Latent Inhibition Of Taste Aversion Learning Research Articles

Fornix transections disrupt the ontogeny of latent inhibition in the rat

In three experiments, we examined the ontogeny of latent inhibition in a conditioned taste-aversion paradigm. In the first experiment, 18-, 25-, and 32-day-old rats received a pairing of a 0.6% Sanka solution with an i.p. injection of LiCl (0.75% b.w., 0.4 M) or physiological saline either after four preexposures to the taste or control treatment without taste preexposure. Impairment of conditioning by taste preexposure (latent inhibition) was evident at 32 days of age, but not at 18 or 25 days of age. In Experiment 2, we investigated the possibility that our failure to observe latent inhibition in 18-day-olds resulted from the particular experimental parameters employed in Experiment 1. In Experiment 2, taste-exposure durations were longer, the retention interval between conditioning and testing was shorter, and deprivation conditions were more typical of those used with preweanling subjects. Again, no evidence of latent inhibition was found. In Experiment 3, we examined the effect of sham or fornix lesions at 18 days of age on latent inhibition at 32 days of age. Lesioned subjects exhibited equivalent conditioned taste aversions but failed to show latent inhibition. Thus, latent inhibition of taste-aversion learning develops between 18 and 32 days of age in the rat, and this development is disrupted by fornix transection during infancy. These findings suggest a role for septohippocampal maturation in the ontogeny of latent inhibition.

Role of central noradrenaline neurons in the contextual control of latent inhibition in taste aversion learning.

Three experiments were performed to examine the effects of noradrenaline (NA) depletion, using 3 different methods: lesions of the dorsal noradrenergic bundle (DB) with 6-hydroxydopamine (6-OHDA), lesions induced by neonatal treatment with 6-OHDA and lesions induced by systemic DSP4 upon latent inhibition, using the taste-aversion learning procedure. NA depleted and control (sham, vehicle or saline) rats were given pre-exposure trials to either novel saccharin or to novel saccharin in a novel type of drinking bottle (the noisy bottle). Later, during conditioning trials saccharin was presented in the noisy bottles for all the rats, followed by lithium chloride injections. Saccharin aversions, tested for in the noisy bottles, indicated considerably weaker saccharin aversions (i.e. more latent inhibition) by the control groups pre-exposed to both saccharin and the noisy bottles. These context-dependent latent inhibition effects were clearly attenuated by all 3 treatments that depleted central NA. Biochemical assays confirmed the NA depletions in each case. The results, demonstrating the intimate role of central NA neurons in contextual control of latent inhibition in taste-aversion learning, appear to conform with current attentional theories of NA function in the forebrain.

Generalized latent inhibition in taste-aversion learning

Rats were preexposed, over 9 days, to either nine different flavors or a single flavor. Then they were given a novel saccharin-lithium pairing (controls were injected with isotonic saline). Generalized latent inhibition was demonstrated in the multiflavor group: Learned aversion to the novel saccharin CS was very transient. One-flavor subjects, in contrast, demonstrated a strong and lasting aversion to saccharin.

Conditioned and latent inhibition in taste-aversion learning: Clarifying the role of learned safety.

Conditioned and latent inhibition in taste-aversion learning: Clarifying the role of learned safety.

Conditioned and latent inhibition in taste-aversion learning: clarifying the role of learned safety.

Experiments 1-3 investigated the applicability of the classical conditioning concept of conditioned inhibition to taste-aversion learning. Rats made ill after drinking saccharin and subsequently administered a "safe" exposure to saline (or casein hydrolysate) evidenced an enhanced preference for the safe fluid (relative to either a third, slightly aversive, solution or to water) when compared to controls in which saccharin was not previously poisoned. Such active condition inhibition was significantly reduced in Experiment 4 when two safe exposures to saline preceded saccharin-illness pairings. These results indicate that conditioned inhibition can be established in a taste-aversion procedure and that a latent inhibition manipulation reduces the ability of a taste to become a signal for safety. Implications of these findings for the learned safety theory of taste-aversion learning and the relevance to bait-shyness of principles established within the classical conditioning paradigm are considered.