Traditionally, theories of addiction have stressed that drug urges are characterized by dysphoria, occur in response to decreasing levels of drug or drug effect, and are associated with withdrawal symptoms/signs or drug-antagonistic responses arising from a homeostatic mechanism. However, recent research has shown that urges, drug self-administration, and relapse all occur concomitant with both positive and negative affect, rising and falling levels of drug, and with drug-agonistic responses, as well as antagonistic/withdrawal responses. In keeping with recent theorizing about motivation and emotions, we believe that affective responding provides a readout of the motivational status of an organism (e.g., Buck, 1985). We conceive of urges as affects, whose activation mediates drug pursuit and self-administration. Moreover, we believe that affects are represented in neural networks comprising information on affect-relevant stimuli, responses, and meaning/expectancy. We believe that there are two types of urge networks. One, a "positive-affect" network, is activated, associatively and nonassociatively, by appetitive stimuli, especially appetitive drug actions that activate "GO" motivational incentive systems. Activation of this network is characterized by positive affect, drug isodirectional responding, attentional focus on a dominant response, and enhanced pursuit of appetitive stimuli--especially the drug. The operating characteristics of the positive-affect network, and the associated motivational systems, result in a drug's instating a positive feedback loop. Appetitive drug actions increase the likelihood of the pursuit of appetitive stimuli, and additional drug constitutes a prepotent candidate from among the available appetitive stimuli. This positive feedback loop may account in part for cardinal features of addiction: for example, the great relapse likelihood once any drug is sampled, the attainment of very high blood levels of a drug, and the pursuit of adjunctive appetitive stimuli while using a drug. The second type of urge network we have labeled a "negative-affect" network, and we believe it is activated, associatively and nonassociatively, by inappetitive stimuli or consequences (punishment, signals of punishment, frustrating lack of reward, etc.) and by withdrawal and signals of withdrawal (e.g., drug cues, which during the course of addiction are associated with both direct drug effects and withdrawal). Activation of the network is characterized by withdrawal symptoms and signs, negative affect, and drug seeking.(ABSTRACT TRUNCATED AT 400 WORDS)
Storage symptoms such as urgency, frequency, and nocturia, with or without urge incontinence, are characterized as overactive bladder (OAB). OAB can lead to urge incontinence. Disturbances in nerves, smooth muscle, and urothelium can cause this condition. In some respects the division between peripheral and central causes of OAB is artificial, but it remains a useful paradigm for appreciating the interactions between different tissues. Models have been developed to mimic the OAB associated with bladder instability, lower urinary tract obstruction, neuropathic disorders, diabetes, and interstitial cystitis. These models share the common features of increased connectivity and excitability of both detrusor smooth muscle and nerves. Increased excitability and connectivity of nerves involved in micturition rely on growth factors that orchestrate neural plasticity. Neurotransmitters, prostaglandins, and growth factors, such as nerve growth factor, provide mechanisms for bidirectional communication between muscle or urothelium and nerve, leading to OAB with or without urge incontinence.
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