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Rats were made sodium deficient by furosemide injection and then offered 20 min of access to 0.05 M NaCl mixed with the sodium channel blocker amiloride. Compared with a sodium deficient control group that was also offered 0.05 M NaCl, these rats drank very little. A subsequent test conducted in the same manner with 20 min of access to 0.3 M NaCl mixed with amiloride produced similar results. It is concluded that amiloride blocks the neural information required for generating the attractive taste of NaCl to the sodium deficient rat.

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The antinociceptive effects of signaled shock and its physiological underpinnings were examined in two experiments. In Experiment 1, rats were exposed to one of three shock conditions: no shock, unsignaled shock, and signaled (by a 10-s, 1000-Hz tone) shock. In each condition the rats were tested hourly in the absence of tones for nociception, with vocalization to shock used as the behavioral measure. Rats receiving signaled shocks had stomach ulcer scores intermediate between those of no-shock and unsignaled shock animals. The signaled shock rats also displayed a pronounced vocalization antinociception effect. This suggested that signaled shock may be less aversive. Experiment 2 was designed to investigate a possible role of endogenous opiate peptides in these effects. In Experiment 2, animals received hourly injections of either the opiate antagonist naltrexone (7 mg/kg, ip) or saline. There were no significant effects of naltrexone on either stomach pathology or nociception scores. The same effects of signaled shock were obtained as in Experiment 1. It is concluded that the role of endogenous opiates in the effects of signaled shock seen here is minimal.