An adjusting-amount procedure was used to measure discounting of reinforcer value by delay. Eight rats chose between a varying amount of immediate water and a fixed amount of water given after a delay. The amount of immediate water was systematically adjusted as a function of the rats' previous choices. This procedure was used to determine the indifference point at which each rat chose the immediate amount and the delayed amount with equal frequency. The amount of immediate water at this indifference point was used to estimate the value of the delayed amount of water. In Experiment 1, the effects of daily changes in the delay to the fixed reinforcer (100 microliters of water delivered after 0, 2, 4, 8, or 16 s) were tested. Under these conditions, the rats reached indifference points within the first 30 trials of each 60-trial session. In Experiment 2, the effects of water deprivation level on discounting of value by delay were assessed. Altering water deprivation level affected the speed of responding but did not affect delay discounting. In Experiment 3, the effects of varying the magnitude of the delayed water (100, 150, and 200 microliters) were tested. There was some tendency for the discounting function to be steeper for larger than for smaller reinforcers, although this difference did not reach statistical significance. In all three experiments, the obtained discount functions were well described by a hyperbolic function. These experiments demonstrate that the adjusting-amount procedure provides a useful tool for measuring the discounting of reinforcer value by delay.

The amphetamine derivative 3,4-methylenedioxymethamphetamine (MDMA) is a drug of abuse and has been shown to be neurotoxic to 5-HT terminals in many species. MDMAengendered neurotoxicity has been shown to be affected by both ambient temperature and core body temperature. We now report that small (2°C) changes in ambient temperature produce changes in core temperature in MDMA-treated rats, but the same changes in ambient temperature do not affect core temperature of saline-treated animals. Furthermore, increases in core temperature of MDMA-treated animals increase neurotoxicity. Rats were given MDMA (20 or 40 mg/kg) or saline and placed in an ambient temperature of 20, 22, 24, 26, 28, or 30°C using a novel temperature measurement apparatus that controls ambient temperature Ϯ0.5°C. Two weeks after MDMA treatment, the rats were killed, and regional 5-HT and 5-hydroxyindole acetic acid levels were analyzed as a measure of neurotoxicity. Rats treated with MDMA at 20 and 22°C showed a hypothermic core temperature response. Treatment with MDMA at 28 and 30°C produced a hyperthermic response. At ambient temperatures of 20-24°C, neurotoxicity was not observed in the frontal cortex, somatosensory cortex, hippocampus, or striatum. At ambient temperatures of 26-30°C, neurotoxicity was seen and correlated with core temperature in all regions examined. These data indicate that ambient temperature has a significant affect on MDMA neurotoxicity, core temperature, and thermoregulation in rats. This finding has implications on both the temperature dependence of the mechanism of MDMA neurotoxicity and human use because fatal hyperthermia is associated with MDMA use in humans.

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