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Activation of receptor-regulated gene expression of striatonigral and striatopal- corticotropin-releasing factor in the limbic system during can- lidal neurons [see comments] cheap permethrin 30gm amex acne free reviews. Addiction generic 30gm permethrin otc skin care 77054, dopamine 30gm permethrin acne 9 days before period, and the molecular norphin gene regulation in rat striatum buy permethrin 30gm online acne 2000. Basal ganglia—input, neural activity, and relation 79. AMPA receptors by the extracellular immediate- early gene prod- 62. D1 dopamine receptor activation uct Narp [see comments]. Regulation of immediate responsive element-binding protein. Proc Natl Acad Sci USA 1992;89: D, a RNA synthesis inhibitor, on long-term potentiation in rat 5764–5768. A macromolecular synthesis-dependent ine, and amphetamine. Proc Natl Acad Sci USA 1992;89: late phase of long-term potentiation requiring cAMP in the me- 4270–4274. AP-1 complex composed of altered Fos-like proteins in brain by 83. Synaptic tagging and long-term potentiation chronic cocaine and other chronic treatments. Blockade of morphine- and am- stage of LTP in hippocampal CA1 neurons. Science 1993;260: phetamine-induced conditioned place preference in the rat by 1661–1664. Influence of novel versus synthesis-dependent late potentiation in the CA1 region of the home environments on sensitization to the psychomotor stimu- hippocampus [see comments]. Proc Natl Acad Sci USA 1995;92: lant effects of cocaine and amphetamine. Sensitization to the behavioral effects nergic D1 receptor blockade during tetanization on the expres- of cocaine: modification by Pavlovian conditioning. Pharmacol sion of long-term potentiation in the rat CA1 region in vitro. Dopaminergic antagonists of sensitization induced by psychomotor stimulants. NIDARes prevent long-term maintenance of posttetanic LTP in the CA1 Monogr 1990 á:208–241. Dopamine D1-defi- tor stimulant effects of amphetamine: modulation by associative cient mutant mice do not express the late phase of hippocampal learning. Models of information processing North Ami 1986;9:413–425. In vivo activity-dependent plasticity diction and stages of change models. Dopamine reverses the putative 'effector' immediate early gene, by cocaine in rat brain. Nature 1989;340: plasticity in an in vitro slice preparation of the rat nucleus accum- 474–476. Requirement of a critical period factor and activity-regulated gene, encodes a novel cytoskeleton- of transcription for induction of a late phase of LTP. Science associated protein that is enriched in neuronal dendrites. Homer: a protein cleus accumbens and prefrontal cortex neurons produced by that selectively binds metabotropic glutamate receptors [see com- previous experience with amphetamine. KOOB DEFINITIONS AND VALIDATION OF butes of a drug (e. This chapter reviews animal models currently used to Definitions of Drug Addiction examine the neurobiological basis of drug addiction and the Drug addiction is defined as a compulsion to take a drug role of reinforcement processes in its initiation, mainte- with loss of control in limiting intake (33). Emphasis is place on more re- a chronic disorder because the risk of relapse remains high cently developed models, and where possible, the models even after completion of treatment and prolonged absti- are evaluated in terms of reliability and predictability to nence. In 1968, the term drug dependence replaced that of the human condition. Potential pitfalls to consider when addiction in the nomenclature of the World Health Organi- interpreting data also are discussed. Defined as a cluster of cognitive, behavioral, and physiologic symptoms ANIMAL MODELS OF THE POSITIVE indicative of an individual continuing substance use despite REINFORCING EFFECTS OF DRUGS significant substance related problems, this term has become the accepted diagnostic term for compulsive use of a psy- Drugs of abuse function as positive reinforcing stimuli; this choactive substance. When defined as described, it is analo- action has provided the framework for currently used animal gous to the term addiction. It is also clear that humans and experi- be confused with physical or psychic dependence, condi- mental animals will readily self-administer these agents in tions in which the cessation or reduction of drug usage the absence of a withdrawal state. Earlier models of drug results in a withdrawal syndrome. Withdrawal and tolerance reinforcement used operant paradigms in nonhuman pri- often are associated with compulsive drug use; however, mates; however, many of these same paradigms now are they are not required for drug addiction. The use of these rodent models, together als suffering from chronic pain may develop tolerance to with the development of modern neurobiological tech- the analgesic effects of an opiate and experience withdrawal niques, has provided important information regarding the symptoms, they do not exhibit signs of compulsive drug- neurobiology of addiction (11,15,36,45,51). The concept of reinforcement has provided the corner- Operant Intravenous Drug stone for current theories and animal models of drug addic- Self-Administration tion. A reinforcer is defined operationally as 'any event that increases the probability of a response' and often is used Drugs of abuse are readily self-administered intravenously interchangeably with 'reward. However, that not all drugs abused by humans are self-administered by experimental animals (e. Furthermore, there are species- and strain-related differences in the degree to which a drug is self-administered Toni S. Shippenberg: National Institutes of Health, National Institute (48,62). A detailed review of intravenous self-administra- on Drug Abuse, Bethesda, Maryland. Koob: Department of Neuropharmacology, The Scripps Re- tion was presented in the previous edition (46); therefore, search Institute, La Jolla, California. The number and pattern of responding required for each infusion is determined by the schedule of reinforcement Multiple Schedules imposed by the experimenter. Drug availability typically is signaled by an environmental stimulus. The dependent Clinical definitions of drug addiction and dependence typi- variables are the number of infusions obtained or the rate cally refer to the disruptive effects of addiction on of responding during a session. In addition to the intrave- non—drug-related activities. The use of multiple schedules nous route of administration, the intragastric or oral route of reinforcement enables the application of concepts of be- can be employed (see the following). It also can provide a control for nonselective effects of drug reinforcement. In Simple Schedules these procedures, self-administration of a drug is incorpo- In fixed-ratio schedules, the number of responses required rated into a multiple component schedule with other rein- for drug infusion is set at a fixed number.

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Acute renal dysfunction appears to be related to loss of postglom erular the tubules generic permethrin 30 gm otc acne 2015, as well as by stim ulating thirst (Continued on next page) 11 permethrin 30gm discount acne 5 benzoyl peroxide cream. Normal condition depletion as during diuretic therapy purchase 30gm permethrin overnight delivery skin care careers, con- Autoregulation gestive heart failure buy permethrin 30gm low cost acne xarelto, 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. This should not be considered drug toxicity because it represents a m odification of a physiologic control "Normalized" renal function m echanism without the production of a true functional disorder in the kidney. Inhibition – – by NSAID Compensatory vasodilation induced by renal prostaglandin synthesis Renal Injury Due To Environmental Toxins, Drugs, and Contrast Agents 11. N SAIDs can induce acute renal decom pensation in patients with various renal and extrarenal clinical conditions that cause a decrease in blood perfu- Severe heart disease (congestive heart failure) sion to the kidney. Renal prostaglandins play an im portant Severe liver disease (cirrhosis) role in the m aintenance of hom eostasis in these patients, so disrup- tion of counter-regulatory m echanism s can produce clinically Nephrotic syndrome (low oncotic pressure) im portant, and even severe, deterioration in renal function. Chronic renal disease Age 80 years or older Protracted dehydration (several days) FIGURE11-19 Physiologic stimulus Inflammatory stimuli Inhibition by nonsteroidal anti-inflam m atory drugs (N SAIDs) on pathways of cyclo-oxygenase (CO X) and prostaglandin synthesis Inhibition - by NSAID -. The recent dem onstration of the existence of functionally dis- tinct isoform s of the cox enzym e has m ajor clinical significance, as COX-1 it now appears that one form of cox is operative in the gastric COX-2 constitutive inducible m ucosa and kidney for prostaglandin generation (CO X-1) whereas Stomach Kidney Inflammatory sites an inducible and functionally distinct form of cox is operative in Intestine Platelets (macrophages, the production of prostaglandins in the sites of inflam m ation and Endothelium synoviocytes) pain (CO X-2). The clinical therapeutic consequence is that an N SAID with inhibitory effects dom inantly or exclusively upon the - cox isoenzym e induced at a site of inflam m ation m ay produce the PGE2 TxA2 PGI2 Inflamma- Proteases O2 tory PGs desired therapeutic effects without the hazards of deleterious effects on the kidneys or gastrointestinal tract. A focal diffuse inflam m atory infiltrate Renal Syndrome Mechanism Risk Factors Prevention/Treatment can be found around the proxim al and dis- Sodium retension ↓ Prostaglandin NSAID therapy (most Stop NSAID tal tubules. The infiltrate consists prim arily and edema common side effect) of cytotoxic T lym phocytes but also con- Hyperkalemia ↓ Prostaglandin Renal disease Stop NSAID tains other T cells, som e B cells, and plasm a ↓ Potassium to Heart failure Avoid use in high-risk patients cells. Changes in the glom eruli are m inim al distal tubule Diabetes and resem ble those of classic m inim al- ↓ Aldosterone/renin- Multiple myeloma change glom erulonephritis with m arked angiotensin Potassium therapy epithelial foot process fusion. Potassium-sparing H yperkalem ia, an unusual com plication diuretic of N SAIDs, is m ore likely to occur in Stop NSAID Acute deterioration of ↓ Prostaglandin and Liver disease patients with pre-existing renal im pairm ent, Avoid use in high-risk patients renal function disruption of Renal disease cardiac failure, diabetes, or m ultiple m yelo- hemodynamic bal- m a or in those taking potassium supple- Heart failure ance m ents, potassium -sparing diuretic therapy, Dehydration Stop NSAID or intercurrent use of an angiotensin-con- Old age Dialysis and steroids (? The m echanism of Nephrotic syndrome with: ↑ Lymphocyte recruit- Fenoprofen Stop NSAID N SAID hyperkalem ia— suppression of Interstitial nephritis ment and activation prostaglandin-m ediated renin release— leads Avoid long-term Papillary necrosis Direct toxicity Combination aspirin analgesic use to a state of hyporeninem ic hypoaldostero- and acetaminophen nism. In addition, N SAIDs, particularly abuse indom ethacin, m ay have a direct effect on cellular uptake of potassium. The renal saluretic response to loop diuretics is partially a consequence of FIGURE 11-20 intrarenal prostaglandin production. This Summary of effects of nonsteroidal anti-inflammatory drugs (NSAIDs) on renal function. Characteristically, the histology of this form of N SAID–induced nephrotic syndrom e Thus, concurrent use of an N SAID m ay consists of m inim al-change glom erulonephritis with tubulointerstitial nephritis. This is an blunt the diuresis induced by loop diuretics. Contrast M edium–Associated Nephrotoxicity FIGURE 11-21 RISK FACTORS THAT PREDISPOSE TO CONTRAST Risk factors that predispose to contrast-associated nephropathy. In ASSOCIATED NEPHROPATHY random populations undergoing radiocontrast imaging the incidence of contrasts associated nephropathy defined by a change in serum creatinine of more than 0. For confirmed high-risk patients (baseline serum creatinine values greater than 1. In addition, there are suspected risk factors Diabetic nephropathy Generalized atherosclerosis Diabetes without that should be taken into consideration when considering the value Severe congestive Abnormal liver nephropathy of contrast-enhanced imaging. The initial glom erular vasoconstriction that follows the injection of radiocontrast m edium induces the ↑Endothelin Systemic ↓ATPase liberation of both vasoconstrictor (endothelin, vasopressin) and ↑PGE2 ↑Vasopressin hypoxemia ↑ANF ↑Adenosine Osmotic load vasodilator (prostaglandin E2 [PGE2], adenosine, atrionatiuretic ↑Blood viscosity to distal tubule ↓PGI factor ) substances. The net effect is reduced oxygen deliv- 2 ery to tubule cells, especially those in the thick ascending lim b of H enle. Because of the system ic hypoxem ia, raised blood vis- ↑RBF ↓↓RBF cosity, inhibition of sodium -potassium –activated ATPase and the – increased osm otic load to the distal tubule at a tim e of reduced Calcium oxygen delivery, the dem and for oxygen increases, resulting in antagonists cellular hypoxia and, eventually cell death. Additional factors Theophylline Net ↓O2 delivery Net ↑O2 consumption that contribute to the acute renal dysfunction of contrast-associ- ated nephropathy are the tubule obstruction that results from increased secretion of Tam m -H orsfall proteins and the liberation of reactive oxygen species and lipid peroxidation that accom pa- Cell injury ny cell death. As noted in the figure, calcium antagonists and theophylline (adenosine receptor antagonist) are thought to ↑TH protein ↑Intrarenal number act to dim inish the degree of vasoconstriction induced by con- of macrophages, T cells trast m edium. Stimulation of mesangium The clinical presentation of contrast-associated nephropathy involves an asym ptom atic increase in serum creatinine within 24 Tubular obstruction Superoxidase hours of a radiographic im aging study using contrast m edium , – – dismutase with or without oliguria. W e have recently reviewed the clinical outcom e of 281 patients with contrast-associated nephropathy according to the presence Reactive O species or absence of oliguric acute renal failure at the tim e of diagnosis. In the absence of oliguric acute renal failure Contrast associated nephropathy the serum creatinine value does not return to baseline in 24% of patients, approxim ately a third of whom require perm anent dialysis. Thus, this is not a benign condition but rather one FIGURE 11-22 whose defined risks are not only perm anent dialysis but also A proposed m odel of the m echanism s involved in radiocontrast death. GFR— glom erular filtration rate; RBF— renal blood flow; m edium –induced renal dysfunction. Based on experim ental m od- TH — Tam m H orsfall protein. Thus it is im portant to select the least invasive diagnostic proce- dure that provides the m ost inform ation, so that the patient can PREVENTION OF CONTRAST m ake an inform ed choice from the available clinical alternatives. ASSOCIATED NEPHROPATHY Since radiographic contrast im aging is frequently perform ed for diabetic nephropathy, congestive heart failure, or chronic renal failure, concurrent adm inistration of renoprotective Hydrate patient before the study (1. The correction of Use nonionic, iso-osmolar contrast media for patients at high risk (see Figure 11-21). Lim iting the total volum e of contrast m edium and using nonionic, isoosm olar FIGURE 11-23 m edia have proven to be protective for high-risk patients. The goal of m an- Pretreatm ent with calcium antagonists is an intriguing but agem ent is the prevention of contrast-associated nephropathy. Bennett W M , Porter GA: O verview of clinical nephrotoxicity. Thadhani R, Pascual M , Bonventre JV: Acute renal failure. Vestergaard P, Am disen A, H ansen AE, Schou M : Lithium treatm ent M ed 1996, 334:1448–1460.

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