Latent inhibition as a performance deficit resulting from CS—context associations

The strain-specific involvement of nucleus accumbens in latent inhibition might depend on differences in processing configural- and cue-based information between C57BL/6 and DBA mice

GABA transmission in the ventral pallidum is not involved in the control of latent inhibition in the rat

In three conditioned taste aversion experiments with rats, latent inhibition (LI) was examined as a function of the time interval (1 or 21 days) between the conditioning and the test phases. In Experiments 1 and 2, the effects of US intensity on LI were examined. LI increased in the 21-day condition, as compared with the 1-day condition, with medium and high US intensity, but not with weak US intensity. Groups not preexposed to the CS flavor had similar aversions when testing was conducted 1 day after conditioning, as compared with 21 days. In Experiment 3A, delay-induced super-LI was obtained when the delay was spent in the home cage and the experimental stages took place in a different context (as in Experiments 1 and 2). In Experiment 3B, when all the stages, including the delay period, were conducted in the home cage, there was no super-LI effect. The modulation of delay-induced super-LI as a function of US intensity and context extinction is discussed in relation to association deficit and retrieval interference theories of LI.

Associative learning and latent inhibition in a conditioned suppression paradigm in humans

Effects of agonists and antagonists at the GABA/benzodiazepine receptor on conditioned suppression in rats

Three experiments with rats demonstrated that preexposure to an experimental environment retarded the level of conditioned freezing observed on a test in that environment after it had been paired with mild footshock. Furthermore, Experiment 1 demonstrated that this latent inhibition effect could be abolished if preexposed rats were exposed to a second experimental environment following conditioning to the preexposed environment. Experiments 2 and 3 demonstrated that this second environment had to be similar, but not identical, to the preexposed environment, and that the influence of exposure to the second environment on latent inhibition could be abolished by exposure to that environment prior to footshock conditioning. These results are considered in terms of the Dickinson-Burke (1996) theory of retrospective revaluation, and their implications for experiments demonstrating a loss of latent inhibition across a delay are considered.

P.3.d.006 Effects of postnatal intermittent hypoxia on prepulse inhibition and locomotor activity in rats

Removing the bar in an appetitive lever-press task, the effects of number of CS-US pairings (1, 2, or 4), modality of the CS (2 tones vs light and tone) and prior CS habituation trials on the development of discriminated conditioned suppression were evaluated. Two or 4 CS-US pairings produced virtually a perfect discrimination with complete suppression to CS and little suppression to CS−. In addition there was a significant interaction of modality × shock, indicating that going from CS+ to CS− had far less effect when the stimuli were in the same modality (T-T) than when modality changed (L-T). The effect of habituation training on suppression while not significant was in the expected direction, attenuating suppression to both CS+ and CS−.

Three experiments were conducted to examine the effect of assessment procedure, either conditioned punishment extinction or conditioned suppression reacquisition, on the associative outcome of backward conditioning in the rat. Each experiment consisted of three phases: (a) magazine and barpress training; (b) Pavlovian training in which groups received one of backward, explicitly unpaired, or no presentation of a conditioned stimulus (CS) and unconditioned stimulus (US); and (c) either conditioned punishment or conditioned suppression transfer of training tests. In Experiment 1, backward conditioning resulted in excitatory associative effects during the conditioned punishment test. In Experiment 2, backward conditioning produced excitatory conditioning when assessed by a conditioned suppression reacquisition test. In Experiment 3, a number of backward conditioning parameters were manipulated, and backward pairings yielded facilitative reacquisition relative to the unpaired group, but did not differ from the no-treatment control group. The pattern of results suggests that backward conditioning produces qualitatively similar outcomes when assessed by a conditioned punishment extinction or conditioned suppression reacquisition test.

Effect of naloxone on conditioned suppression in rats.

Loss of control by a less valid or by a less salient stimulus compounded with a better predictor of reinforcement

We utilized a potent, selective, and orally‐bio‐available antagonist with documented engagement with nociceptin receptors (NOP) to assess antidepressant‐ and anxioltyic‐related effects of blockade of NOP receptors. The NOP receptor antagonist, Cpd 1, displayed antidepressant‐like neurochemical and behavioral effects in rats and mice. Serotonin outflow in rat prefrontal cortex was enhanced without affecting norepinephrine or dopamine. Correspondingly Cpd 1 decreased immobility in the forced swim test (FST). Cpd 1 augmented the effects of fluoxetine without changing target occupancies of either drug. Anti‐immobility effects of Cpd 1 were absent in mice without NOP receptors. Cpd 1 also produced anxiolytic‐like effects in some rodent models: decreased stimulus‐elicited freezing in mice and decreased stress‐induced hyperthermia in rats. Cdp 1 was not active in: marble‐burying in mice, novelty‐suppressed feeding in mice, conditioned suppression in rats, punished food‐maintained responding in rats, and the 4‐plate test in mice. Cpd 1 did not disrupte performance in 5‐choice serial reaction time tests or delayed matching‐to‐position in rats. Cpd 1 was mildly wake promoting in rats. These data suggest that Cpd 1 has unique antidepressant‐ and anxiolytic‐related pharmacological effects in rodents.

With number of preexposures constant latent inhibition increases with preexposure CS duration or total CS exposure

Extinction is the reduction in drug seeking when the contingency between drug seeking behavior and the delivery of drug reward is broken. Here, we investigated a role for the nucleus accumbens shell (AcbSh). Rats were trained to respond for 4% (v/v) alcoholic beer in one context (Context A) followed by extinction in a second context (Context B). Rats were subsequently tested in the training context, A (ABA), or the extinction context, B (ABB). Pre-test injections of the glutamate AMPA receptor antagonist, NBQX (1 µg) into AcbSh had no effect on renewal of alcoholic beer seeking when rats were returned to the training context (ABA). However, NBQX increased responding when rats were tested in the extinction context (ABB). In a second experiment, rats received training, extinction, and test in the same context. Pre-test injections of NBQX (0, 0.3, and 1 µg) into the AcbSh dose-dependently attenuated expression of extinction. We also found that NBQX in the AcbSh had no effect on initial acquisition of extinction or the motivation to respond for reward as measured by break point on a progressive ratio schedule. Finally, we show that pharmacological disconnection of a basolateral amygdala (BLA) → AcbSh pathway via NBQX in AcbSh combined with reversible inactivation of the contralateral BLA attenuates expression of extinction. Together, these results suggest that AcbSh AMPA receptors mediate expression of extinguished reward seeking through glutamatergic inputs from the BLA.

Two groups of rats--1 with electrolytic lesions of the hippocampus and 1 consisting of sham-operated controls--received flavor-aversion conditioning with 2 flavors. All subjects had received prior nonreinforced exposure to Flavor A. Latent inhibition was apparent in slower acquisition of the aversion to Flavor A than to Flavor B. Hippocampal lesions had no effect on acquisition to the nonpreexposed Flavor B but produced a marked enhancement of the latent inhibition effect. The contrast between this result and previous findings of an attenuation of latent inhibition in subjects with hippocampal lesions is discussed.