Naloxone attenuates rat’s preference for signaled shock

Abstract

Rats were confined and given signaled shock on one side of a shuttlebox and unsignaled shock on the other side. Preference tests revealed that rats injected with the opiate antagonist naloxone during training showed no subsequent side preference, whereas saline control rats preferred the signaled side. The second and third experiments showed that this naloxone effect could not be due to state-dependent learning (generalization decrement), interference with exploratory activity, or the drug making the signal aversive. The results suggest that release of endogenous analgesic substances may constitute a central nervous system preparatory response which mediates a preference for signaled shock. Given a choice between two situations, one in which aversive electric shock is reliably preceded by a stimulus and one in which identical aversive events are not signaled, rats typically choose the signaled shock situation (Lockard, 1963). If rats are given controlled exposure to both conditions (signaled and unsignaled shock), and therefore receive an equivalent number, duration and intensity of shock, they spend most of their time in the place where accurate temporal information is given about shock, even if tests are made in the absence of shock and signals (Collier, 1977). The rat behaves as if the signaled shock was less aversive than the unsignaled shock. It has been suggested that the signal allows the animal to make a preparatory response which modifies the aversiveness of the shock (Biederman &

Classically conditioned tail flexion in rats: CR-contingent modification of US intensity as a test of the preparatory response hypothesis

“…Recently, Marlin, Sullivan, Berk, .and Miller (1979), using a modified version of the PSS preparation, reported that a preference remained after differences in signaled safety had been eliminated as contributing factors and information-seeking had been rejected on the particulars of the data. Their results were consistent with those of D ' Amato and Safarjan (1979), and Fanselow's (1979) observation that naloxone attenuates PSS in rats suggests that part of the PR may include the release of endogenous opiates. As a consequence of observing this preference in a situation in which two of the three traditional explanations of the PSS effect could be discounted, Marlin et aI.…”

Triggering of the endorphin analgesic reaction by a cue previously associated with shock: Reversal by naloxone

“…However, their lack of conditioning controls leaves open the possibility that these effects were due simply to the unconditioned effects of the shock US and were not a conditioned triggering of the endogenous analgesic system by the CS. Other evidence for triggering of the endogenous analgesic system by a signal predicting shock was reported by Fanselow (1979), who found that naloxone attenuates the rat's preference for signaled shock. This result suggests that the rat prefers signaled shock because the signal causes conditioned release of endogenous opiates that reduce the aversiveness of the shock on the signaled side.…”

Naloxone pretreatment enhances shock-elicited aggression

“…According to this model, fear-provoking stimuli that trigger defensive behavior should also trigger the endogenous analgesic system. Support for the model comes from findings that show that, in the presence of fear-provoking stimuli, such as innately recognized predators (Blanchard & Blanchard, 1971) or stimuli associated with electric shock (Chance, White, Krynock, & Rosecrans, 1978;Fanselow, 1979; Fanselow & Bolles, 1979b), an animal is more tolerant of nociceptive stimuli. The analgesia produced by stimuli associated with electric shock seems to be mediated by endogenous opiates, since these stimuli increase endogenous opiate activity in the brain (Chance et aI., 1978), and the analgesia produced by these stimuli is eliminated by the opiate antagonist, naloxone (Fanselow, 1979; Fanselow & Bolles, 1979b).…”

“…Support for the model comes from findings that show that, in the presence of fear-provoking stimuli, such as innately recognized predators (Blanchard & Blanchard, 1971) or stimuli associated with electric shock (Chance, White, Krynock, & Rosecrans, 1978;Fanselow, 1979; Fanselow & Bolles, 1979b), an animal is more tolerant of nociceptive stimuli. The analgesia produced by stimuli associated with electric shock seems to be mediated by endogenous opiates, since these stimuli increase endogenous opiate activity in the brain (Chance et aI., 1978), and the analgesia produced by these stimuli is eliminated by the opiate antagonist, naloxone (Fanselow, 1979; Fanselow & Bolles, 1979b).We have applied this model to posts hock freezing, one of the defensive behaviors of the rat (Fanselow & Bolles, 1979a). As the nociceptiveness of shock is increased, by increasing the current flow through the animal, the amount of postshock freezing likewise increases (Blanchard & Blanchard, 1969; Fanselow & Bolles, 1979a).…”