Studies on the neural mechanisms of baitshyness in rats

Abstract

The effects on taste aversion learning of lesions in a variety of brain areas known to alter taste avoidance and/or shock avoidance behavior were examined in 72 adult male rats. Bilateral lesions of the medial frontal cortex, orbital or sulcal frontal cortex, cingulate cortex, caudate nucleus. medial thalamus, or hippocampus failed to significantly alter taste aversion learning, while bilateral lesions to the amygdala impaired this learning. Lesions to the septum produced equivocal results. There does not appear at present to be a general conceptual framework that can account for the data described here as well as do previous studies in the literature.

Strength of conditioning determines the effects of septo-hippocampal lesions on taste aversion learning

“…Perhaps the most striking of these differences is the nature of the UCS employed. For example, four of the five studies that reported no impairment of taste aversion acquisition after large hippocampal lesions (Kolb et al, 1977;Murphy & Brown, 1974;Thomka & Brown, 1975; present study) used LiCl as the US; the fifth (Miller et al, 1975) used cyclophosphamide. On the other hand, two of the three studies reporting an acquisition deficit after hippocampal lesions (Best & Orr, 1973;Krane et al, 1976) used apomorphine as the US; the third (Miller et al, 1971) used X-ray.…”

“…Best and Orr (1973) and Miller et al (1971) had previously reported that hippocampal lesions disrupt taste aversions learned under weak conditioning paradigms that paired a preferred sacch~rin C.S and an apomorphine or X-ray US. At the tlme thls research was conducted, there were no such reports in which LiCI had served as the US, although, in one study that preceded this one, Kolb et al (1977) found a taste aversion deficit in rats with septal lesions when LiCl served both as the US and CS.l This result suggested that under appropriate conditions, septo-hippocampal lesions might disrupt taste .aversions supported by LiCl. The second expenment tested this notion by pairing a preferred sucrose CS with a reduced dose of LiCl as the US.…”

“…The procedure was essentially the same as that reported by Kolb et al (1977). The animals were adapted to a 23 Y2-h water-deprivation schedule for 1 week prior to testing.…”

“…In these studies, locomotor passive avoidance was severely disrupted, but taste aversion learning was unaffected by the lesions. However, other studies have reported deficits either in the acquisition or extinction of a conditioned taste aversion after lesions of th~ septum (Kolb, Nonneman, & Abplanalp, 1977) or the hippo-campus (Best & Orr, 1973;Krane, Sinnamon, & Thomas, 1976;McFarland, Kostas, & Drew, in press;Miller, Elkins, Fraser, Peacock, & Hobbs, 1975;Miller, Elkins, & Peacock, 1971). These studies differ in a number of respects, including size and location of the lesion within the septo-hippocampal system, the nature of the CS, the nature and route of administration of the US, presence or absence of preconditioning exposure to the CS, the dependent measures employed, and a number of other procedural variables.…”

“…This interpretation is consistent with the results of a number of other studies as well. In general, those studies reporting large hippocampal lesions that include the fimbria (Krane et aI., 1976;Miller et aI., 1971) report a stronger disruption of conditioned taste aversion than do those studies with lesions that largely spare the fimbria (Kolb et al, 1977;McGowan et aI., 1972;Murphy & Brown, 1974;Thomka & Brown, 1975). In like manner, those studies using restricted septal lesions that largely spared the fimbria-fornix (Hobbs et aI., 1974;McGowan et aI., 1969;McGowan et aI., 1972) found no taste aversion deficit, whereas Kolb et ai.…”