Basolateral amygdala lesions in the rat produce an abnormally persistent latent inhibition with weak preexposure but not with context shift

The role of test context in latent inhibition of conditioned inhibition: Part of a search for general principles of associative interference

“…Thus, in Experiment 2, test behavior was consistent with whatever was previously learned in the test context (A or B). The results of Experiment 2 are in accord with analogous studies that assessed the context specificity of interference by latent inhibition on subsequent excitatory conditioning (e.g., Bailey & Westbrook, 2008; Dexter & Merrill, 1969; Gray et al, 2001; Hall & Channel, 1985; Kaplan & Lubow, 2001; Lovibond et al, 1984; Nakajima et al, 2006; Nelson & Sanjuan, 2006; Rosas & Bouton, 1997; Rudy, 1994; Schiller & Weiner, 2005; Zalstein-Orda & Lubow, 1995). For example, Dexter and Merrill exposed rats to a CS in one of two Skinner boxes used for test (“modified” or “unmodified”), in a holding cage, or they received no exposure.…”

“…Alternatively stated, here we assessed how test context influenced latent inhibition’s interference with conditioned inhibition, now with latent inhibition treatment and conditioned inhibition training administered in distinctively different contexts, by administering a summation test in each of these two contexts. This allowed us to compare our findings in this situation with conditioned inhibition training in Phase 2 to prior reports of test-context specificity of a latent inhibition treatment on subsequent excitatory conditioning that used analogous context shifts (e.g., Bailey & Westbrook, 2008; Gray et al, 2001; Hall & Channel, 1985; Kaplan & Lubow, 2001; Lovibond et al, 1984; Nakajima et al, 2006; Nelson & Sanjuan, 2006; Rosas & Bouton, 1997; Rudy, 1994; Schiller & Weiner, 2005; Zalstein-Orda & Lubow, 1995). Based on Bouton’s 1993 model, we expected weak conditioned inhibition to be evident in Context A relative to Context B because both nonreinforcement (i.e., latent inhibition treatment in Context A) and a second-learned relationship concerning a cue (here conditioned inhibition treatment in Context B) are posited to be context specific.…”

“…This is not surprising for two reasons. First, prior research with excitation training following a latent inhibition treatment has found latent inhibition to be context specific (despite its being the first-learned information concerning X; e.g., Bailey & Westbrook, 2008; Bouton & Swartzentruber, 1989; Gray et al, 2001; Hall & Channel, 1985; Kaplan & Lubow, 2001; Lovibond et al, 1984; Maes, 2002; Nakajima et al, 2006; Nelson & Sanjuan, 2006; Rosas & Bouton, 1997; Rudy, 1994; Schiller & Weiner, 2005; Wheeler et al, 2003; Yap & Richardson, 2005; Zalstein-Orda & Lubow, 1995). Second, Group ABA-X was tested in the context of the latent inhibition treatment (A), whereas Group ABB-X was tested in the context in which conditioned inhibition training had occurred (B), which might have allowed Context B to serve as an occasion setter for X acting as a conditioned inhibitor because in this situation conditioned inhibition was second learned (e.g., Nelson 2002, Experiment 2; see also Sissons & Miller, 2009).…”

“…Data from outcome interference preparations other than extinction also speak to the dependency of outcome interference on the test context. For instance, a context shift between a latent inhibition treatment in Phase 1 and Pavlovian excitatory conditioning in Phase 2 results in less interference with expression of the CS-US association (i.e., stronger responding) when the CS is tested in the context in which excitation was trained, compared to testing of the CS in the context of the latent inhibition treatment (i.e., ABA renewal vs. an ABB control; Bailey & Westbrook, 2008; Gray, Williams, Fernandez, Ruddle, Good, & Snowden, 2001; Hall & Channel, 1985; Kaplan & Lubow, 2001; Lovibond, Preston, & Mackintosh, 1984; Nakajima, Takahashi, & Blaisdell, 2006; Nelson & Sanjuan, 2006; Rosas & Bouton, 1997; Rudy, 1994; Schiller & Weiner, 2005; Zalstein-Orda & Lubow, 1995) or in a novel context (Bouton & Swartzentruber, 1989; Maes, 2002; Wheeler, Chang, & Miller, 2003; Yap & Richardson, 2005). Moreover, when a latent inhibition treatment is administered in Context A and excitatory conditioning is administered in Context B, a greater decrement in excitatory responding has been observed in Context C relative to Context B than is seen with the same context switch without the initial latent inhibition treatment.…”

From attention to memory along the dorsal-ventral axis of the medial prefrontal cortex: some methodological considerations

“…Weakened latent inhibition is produced experimentally either by using a low number of stimulus pre-exposures or a high number of conditioning trials (Weiner and Arad, 2009). Indeed, such parametric manipulations have been found to be critical to the demonstration of the effects of lesions in BLA or core NAc and which do not disrupt latent inhibition under conditions which reliably produce latent inhibition in control (in this case sham-operated) animals, but which enhance latent inhibition under behavioral conditions known to be insufficient to produce latent inhibition in controls (Gal et al, 2005; Schiller and Weiner, 2005). In one previous study which similarly examined the effects of lesions to mPFC under conditions which did not produce latent inhibition in controls (in this case using a high number of conditioning trials), still no effects of mPFC lesions were demonstrated (Schiller and Weiner, 2004).…”