Morphine-induced suppression of conditioned stimulus intake: Effects of stimulus type and insular cortex lesions

Abstract

Intake of an unconditionally preferred taste stimulus (e.g., saccharin) is reduced by contingent administration of a drug of abuse (e.g., morphine). We examined the influence of insular cortex (IC) lesions on morphine-induced suppression of an olfactory cue and two taste stimuli with different levels of perceived innate reward value. Two major findings emerged from this study. First, morphine suppressed intake of an aqueous odor as well as each taste stimulus in neurologically intact rats. Second, IC lesions disrupted morphine-induced suppression of the taste stimuli but not the aqueous odor cue. These results indicate that the perceived innate reward value of the CS is not a factor that governs drug-induced intake suppression.

Role of the insular cortex in morphine-induced conditioned taste avoidance

“…Thus, it would appear that the failure of ICX rats to show the same degree of conditioned taste avoidance as SHAM subjects at asymptote in the present study cannot be explained as a consequence of a lesion-induced deficit in the perception of taste danger/novelty. Nor, as shown by the normal performance of the ICX rats in the morphine-induced odor avoidance experiment of Lin et al (2009b), can this deficit in the present study be attributed to a disruption in the detection/processing of the morphine US.…”

“…An immediately obvious candidate is that the lesions may blunt sensitivity to the US property of morphine that is responsible for taste avoidance. However, this account appears untenable because Lin et al (2009b) found that ICX rats showed normal acquisition of morphine-induced odor avoidance in a procedure that was identical to the taste avoidance task. Thus, the failure of ICX rats to show the same level of taste avoidance as SHAM-Morphine subjects cannot be reduced to a deficit in the perception of, or responsivity to, the US property of the morphine drug state.…”

“…However, that earlier research employed CS presentations that were only 5 min in duration. As shown by Lin et al (2009b) such short CS access may obscure important differences because of a ceiling effect in consumption, if not always in the drug-injected experimental rats then certainly in the saline-injected control subjects. To avoid this problem, the present work used 15-min CS access periods, a duration that also permits more direct comparison with our research on the effects of IC lesions on toxicosis-induced CTA learning.…”

“…Our earlier experiment, like that of Geddes et al (2008), involved 5-min CS access per trial. Recent research (Lin, Roman & Reilly, 2009b) indicates that such a short access time may obscure important group differences, which become evident only when the CS is available for 15 min, because of a tendency towards ceiling effects in the fluid consumption of the water deprived rats. Additionally, to maintain comparability with our earlier experiment, the rats were trained (trials 1–13) using our standard 15-mg/kg dose of morphine.…”

Role of the gustatory thalamus in taste learning

“…Of particular relevance to present purposes, bilateral lesions of either the GC or BLA disrupt taste neophobia which is characterized by an elevated intake of the novel taste stimulus on first encounter and a subsequent latent inhibition-like delay in the acquisition of CTAs [25,32,30,33,57,41,64]. A similar elevated consumption of a novel taste CS was seen in the GTX rats in the present study but this deficit appeared to have no influence on the rate of taste aversion learning.…”