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A computational model of nervous system function during classical and instrumental conditioning is proposed. The model assumes the form of a hierarchical network of control systems. Each control system is capable of learning and is referred to as an associative control process (ACP). Learning systems consisting of ACP networks, employing the drive-reinforcement learning mechanism (Klopf, 1988) and engaging in real-time, closed-loop, goal-seeking interactions with environments, are capable of being classically and instrumentally conditioned, as demonstrated by means of computer simulations. In multiple-T mazes, the systems learn to chain responses that avoid punishment and that lead eventually to reward. The temporal order in which the responses are learned and extinguished during instrumental conditioning is consistent with that observed in animal learning. Also consistent with animal learning experimental evidence, the ACP network model accounts for a wide range of classical conditioning phenomena. ACP networks, at their current stage of development, are intended to model sensorimotor, limbic, and hypothalamic nervous system function, suggesting a relationship between classical and instrumental conditioning that extends Mowrer's (1956, 1960a/1973) two-factor theory of learning. In conjunction with consideration of limbic system and hypothalamic function, the role of emotion in natural intelligence is modeled and discussed. ACP networks constitute solutions to temporal and structural credit assignment problems, suggesting a theoretical approach for the synthesis of machine intelligence.

A hamster model of schistosomiasis has provided the first opportunity to sequentially examine the early phases of the development of portal hypertension in a natural model of chronic liver disease. Groups of hamsters were infected with 50 cercariae of Schistosoma mansoni and underwent hemodynamic evaluation at intervals of 5, 8, 12 and 20 wk after infection. A progressive rise in intrahepatic resistance (from 4.0 +/- 0.4 to 8.4 +/- 1.0 mm Hg min.ml-1.gm liver weight [p less than 0.01]) appeared to play a major role in the initial stages of evolving portal hypertension. A gradual decline in portal blood flow (from 2.1 +/- 0.3 to 1.3 +/- 0.1 ml.min-1.gm-1 liver weight [p less than 0.01]) was only partially compensated for by an increase in hepatic arterial flow. Accordingly, by week 20, total hepatic blood flow decreased 23%. Liver weight that increased markedly between 5 and 12 wk after infection, as a result of the acute accumulation of obstructing granulomas, stabilized between wk 12 and 20, while a gradual but progressive rise in hepatic collagen content was seen. Portal pressure increased 75% during the study period. Chronic examination of this natural model should help define the pathogenesis of the complications of portal hypertension and contribute to the basis for effective intervention in this disease process.