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Biomedical subjects

R A Rosellini

Publications and source records attributed to R A Rosellini.

27 records · Page 2Linked to original sources

Cross-motivational effects of inescapable shock are associative in nature.

Exposure to inescapable shock interferes with the subsequent acquisition of an appetitive operant. This deficit may be due to either associative interference or activity reduction from the inescapable shock pretreatment. The relative importance of these two factors was examined by using an appetitive response choice discrimination procedure and concurrently measuring activity. Experiment 1 demonstrated separate associative and activity effects of inescapable shock, in that the animals exposed to inescapable shock made more incorrect responses than controls and were lower in activity. Experiment 2 demonstrated that these effects resulted from the uncontrollability of the shock, not from shock exposure per se. In Experiment 3, residual effects of inescapable shock were investigated by exposing animals to discrimination reversals. On these tests, inescapably shocked animals showed performance inferior to nonshocked controls, a result indicating that the effects of inescapable shock are not completely reversed by experience with contingent reward in the discrimination task. No evidence of an activity deficit was observed during this discrimination reversal. These results strongly suggest that associative factors play a more important role than activity reduction in mediating the effects of inescapable shock, at least when these are measured in an appetitive context.

Animals↗

Frustation and learned helplessness.

This article reports the transfer of learned helplessness from one aversive motivator, shock to another, frustration. In experiment 1, animals were trained to approach food in a runway and concomitantly exposed to either escapable, inescapable, or no shock in a different situation. Extinction was conducted in the runway, and subsequently the animals were tested for hurdle-jump escape from the frustrating goal box. Inescapably shocked rats failed to learn to hurdle-jump, whereas escapably or nonshocked animals learned the frustration escape response. Experiment 2 replicated the basic finidngs of Experiment 1 and showed transfer of learned helplessness from shock to frustration when no running response had been first acquired in the runway.

Animals↗

Learned helplessness in the rat: time course, immunization, and reversibility.

Rats, like dogs, fail to escape following exposure to inescapable shock. This failure to escape does not dissipate in time; rats fail to escape 5 min, 1 hr., 4 hr., 24 hr., and 1 wk. after receiving inescapable shock. Rats that first learned to jump up to escape were not retarded later at bar pressing to escape following inescapable shock. Failure to escape can be broken up by forcibly exposing the rat to an escape contingency. Therefore, the effects of inescapable shock in the rat parallel learned helplessness effects in the dog.

Animals↗

Conditioned fear exacerbates acute morphine dependence.

A variety of physical stressors have been shown to enhance reactivity to opioid drugs. Few studies have examined the effects of nonphysical stressors on opioid drug reactivity. In this regard, it has previously been shown that animals administered morphine in the presence of shock-associated cues demonstrate increases in hypoalgesia relative to nonshock control animals. These findings have typically been viewed as being mediated by the activation of endogenous pain inhibition systems via conditioned fear. In this series, we further examined the nature of these effects by assessing the effects of conditioned fear on acute morphine dependence. Experiment 1 revealed that animals administered 3 mg/kg morphine in the presence of context fear cues demonstrated an enhanced withdrawal response when removed and administered 3 mg/kg naloxone. Because it is known that conditioning effects do not diminish over time, a second experiment examined whether the enhancement of acute dependence by context fear would still be evident 72 h postconditioning. As in Experiment 1, animals administered morphine in a context associated with shock demonstrated an enhancement of acute dependence. Experiment 2b revealed that the shock parameters used in these studies can induce a hypoalgesic response on the test that is opioid mediated. These findings are discussed with regard to the neuroanatomy of fear systems as they relate to the neuropharmacological study of opioid withdrawal.

Animals↗

Sudden death in the laboratory rat.

Vulnerability to sudden death was produced in laboratory rats by manipulating their developmental history. Rats who were reared in isolation died suddenly when placed in a stressful swimming situation. Handling of these singly-housed rats from 25 to 100 days of age potentiated the phenomenon. However, animals who were group housed did not die even when they had been previously handled.

Animals↗

Acquisition of an unsignalled avoidance task in rats exposed to alcohol prenatally.

Although numerous studies have investigated the effects of prenatal alcohol exposure on both passive and active avoidance, its effect on an unsignalled, or Sidman, avoidance task has not been ascertained. Rats consumed liquid diets containing either 35% or 0% ethanol derived calories (EDC's) during days 6 thru 20 of pregnancy. These liquid diets were isocaloric and a pair-feeding procedure was employed. An ad lib lab chow control group was also included. At approximately 60 or 120 days of age, female offspring were tested for 2 hours on each of 3 consecutive days. Shock was programmed to occur every 10 seconds unless a response was made, in which case the next shock was postponed for 20 seconds. The results demonstrated that prenatal alcohol exposure produced a facilitation in the acquisition of this task at both ages. The 35% EDC offspring made significantly more responses than controls and received fewer shocks. In addition, an analysis of interresponse times for the older animals revealed that the 35% EDC group learned to space their responses better than control animals. Possible explanations of the facilitation in Sidman avoidance performance shown by the 35% EDC progeny are discussed in terms of an inhibition deficit.

Animals↗