An acylated mannan in the membrane of Micrococcus lysodeikticus.
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Biomedical subjects
Publications and source records attributed to D A Powell.
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Rats were trained in shock-induced aggression, free operant avoidance, or were presented with unavoidable shocks. Fighting in response to shock was subsequently measured by intermatching individual animals that had received the three training procedures. The fighting probabilities of animals with histories of avoidance and dominant animals with histories of fighting were higher than the fighting probabilities of non-dominant fighting rats or rats with a history of unavoidable shocks. Animals with higher fighting probabilities disrupted avoidance baselines more than animals with lower fighting probabilities. Control experiments suggested that fighting decrements produced by administration of prior grid-shock were due to the acquisition of behaviors incompatible with aggression.
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Fighting rates between paired rats were investigated as a function of the probability of attack by a single animal. Animals from stable high-fighting and low-fighting frequency pairs were intermatched to detect individual high-fighting and low-fighting rats. Pairs of high-fighting animals then received saline or different chlorpromazine dosages during successive sessions. Finally, single high-fighting members of each pair also received the different drug dosages. The chief findings were that: (a) rats showing high fighting rates when matched against each other revealed low fighting rates when matched against one, but not the other member of a low-fighting pair; and (b) high-fighting rats decreased their fighting rates as their own or their opponent's chlorpromazine dosage increased. These results indicated that a low rate of fighting on the part of one rat results in a low fighting rate on the part of its opponent.
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Several recent studies have investigated relationships between post-traumatic stress disorder (PTSD) and learning and memory problems. These reports have found in general that not only does PTSD affect trauma-related memories, but when patients with PTSD are compared with similar trauma patients without PTSD, general memory impairments have been found. The present paper reports a study in which associative learning, using Pavlovian eyeblink conditioning, was investigated in combat veterans with and without chronic PTSD, using interstimulus intervals of 500 and 1000 msec in two separate experiments. Although several recent reports suggest that larger-magnitude autonomic conditioned responses occur in patients with PTSD during Pavlovian conditioning, the present study found evidence of impaired Pavlovian eyeblink conditioning in combat veterans with and without PTSD, compared to non-combat veterans. Although these data suggest that combat leads to an impaired associative learning process regardless of whether PTSD is apparent, a group of community-dwelling combat veterans not under medical treatment showed normal conditioning, suggesting that variables other than prior combat must also be involved.
It has become clear from the study of different response systems during classical conditioning that some responses are acquired quite rapidly and others show a much slower rate of acquisition. The most often studied rapidly acquired responses have been classically conditioned autonomic changes (e.g., heart rate); the slowly acquired responses most often studied are skeletal responses, such as the eyeblink or leg flexion response. Although there are various other differences between rapidly acquired and slowly acquired responses, we have suggested that the most important difference is the possibility that they represent different stages of the learning process. In the present review I describe research in our laboratory that has focused on conditioned bradycardia as a model system of a rapidly acquired associative system and contrast it with the more slowly acquired Pavlovian conditioned eyeblink response. I also describe the generality of conditioned bradycardia and discuss the differential role of subdivisions of the prefrontal cortex as a substrate for mediating this response. Finally, I briefly discuss the other brain areas involved in conditioned bradycardia, and its functional significance as it relates to the learning process.
Using the New Zealand albino rabbit as an animal model, it has been determined that the medial prefrontal cortex is intimately involved in, and may be necessary for, acquisition of classically conditioned bradycardia. The interconnected nuclei of the medial thalamus, most notably the mediodorsal nucleus, conversely appear to be associated with the development of the tachycardia that accompanies classical conditioning of the eyeblink and nictitating membrane response. Neuroanatomical, electrophysiological, brain stimulation, and lesion data are reviewed, which support the conclusion that the prefrontal-thalamic axis is intimately involved in acquisition of classically conditioned visceral changes.
Two experiments were conducted to ascertain the cardiovascular accompaniments of differential Pavlovian jaw movement (JM) conditioning. The first examined the blood pressure (BP) changes that accompany the tachycardiac conditioned responses (CRs) associated with JM conditioning. The BP response in all instances consisted of a depressor response that was greater to the reinforced CS+ than CS-, although the magnitude of the CR was quite small. The second experiment determined the effects of peripheral autonomic antagonists on the cardiac accelerations associated with JM conditioning. It was found that the peripheral vagal antagonist methyl scopolamine completely abolished responses to both CS+ and CS-, whereas atenolol, a beta adrenergic antagonist, augmented the response, compared to saline control injections. The JM responses were also affected by the autonomic blockades, with minimal responding occurring in the scopolamine group but slightly more JM CRs in the atenolol group, compared to saline control animals. These results suggest that the major cardiovascular response to an appetitive stimulus, which evokes JM conditioning, consists of cardiac accelerations with the BP depressor responses playing a minimal, if any, role. Moreover, these conditioned cardiac increases appear to be due solely to the release of vagal inhibition.