexisting histologic lesions, donor hypotension, or preop- erative com plications. The gold standard for this im portant dis- tinction rem ains renal biopsy. In addition, cyclosporine has been associated with hem olytic-ure- m ic syndrom e with throm bocytopenia, red blood cell fragm enta- tion, and intravascular (intraglom erular) coagulation. Again, this drug-related intravascular coagulation has to be differentiated from that of acute rejection. The absence of clinical signs and of rejec- FIGURE 11-13 (see Color Plate) tion-related interstitial edem a and cellular infiltrates can be helpful. Intravascular coagulation in a cyclosporine-treated renal transplant Vanrenterghem and coworkers found a high incidence of recipient. Recent of the afferent arteriole entering the glom erulus. W hen severe studies have shown that im paired fibrinolysis, due m ainly to enough, this can decrease glom erular filtration rate. Although the excess plasm inogen activator inhibitor (PAI-1), m ay also contribute precise pathogenesis of the renal hem odynam ic effects of to this im balance in coagulation and anticoagulation during cyclosporine are unclear, endothelin, inhibition of nitric oxide, cyclosporine treatm ent. Lithium-Induced Acute Renal Failure FIGURE 11-14 SIGNS AND SYM PTOM S OF Sym ptom s and signs of toxic effects of lithium. Lithium can cause TOXIC EFFECTS OF LITHIUM acute functional and histologic (usually reversible) renal injury. W ithin 24 hours of adm inistration of lithium to hum ans or ani- m als, sodium diuresis occurs and im pairm ent in the renal concen- Toxic Effect Plasma Lithium Level Signs and Symptoms trating capacity becom es apparent. The defective concentrating capacity is caused by vasopressin-resistant (exogenous and endoge- Mild 1–1. The clinical picture features nonspecific signs of progression to coma), delirium, degenerative changes and necrosis of tubule cells. The m ost ataxia, generalized fasciculations, distinctive and specific acute lesions lie at the level of the distal extrapyramidal symptoms, tubule. They consist of swelling and vacuolization of the cyto- convulsions, impaired renal plasm of the distal nephron cells plus periodic acid-Schiff–positive function granular m aterial in the cytoplasm (shown to be glycogen). Renal Injury Due To Environmental Toxins, Drugs, and Contrast Agents 11. Acute renal failure, with or without oliguria, can be associated with lithium treatm ent, and with severe dehydration. In this case, acute renal failure can be consid- Salt depletion strongly impairs renal elimination of lithium. Indeed, the histologic appearance in such cases is Salt loading increases absolute and fractional lithium clearance. Conditions that Diuretics stim ulate sodium retention and consequently lithium reabsorption, Acetazolamide Increased lithium clearance such as low salt intake and loss of body fluid by way of vom iting, Thiazides Increased plasma lithium level due to decreased diarrhea, or diuretics, decreasing lithium clearance should be avoid- lithium clearance ed. W ith any acute illness, particularly one associated with gastroin- Loop diuretics Acute increased lithium clearance testinal sym ptom s such as diarrhea, lithium blood levels should be Amiloride Usually no change in plasma lithium level; may be closely m onitored and the dose adjusted when necessary. Indeed, used to treat lithium-induced polyuria m ost episodes of acute lithium intoxication are largely predictable, and thus avoidable, provided that precautions are taken. Nonsteroidal Increased plasma lithium level due to decreased Removing lithium from the body as soon as possible the is the anti-inflammatory drugs renal lithium clearance (exceptions are aspirin mainstay of treating lithium intoxication. W ith preserved renal func- and sulindac) tion, excretion can be increased by use of furosemide, up to 40 mg/h, Bronchodilators (amino- Decreased plasma lithium level due to increased phylline, theophylline) obviously under close monitoring for excessive losses of sodium and renal lithium clearance water induced by this loop diuretic. W hen renal function is impaired Angiotensin-converting May increase plasma lithium level enzyme inhibitors in association with severe toxicity, extracorporeal extraction is the Cyclosporine most efficient way to decrease serum lithium levels. One should, Decreased lithium clearance however, remember that lithium leaves the cells slowly and that plas- ma levels rebound after hemodialysis is stopped, so that longer dialy- sis treatment or treatment at more frequent intervals is required. Inhibitors of the Renin-Angiotensin System efferent arteriolar vascular tone and in Pre-kallikrein general is reversible after withdrawing the angiotensin-converting enzym e (ACE) inhibitor. Angiotensinogen Kininogen Activated factor XII Inhibition of the ACE kinase II results in at least two im portant effects: depletion Renin + + Kallikrenin of angiotensin II and accum ulation of +: stimulation bradykinin. The role of the latter effect Angiotensin I Angiotensin Bradykinin converting on renal perfusion pressure is not clear, A. W hen renal per- Potentiation of sympathetic activity fusion drops, renin is released into the plas- m a and lym ph by the juxtaglom erular cells Increased Ca2+ current Prostaglandins of the kidneys. Renin cleaves angiotensino- gen to form angiotensin I, which is cleaved further by converting enzym e to form Cough? Angiotensin II partici- pates in glom erular filtration rate regulation in a least two ways. First, angiotensin II FIGURE 11-16 increases arterial pressure— directly and Soon after the release of this useful class of antihypertensive drugs, the syndrom e of func- acutely by causing vasoconstriction and tional acute renal insufficiency was described as a class effect. This phenom enon was first m ore “chronically” by increasing body fluid observed in patients with renal artery stenosis, particularly when the entire renal m ass was volum es through stim ulation of renal sodi- affected, as in bilateral renal artery stenosis or in renal transplants with stenosis to a soli- um retention; directly through an effect on tary kidney. Acute renal dysfunction appears to be related to loss of postglom erular the tubules, as well as by stim ulating thirst (Continued on next page) 11. Normal condition depletion as during diuretic therapy, con- Autoregulation gestive heart failure, cirrhosis, and +– +– nephrotic syndrom e. W hen activated, this Afferent Efferent reninangiotensin system plays an im por- arteriole Glomerulus arteriole tant role in the m aintenance of glom erular pressure and filtration through preferen- M yogenic reflex (Laplace) tial angiotensin II–m ediated constriction Tubuloglomerular feedback of the efferent arteriole. Thus, under such Tubule conditions the kidney becom es sensitive B2. Perfusion pressure reduced to the effects of blockade of the renin- but still within autoregulatory range PGE2 (congestive heart failure, angiotensin system by angiotensin I–con- – renal artery stenosis, verting enzym e inhibitor or angiotensin II diuretic therapy, receptor antagonist. Perfusion pressure com prom ised renal function and congestive seriously reduced PGE2 heart failure, the incidence of serious (prerenal azotemia) – changes in serum creatinine during ACE Intra- glomerular inhibition depends on the severity of the pressure pretreatm ent heart failure and renal failure. Second, angiotensin II preferentially constricts the efferent am ong the appropriate m easures for arteriole, thus helping to preserve glom erular capillary hydrostatic pressure and, conse- patients at risk. Acute interstitial nephritis associated with W hen arterial pressure or body fluid volum es are sensed as subnorm al, the renin- angiotensin I–converting enzym e inhibition angiotensin system is activated and plasm a renin activity and angiotensin II levels has been described. This m ay occur in the context of clinical settings such as renal artery stenosis, O pie; with perm ission. M ost of the renal abnorm alities encountered clinically as a result of N SAIDs can be attributed to the action of these com pounds on prostaglandin production in the kidney. Renal vasoconstriction Sodium chloride and water retention are the m ost com m on side ↓Renal function effects of N SAIDs.

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Davidson: Laboratory for Affective Neuroscience cialis jelly 20mg mastercard, University other than to underscore that a major function of the PFC of Wisconsin purchase cialis jelly 20mg with visa, Madison purchase cialis jelly 20mg on line, Wisconsin buy discount cialis jelly 20mg on-line. One of the principal roles tive and negative affective states shift the asymmetry in pre- of the PFC is to represent goal-relevant information, a key frontal brain electrical activity in lawful ways. For example, component of both complex thought and emotion. As many film-induced negative affect increases relative right-sided studies at the nonhuman primate level have now docu- prefrontal and anterior temporal activation (15), whereas mented, reward-related information plays a key role in mod- induced positive affect elicits an opposite pattern of asym- ulating the activity of PFC neurons. This general pattern has been replicated and ventromedial zones of the PFC is associated with the by others using similar measures (16,17). In positron emis- identity and size of expected rewards (2). This component sion tomography (PET) and functional magnetic resonance of PFC activity is likely governed by a dopaminergic input imaging (fMRI) studies, with considerably better spatial res- from the ventral tegmental area of the midbrain (see ref. Our notion of the role of the PFC in pre-goal though many important methodologic details must be con- attainment positive affect is based on this corpus of research, sidered in interpreting the findings (see ref. The most important of these is considered in a later section. The case for the differential importance of left and right In addition, a body of evidence supports the conclusion PFC sectors in emotional processing was first made system- that individual differences in baseline levels of asymmetric atically in a series of studies of patients with unilateral corti- activation in these brain regions are lawfully related to varia- cal damage (5–7). Each of these studies compared the mood tions in dispositional affective style (18). Bechara and colleagues (19) have reported that fairly gross and likely included more than one sector of the patients with bilateral lesions of the ventromedial PFC have PFC and often other brain regions as well. The general difficulty anticipating future positive or negative conse- interpretation that has been placed on these studies is that quences, although immediately available rewards and pun- depressive symptoms are increased following left-sided ante- ishments do influence their behavior. Such patients show rior PFC damage because this brain territory participates in decreased levels of electrodermal activity in anticipation of certain forms of positive affect, particularly pre-goal attain- a risky choice in comparison with controls, whereas controls ment positive affect; damage leads to deficits in the capacity exhibit such autonomic change before they explicitly know to generate this form of positive affect, a hallmark feature that a choice is risky (20–22). It should be noted that not all studies The findings from the lesion method when effects of support this conclusion. In a recent metaanalysis of lesion small unilateral lesions are examined and from neuroimag- studies, Carson et al. Davidson (10) has previously reviewed many of disorders converge on the conclusion that increases in right- these studies and has addressed a number of critical meth- sided activation in various sectors of the PFC are associated odologic and conceptual concerns in this literature. Less evidence is available for most important of these issues is that according to the dia- the domain of positive affect, in part because positive affect thesis stress model of anterior activation asymmetry pro- is much harder to elicit in the laboratory and because of posed by Davidson and colleagues (11–13), individual dif- the negativity bias (23,24). This latter phenomenon refers ferences in anterior activation asymmetry, whether lesion- to the general tendency of organisms to react more strongly induced or functional, represent a diathesis. As such, they to negative than to positive stimuli, perhaps as a conse- alter the probability that specific forms of emotional reac- quence of evolutionary pressures to avoid harm. The find- tions will occur in response to the requisite environmental ings of Bechara et al. In the absence of such a challenge, the pattern PFC lesions on the anticipation of future positive and nega- of asymmetric activation will simply reflect a propensity but tive affective consequences are based on studies of patients will not necessarily culminate in differences in mood or with bilateral lesions. In a recent study of mood sequelae in patients to examine patients with unilateral ventromedial lesions to with unilateral lesions with the largest sample size to date ascertain whether valence-dependent asymmetric effects are (n 193), Morris et al. It is likely that larger lesions intrude on other role played by various sectors of the PFC in emotion are brain territories and mask the relation between left PFC lacking, although a growing corpus of work illustrates the damage and depression. Many consistent with the findings derived from the lesion studies. This pro- learning, although the human data imply a more heteroge- cess requires that the organism have some means of repre- neous contribution. Such a pro- the amygdala is small, they have provided unique informa- cess may be conceptualized as a form of affective working tion about the role of this structure in emotional processing. It is likely that the PFC plays a key role in this A number of studies have now reported specific impair- process (28). Recogni- comes and consequently results in an inability to behave in tion of facial signs of other emotions have been found to an adaptive fashion. This proposal can bilateral amygdala damage judged the unfamiliar persons to be tested with current neuroimaging methods (e. Recognition of vocalic signs of fear and anger the different functional roles of the dorsolateral, orbitofron- was found to be impaired in a patient with bilateral amyg- tal, and ventromedial sectors of the PFC, Davidson and dala damage (42), which suggests that this deficit is not Irwin (4) suggested on the basis of both human and animal restricted to facial expressions. Other researchers demon- studies that the ventromedial sector is most likely involved strated an impairment of aversive autonomic conditioning in the representation of elementary positive and negative in a patient with amygdala damage despite the fact that the affective states in the absence of immediately present incen- patient demonstrated normal declarative knowledge of the tives. The orbitofrontal sector has most firmly been linked conditioning contingencies (43). Collectively, these find- to rapid learning and unlearning of stimulus-incentive asso- ings from patients with selective bilateral destruction of the ciations and has been particularly implicated in reversal amygdala suggest specific impairments on tasks that tap as- learning (29). As such, the orbitofrontal sector is likely key pects of negative emotion processing. Most of the studies to understanding aspects of emotion regulation (30). One have focused on perception; the data clearly show the amyg- critical component of emotion regulation is the relearning dala to be important in recognizing cues of threat or danger. The dorsolateral sector is most directly involved of stimulus–punishment contingencies. In one of the few in the representation of goal states toward which more ele- studies to examine the role of the amygdala in the expression mentary positive and negative states are directed. Among control subjects, they observed the has established the importance of the amygdala in emotional well-known effect of startle potentiation during the presen- processes (31–33). Because many reviews of the animal lit- tation of aversive stimuli. In the patient with right amygdala erature have appeared recently, a detailed description of damage, no startle potentiation was observed in response these studies is not presented here. LeDoux and colleagues to aversive versus neutral stimuli. These findings suggest have marshaled a large corpus of compelling evidence to that the amygdala may be necessary for the expression of suggest that the amygdala is necessary to establish condi- an already learned negative affect. Whether the amygdala is necessary to express that fear following learning and whether the amygdala is Hippocampus and Anterior Cingulate the actual locus where learned information is stored is still Cortex a matter of some controversy (34,35). The classic view of amygdala damage in nonhuman primates (resulting in In this section, the contributions of the hippocampus and major affective disturbances as expressed in the Klu- anterior cingulate cortex (ACC) to emotion and cognition ver–Bucy syndrome, in which the animal exhibits an abnor- are briefly mentioned. A more extensive discussion of the mal approach, hyperorality and hypersexuality, and little contributions of this circuit to emotional and cognitive pro- fear) is now thought to be a function of damage elsewhere cessing can be found in several recent reviews (4,45–47). When very selective excitotoxic The hippocampus has been implicated in various aspects lesions of the amygdala are made that preserve fibers of of memory (47), particularly declarative memory of the sort passage, nothing resembling the Kluver–Bucy syndrome is we experience when we consciously recall an earlier episode. This diverse array of findings suggests a more The contribution of the hippocampus to emotion and affec- 376 Neuropsychopharmacology: The Fifth Generation of Progress tive style has only recently begun to be gleaned from the pal lesion in failing to modulate emotional responses in available corpus of animal studies on its role in context- a context-appropriate manner. This literature has generally sup- inferential at the present time. Neuroimaging studies are ported a role for the hippocampus in the learning of context. In addition, which a discrete cue is paired with an aversive outcome, in further study is needed to understand how and why the addition to learning the specific cue–punishment contin- hippocampus may preferentially extract and process infor- gency, the animal learns to associate the context in which mation about context.

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Noninvasive measurements of and glial glutamate transporters discount cialis jelly 20 mg line. Metabolic coupling between tic pathway and amino acid metabolism in the brain: an ex vivo glia and neurons cheap cialis jelly 20 mg fast delivery. Glutamine 13C]glucose with or without ammonium acetate order 20mg cialis jelly mastercard. Metabolism and role of glutamate in metabolism: neuronal-astroglial relationships buy cialis jelly 20mg low cost. An [Na -K ] onstration by [13C]NMRspectroscopy that glutamine from coupled L-glutamate transporter purified from rat brain is lo- astrocytes is a precursor for GABA synthesis in neurons. Transport of neuroactive amino brane vesicles isolated from rat brain. Amino acid neurotransmission: membrane vesicles and reconstituted preparations from rat spotlight on synaptic vesicles. Chaudhry FA, Lehre KP, van Lookeren Campagne M, et al. Glutamate transporters in glial plasma membranes: highly dif- 61. Neu- ferentiated localizations revealed by quantitative ultrastructural ronal-glial metabolism under depolarizing conditions. Biochemistry and physiology of brain of two glial glutamate transporters in the rat brain: quantitative ammonia. Expression of the glial Dev Neurosci 1998;20:389–398. Chronic inhibition tion, hyperammonemia and energy deprivation. Neurochem Int of glutamate uptake produces a model of slow neurotoxicity. Knockout of sor for the GABA and glutamate transmitter pools. Neurosci glutamate transporters reveal a major role for astroglial transport Lett 1978;10:171–174. NMRmeasurements of GABA levels in human brain in vivo. Regional deafferenta- Proc Natl Acad Sci USA 1993;90:5662–5666. Carbon dioxide fixation transporter and glutamate receptor proteins in septum and hip- in the brain. Synaptic activation of glutamate trans- rate of glutamine synthesis and utilization at steady state in porters in hippocampal astrocytes. Glutamate uptake into astrocytes of ammonia on rat brain metabolism in vivo. Biochem J 1973; stimulates aerobic glycolysis: a mechanism coupling neuronal 134:1001–1008. Effects of conditions explain the discrepancy over glutamate stimulation acute hyperammonemia on cerebral amino acid metabolism and of aerobic glycolysis? Metabolic control analysis: a survey of its theoretical 2:741–479. The role of glia in the inactivation of neurotransmit- 25: Glutamate and GABA Neurotransmitter Cycles 341 ters. Oxford: have distinct intraneuronal distributions and cofactor interac- Oxford University Press, 1995:732–745. The level of GAD67 protein is highly trical stimulation of sciatic nerve on metabolic activity in spinal sensitive to small increases in intraneuronal gamma-aminobu- cord and dorsal root ganglion in the rat. Metabolic mapping vigabatrin (gamma-vinylGABA) differentially affects GAD65 of the primary visual system of the monkey by means of the and GAD67 expression in various regions of rat brain. J Neurosci autoradiographic [14C] deoxyglucose technique. Frequency-dependent kDa isoform of glutamic acid decarboxylase (GAD65) maintain activation of glucose utilization in the superior cervical ganglion normal levels of GAD67 and GABA in their brains but are by electrical stimulation of cervical sympathetic trunk. Biochem Biophys Res Commun 1996;229: Acad Sci USA 1983;80:4179–4183. Cleft palate and Resonance Spectroscopy to studies of neuronal/glial relation- decreased brain -aminobutyric acid in mice lacking the 67- ships. Topiramate increases J Cereb Blood Flow 2000;in press.. GABAergic mechanism in the pathogenesis and with epilepsy. Epilepsia 1997; tin on brain GABA, homocarnosine, and pyrrolidinone in epi- 38:399–407. Acute and chronic molecule resonances in 1H NMRspectra of human brain. Magn alterations in human cerebral GABA levels in response to topira- Reson Med 1994;32:294–302. GABA changes with viga- spectroscopic study of rat brain in vivo. J Cereb Blood Flow batrin in the developing human brain. GABA levels in the brain: a target for vigabatrin-induced increases in cerebral GABA. New NMR measure- assessed using 1H-magnetic resonance spectroscopy. Measuring brain GABA in patients with com- Psychiatry 1999;56:1043. Measuring human brain GABA dence of reduced cortical GABA levels in localized 1-H-MR in vivo: effects of GABA-transaminase inhibition with vigaba- spectra of alcohol-dependent and hepatic encephalopathy pa- trin. Functional imaging in the epilepsies proton MRS: GABA and glutamate. Adv Neurol measurements of 2-pyrrolidinone in human brain in vivo. Nonoxidative glucose and the measurement of neuronal pH in patients with epilepsy. Wenner-Gren International Symposium regulatory properties of the brain glutamate decarboxylases. Two forms of the gamma- functional magnetic resonance imaging of the brain. Annu Rev aminobutyric acid synthetic enzyme glutamate decarboxylase Biophys Biomol Struct 1998;27:447–474. Adv Exp Med Biol 1999;471:99–109 into tricarboxylic acid cycle derived metabolic pools in neurons 136. Lactate rise and glia during and after sensory stimulation. Proceedings of detected by 1H NMRin human visual cortex during physiologi- the International Society for Neurochemistry 3rd International cal stimulation.