Interpersonal perception in group therapy: a social relations analysis.

Although group therapists have emphasized the importance of interpersonal perception and feedback during therapy, there has been little systematic research on how group members form impressions of one another. D.J. Kiesler's (1983) interpersonal circle provides a framework for studying interpersonal perception and relations. Twenty-seven women and 18 men from 9 time-limited therapy groups reported their impressions of their fellow group members using the Impact Message Inventory, and they also completed 2 self-report scales. A social relations analysis of this data indicated that Subjects' perceptions included both assimilation and consensus. There was also a relationship between how Subjects saw themselves before therapy and how they were seen by other group members. The results demonstrated the utility of the social relations model for group therapy research and provided modest support for Kiesler's interpersonal circle.

Antagonism by d-amphetamine of trimethyltin-induced hyperactivity evidence toward an animal model of hyperkinetic behavior.

In male rats of the Long-Evans strain, either 7.0 mg/kg of trimethyltin (TMT) or 0.9% NaCl was administered by intragastric gavage. After a period of recovery from the typical signs of trimethyltin toxicity, each rat was tested at 72-hr intervals for its locomotor activity in an open field apparatus, the floor of which was divided into square grids. The baseline activity of each of the trimethyltin-treated rats was significantly greater than the saline-treated controls. d-Amphetamine, injected intraperitoneally in a dose of 0.5 or 2.0 mg/kg, augmented the hyperactivity of the trimethyltin-treated animals. However, a 4.0 mg/kg dose of d-amphetamine markedly attenuated the hyperactivity of trimethyltin-treated rats while elevating that of the controls. Since trimethyltin produced an autism-like behavioral disorder involving hyperactivity, preservation, aggressiveness and impairment in problem-solving and memory function, the placating effect of amphetamine supports the proposition that the pathology due to trimethyltin may represent an experimental analogue to the hyperkinetic syndrome in children.

Effect of hippocampal lesions produced by intracerebroventricular kainic acid on alcohol drinking in the rat.

An alcohol self-selection test was first given to adult male rats of either the Sprague-Dawley or Long-Evans strain in which the concentrations available with water were increased from 3% to 30% over an eight-day period. Subsequently, the animals were anesthetized and, using stereotaxic procedures, a 1.2 or 2.4 nmole dose of kainic acid was infused bilaterally into the cerebral ventricle (ICV) over a 30-sec interval and in a total volume of 10 microliters. When the same alcohol self-selection test was repeated two weeks post-operatively, alcohol intake was significantly suppressed in terms of both g/kg intake per day as well as proportion of alcohol to water selected. Alcohol intake of the control rats infused with the CSF carrier vehicle was unchanged. When a much longer interval of 7-10 min was used to infuse the 2.4 nmole dose of kainic acid ICV, the intake of alcohol of this group also was not significantly changed. Post-mortem histological analysis of forebrain tissue of the kainic acid infused rats confirmed cytological damage to the hippocampus, particularly in cell fields CA3 and CA4, which has been reported previously. Since the hippocampus has been implicated recently in the mechanisms underlying alcohol drinking, our results suggest that a pathological lesion of this limbic-forebrain structure could influence the degree to which alcohol is self-administered in a free-choice situation.

Action of anorexigenic peptide injected into the brain: dissociation of effect on body weight and feeding in the rat.

Previous reports on the effect of anorexigenic peptide (AXP) administered systemically in the rodent are inconsistent in terms of the effect of the tri-peptide on food intake and body weight. The purpose of this study was to examine the effect of AXP infused into the brain on these measures. In post-pubescent female rats of the Sprague-Dawley strain, guide cannulae were permanently implanted in the lateral cerebral ventricle for repeated intracerebroventricular (ICV) infusion. Postoperatively, measures of food and water intake and body weight were obtained every day at the same time. After a 7-day base-line period, AXP was infused bilaterally in a total volume of 15 microliter and in a dose of either 0.25 microgram (n=7) or 1.25 micrograms (n=5), with artificial CSF vehicle serving as the control solution (n=6). ICV infusions were given once daily for 20 consecutive days, after which the same intake and body weight measures were recorded for another 7-day period. The rats given 0.25 micrograms AXP showed a significant suppression in weight gain with the overall slope of the growth curve being 0.358. In contrast, the growth slope of the rats given the 1.25 micrograms dose of AXP was 0.621, whereas those given the CSF was 0.823. Although the trends of intake of food tended to follow the curves of the rats body weight, the difference between g/kg food intake of rats during ICV infusions of either dose of AXP was not significantly different from that of the CSF controls. Water intake also was unaffected by either dose of AXP. These results demonstrate that this tri-peptide derived from urine of patients afflicted with anorexia nervosa exerts a direct effect on the brain. Since the 0.25 micrograms dose of AXP infused acutely ICV caused a sustained hyperthermia, its mechanism of action is apparently a metabolic one; that is, the interruption in the gain in body weight of the rat is independent of the amount of food it ingests.

Imparied maze performance in the rat caused by trimethyltin treatment: problem-solving deficits and perseveration.

Trimethyltin (TMT) produces cytological damage to several limbic-forebrain structures which is accompanied by behavioral changes including hyperactivity and aggressiveness. The purpose of this investigation was to determine whether the problem-solving capacity of the rat is affected by TMT treatment. Either 7.0 mg/kg of TMT ([CH3]3SnCl) or 0.9% saline was injected by gavage into the gastric lumen of each rat. The treated and non-treated animals were divided into two groups of nine each and tested subsequently on a series of Hebb-Williams maze problems. In comparison to the controls, the tin-treated rats made markedly more errors on all but one of the maze patterns. Moreover, the rate of error reduction across problems over the 10 daily trials was significantly retarded in the lesioned animals. In addition to these severe problem-solving deficits, the TMT-treated rat often exhibited a characteristic pattern of perseverative behavior while running in the maze. The pattern was not unlike stereotypies associated with the psychomotor pathology observed following treatment with certain drugs. Overall, the results of the performance of the animal in the Hebb-Williams task provides a corollary with the child afflicted with minimal brain dysfunction (MBD) and, thus, a model for MBD is suggested.

Activity changes in rats following acute trimethyltin exposure.

The aliphatic organo-metal derivative, trimethyltin, causes marked morphological damage to the central nervous system (CNS), when the compound is administered by the intragastric route. This report describes certain behavioral consequences of [CH3]3Sn treatment. Either 7.0 mg/kg [CH3]3SnCl or 0.9% saline was injected intragastrically in male rats of Long-Evans strain divided into two equal groups of nine each. Forty days later open-field activity during a 2-min interval was measured for each rat. Following activity testing, the animals were trained to press a lever for food reinforcement on an ascending fixed-ratio series ranging from FR 2 to FR 99. The results showed that rats treated with [CH3]3SnCl were three times as active as controls in the open field, and emitted lever responses at a significantly higher rate than controls throughout the fixed-ratio series regardless of the reinforcement schedule. The possible neuropathological consequences and the relative permanence of the neurobehavioral changes following tin treatment are discussed.